Volume 35 June 2009 Number 1 - University of Mosul

Annals of 

the College 

of Medicine 

Mosul 

Volume 35 June 2009 Number 1 

Editorial Board 

Taher Q. AL‐DABBAGH 

Hisham A. Al‐ATRAKCHI 

Budoor A. K. AL‐IRHAYIM 

Kahtan B. IBRAHEEM 

Ilham K. AL‐JAMMAS 

Sahar K. OMAR 

Rami M. AL‐HAYALI 

Editor 

Deputy Editor 

Member 

Member 

Member 

Member 

Member & Manager 

Faiza A. ABDULRAHMAN 

Administration 

A publication of the College of Medicine, University of Mosul, Mosul, Iraq


the College 



(Ann Coll Med Mosul) 

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ISSN 0027-1446 

CODE N: ACCMMIB 

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the College 



CONTENTS 

Volume 35 Number 1 June 2009 

Childhood mortality in Mosul city during the year 2007 

Amaema A. Al-Zubeer………………………………………………………………………………...………1- 7 

Effect of amlodipine on serum lipid profile in hypertensive patients 

Ashraf H. Ahmed, Rami M. A. Al-Hayali………………………………………………………………….… 8- 12 

Bell’s palsy in Mosul 

Estabrak M. Alyouzbaki………………………………………………………………………...….……….. 13-17 

Effects of dairy-products' consumption on sebum lipids and fatty acids 

Y.Y. Al-Tamer, A. A. Mahmood…………………………………………………………………………...… 18-25 

Spontaneous healing of traumatic perforations of the tympanic membrane 

Salim H. Al-Obiedi………………………………………………………………………………………..…... 26-32 

Platelet indices in the differential diagnosis of thrombocytosis 

Bashar A. Saeed, Sana M. Taib, Khalid Nafih………………………………………………………….…. 33-36 

Histopathological changes of decidua and decidual vessels of early pregnancy 

Rana A. Azooz, Noel S. Al-Sakkal……………………………………………………………………....…. 37-41 

Seasonal variation of glycated hemoglobin A 1c % among diabetic patients in Mosul 

Nabeel N. Fadhil, Omar A. Jarjees………………………………………………………………..…….….. 42-49 

The prevalence of fatty liver disease among diabetics in Mosul 

Dhaher J. S. Al-Habbo, Younise A. Khalaf, Nabeel Alkhiat, Ali K. Habash……….……………….…… 50-57 

Diagnostic laparoscopy in female infertility 

Raida M. Al-Wazzan, Entessar Abdel Jabbar………………………………………………………...….… 58-64 

Coronary angiographic findings among diabetic and non-diabetic patients 

Dhiyaa A. Alhamadani, Fakher Y. Husain, Mahmood A. Abbo ………………………………………..… 65-72 

Renin – angiotensin system (RAS) and hypertensive disease 

"From the link in pathophysiology to the outcomes of inhibition" 

Asim M. Al-Chalabi …………………………………………………………….………….………….….…… 73-86 

Case report: Accidental cooking gas intoxication 

Dhaher J. S. Al-Habbo…………………………………………………………………….………….….…… 87-92 

Printing of this issue was completed on Mar, 2010.

Annals of the College of Medicine Vol. 35 No. 1, 2009 

Childhood mortality in Mosul city during the year 2007 

Amaema A. Al-Zubeer 

Department of Community Medicine, College of Medicine, University of Mosul. 

(Ann. Coll. Med. Mosul 2009; 35(1): 1-7). 

Received: 20 th May 2008; Accepted: 24 th Sept 2008. 

ABSTRACT 

Objectives: To calculate infant and under five mortality rates and to find out the most common 

causes of death among children. 

Methods: 

Study period: The study was done over a period of one month, during Dec. 2007. 

Study design: Rapid epidemiological survey using UNICEF “last birth technique”. 

Study setting: The study was done at Al-Hadbaa Primary Health Care Center in Mosul city. 

Study population: Data was collected from 1046 mothers in child bearing age (15-49 years), who were 

attending at the antenatal clinic by direct interviewing using a questionnaire form based on the model 

formulated by UNICIF for childhood mortality survey. 

Results: The present study showed that the estimated under five mortality rate is 107 /1000 of last 

live births which represents a rise of 2.5 fold since WHO Maternal and Child Mortality Survey was 

done at 1990 in Iraq. The Infant mortality rate was estimated to be 95.6 death / 1000 of last live births. 

The study also showed that the neonatal mortality (0-28 days) constitutes 40.9/1000 last live birth 

which accounts for 42% from all deaths that occur during 1 st year of life. Other findings showed that 

more than a quarter of all causes of deaths among under five were related to respiratory problems 

and 15.5% of all causes were linked to congenital abnormalities. Diarrheal disease accounted for 

8.6% of causes. 

Conclusion: Results showed that under five mortality is still considered a major health problem and 

reflecting defect in health system of the community, needs to be re-evaluated and minimized to be as 

least as possible. 

الخلاصة 

أهداف البحث:‏ لحساب وفيات الأطفال دون السنة ودون الخامسة من العمر في مدينة الموصل ولاآتشاف سبب الوفاة 

الأآثر شيوعا بين الأطفال.‏ 

طريقة إجراء البحث:‏ تم إجراء مسح وبائي سريع باستخدام حساب تقنية الولادة الأخيرة التابع لليونيسيف في مرآز الحدباء 

أماً‏ تتراوح 

جمعت العينات من للرعاية الصحية الأولية في مدينة الموصل خلال مدة شهر في آانون الثاني من النساء اللواتي يراجعن عيادة رعاية الحوامل بواسطة المقابلة المباشرة مستخدمين استمارة 

أعمارهن من استبيان معتمدة على موديل مصاغ من اليونيسيف لمسح وفيات الأطفال.‏ 

أخر ولادة 

وفاة لكل النتائج:‏ أظهرت الدراسة الحالية أن المعدل المحسوب لوفيات الأطفال دون الخامسة هو حية والتي تمثل ارتفاع بمقدار مرتين ونصف منذ مسح منظمة الصحة العالمية لوفيات الأمومة والطفولة الذي تم في 

أخر ولادة حية.‏ 

وفاة لكل في العراق.‏ أن المعدل المحسوب لوفيات الرضع دون السنة من العمر هو من آل 

أخر ولادة حية والتي تمثل لكل يوم)‏ تشكل آما وأظهرت الدراسة أن وفيات الخدج الوفيات الحاصلة خلال السنة الأولى من الحياة.‏ نتائج أخرى أظهرت أنه أآثر من ربع أسباب وفيات الأطفال دون الخامسة 

%٤٢ 

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٩٥,٦ 

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٤٠,٩ 

٢٨ -٠) 

،(٤٩-١٥) 

١٩٩٠ 

© 2009 Mosul College of Medicine 1


من آل 

من آل الأسباب مرتبطة بتشوهات خلقية بينما يشكل الإسهال لها علاقة بالمشاآل التنفسية و الأسباب.‏ 

الاستنتاج:‏ أظهرت النتائج أن وفيات الأطفال دون الخامسة من العمر ما تزال تعتبر مشكلة صحية مهمة وتعكس الخلل في 

النظام الصحي للمجتمع،‏ و تحتاج إلى تقييم و تحسين.‏ 

% ٨,٦ 

%١٥,٥ 

C 

hildren are the future of society and their 

mothers are guardians of that future (1) . 

Pregnancy, child birth and their consequences 

are still the leading causes of death, disease 

and disability among women of reproductive 

age in developing countries 

(2) . Childhood 

mortality which comprises infant mortality rate 

and under five mortality rate are key indicators 

used internationally, nationally and locally as a 

sensitive but not specific way of comparing 

health status and development within 

countries (3) . Under five mortality rate is also a 

good reflection of the general wellbeing of 

children in an area (4, 5) . Across the world there 

is an overall downward trend in under five 

mortality rates (6, 7) . However, this trend was 

showing sign of slowing lately, though till the 

year 2005, almost 11 million children under 

five years of age died from causes that are 

largely preventable globally. Among them are 

4 million who will not survive the first month of 

life 

(1,8) . Poor or delayed care-seeking 

contributes up to 70% of child death. More 

than 50% of all child deaths globally occur in 

just six counties: China, the Democratic 

Republic of Congo, Ethiopia, India and 

Pakistan (8) . There are several factors 

contributing to the death of infants and 

children (9) , these include socio-demographic 

status of family, level of community 

development and education, (availability, 

access and quality of health services) with 

neonatal mortality is associated with maternal 

health and access to care around the time of 

delivery and the presence of preventive and 

curative health services (10,11) which in fact are 

still poor in Iraq. 

The aim of the present study is to determine 

the under five mortality in the catchment area 

of Al- Hadbaa Primary Health Care Center in 

Mosul city during the year 2007 using rapid 

epidemiological survey and to find out the 

most common causes of death among the 

study sample. 

Specific objective 

To estimate the under five mortality rate, 

infant mortality rate and neonatal mortality 

among the study sample. 

To find out the most common causes of 

death among children under five years of age. 

To compare the estimated present under five 

mortality rates with previous rates that have 

been estimated in Iraq. 

Methods 

The survey was conducted at Al-Hadbaa 

Primary Health Care Center which represents 

one of the most crowded centers in Mosul city. 

The study sample included 1046 mothers in 

child bearing age (15-49 years) who attended 

at the antenatal clinic in the center which 

represent 87% of all mothers attending the 

center during one month period. This center 

has a catchment area of approximately 13000 

women in child bearing age and 11500 

children under five years (12) . The study was 

conducted during Dec. 2007. A questionnaire 

form was prepared using “last birth technique” 

module formulated by UNICEF for childhood 

mortality survey in developing countries (11) . 

The questionnaire included information about 

mother’s age, previous deliveries and the outcome 

of each delivery, causes of death if 

present and age of child at death. It was 

reviewed with teaching staff of community 

department to assess its validity which was 

92%. Results approach was applied on it to 

measure the reliability of the answers, and it 

was correct in 81%. Filling up the 

questionnaire form was done by direct 

interview with the mothers at the antenatal 

clinic. The response rate was 97%. In addition 

to that, the investigator had visited the 

Statistical Unit in Nineveh Health Office and 

Al-Khannsa Hospital and the under five 

mortality rates were calculated from the 

registered deaths in the records of those units 

for comparison purposes. 



Age specific parity was calculated by dividing 

the number of children ever born in a specific 

age group over the total number of mothers in 

that age group. The under five mortality rates 

were calculated by dividing the total number of 

children died below five years over the total 

number of last live birth multiplied by one 

thousand. Similar procedure was done to 

calculate the infant and neonatal mortality 

rates (13,14) . 

Data collection, computer feeding, tabulation 

and statistical analysis were conducted by the 

investigator herself using Minitab statistical 

software version XIII. Chi square test was 

used and odds ratio for finding association. 

Results 

Table (1) shows that the overall estimated 

under five mortality rate is 107 / 1000 live 

births. From the analysis of data of the present 

study, the estimated infant mortality rate is 

95.6 deaths/1000 last live birth. Neonatal 

mortality (0-28 days) constitutes 40.9/1000 last 

live birth which account for 42% of all deaths 

that occur during 1 st year of life. The table also 

indicates that less than five mortality is higher 

among age group (45-49), as it reaches 208.5 

per 1000 live births. 

Table (2) represents the estimation of risk of 

under five deaths among women age 45-49 

years in comparison with the other age groups. 

Children whose mothers’ age among the age 

range 45-49 year have significantly 2 fold risk 

of under five death than other children 

(OR=2.2, 95% CI= (1.510, 2.917), P value 


Table (3): Age distribution of women with their total children ever born and average parity 

No. of children ever born Average 

Mother’s age group All women 

parity 

Male Female Total /mother 

15- 48 32 24 56 1.16 

20- 298 315 289 604 2.02 

25- 228 279 319 598 2.62 

30- 140 255 281 536 3.82 

35- 176 469 435 904 5.13 

40- 113 389 355 744 6.58 

45-49 43 166 118 284 6.60 

Total 1046 1905 1821 3726 Sum 

Table (4): Distribution of death cases by causes and sex 

Causes Male Female Total Percent 

Respiratory* problem 59 36 95 26.38 

Congenital abnormality 27 29 56 15.55 

Fever* 22 27 49 13.6 

Premature 15 18 33 9.1 

Diarrhea* 15 16 31 8.6 

Unknown* 18 12 30 8.3 

Others** 36 30 66 18.3 

Totals 192 168 360 100% 

*These causes are classified under international classification of diseases 10 th revision (15,16,17) . 

**Others: Include injury, accidents, meningitis, septicemia. 

Discussion 

Childhood mortality rates are used to 

determine the level of human and economic 

development of the country (18,19) . The present 

survey indicates that under five mortality rates 

is 107/1000 last live birth which represents 2.5 

fold rise of under five mortality rates estimated 

by UNICIF/WHO maternal and child mortality 

survey done at 1990 which was 41/1000 live 

birth (20 ,21) . The results that were obtained from 

the vital registration system show that the 

estimated under five mortality for the year 

2007 is 24/1000 live birth and the infant 

mortality rate is 19.5/1000 live birth that occur 

during the year 2007. Another datum that has 

been taken from the Statistics Unit of Al- 

Khannsa Hospital shows more or less similar 

results as under five mortality rate was 

32/1000 live birth and the IMR was 28.58/1000 

live birth. These findings yield that only 20.4 % 

of all infant mortality which occurred has been 

registered and only 22.4 % of real under five 

mortality has been registered as compared 

with the present survey results (22) . Similarly, 

almost one third of deaths (29.8 %) has been 

registered in Al-Khannsa Hospital Statistical 

Unit for both infant and under five mortality 

when compared with the result of the present 

survey (23) . This is due to information on deaths 

from the health information system, 

unfortunately, does not reflect the mortality 

picture from population perspective because it 

is government facility – based data and thus 

does not include deaths that occur outside 

such facilities or from private heath institutions 

(24) . In many developing countries, vital 

registration data are incomplete. The severity 

of the under-reporting varies from country to 

country, and also varies over time within 



countries (25) . This under reporting of the 

registration system represents the top of the 

iceberg phenomena (14) . Birth history 

information from surveys provides the most 

robust estimation of infant and child mortality 

(12, 26) . 

A survey done at rural area near Mosul 

during 1992 showed rise in under five mortality 

rates of 61 death /1000 live birth (28) . Another 

survey done at Al-Zangelle district in Mosul 

city during the year 2002 showed that under 

five mortality rates was 166/1000 live birth (29) . 

The present study picture may reflect slight 

decline in childhood mortality since 2002 but it 

is still very high and unless progress is 

accelerated significantly, there is little hope of 

reducing child mortality by two thirds by the 

target date of 2015 – the targets set by the 

millennium declaration (8) . Globally there is 

decline in the child mortality as mentioned by 

WHO (8) , while, the actual number of deaths is 

highest in Asia 

(30,31) , the rates for both 

neonatal deaths and still births are greatest in 

Sub Sahara Africa (27) . In addition to that, it 

was reported that there are some regions of 

the world which underwent humanitarian crisis 

where mortality rates are “stagnating” and Iraq 

is one of these regions (8) . A study done during 

2004 for estimation of mortality before and 

after 2003 invasion of Iraq showed that the risk 

of death was estimated to be 2.5 higher after 

invasion when compared with pre invasion 

period (32) . The present study revealed that 

there is a steady increase in the average parity 

per mother with increase of age of mothers. 

This gives explanation of why mortality rate is 

still stagnating because modest reductions of 

mortality rates are too small to keep up with 

the increasing numbers of births (8) . 

The present study also showed that the 

estimated infant mortality rate is 95.5 / 1000 

last live birth and neonatal mortality is 40/ 

1000 last live birth. Thus the neonatal mortality 

constitutes 42% of all deaths that occur during 

1 st year of life. Across the world, newborn 

deaths contribute to about 40 % of all deaths 

in children under five years of age and more 

than half of infant mortality (8) . A survey done 

by UNICEF at early nineties showed that infant 

mortality rate was 32 per thousand live births 

during 1990 and increased afterwards to 93 

deaths per thousand live births 1994 (20) . 

Another result of the present study indicated 

that the most common cause of deaths among 

under five was respiratory problems as they 

constitute 26.3% of all causes, these problems 

occur most commonly within the 1 st year of life. 

Across the world, deaths among under five are 

still attributable to just handful of conditions 

that are avoidable through existing 

interventions 

(1) . These are acute lower 

respiratory infection mostly pneumonia (10%) 

of all death, diarrhea (15%), measles (4%), 

HIV/AIDS (3%), and neonatal conditions and 

mainly preterm birth, birth asphyxia and 

infections (37%) (8) . The present study also 

revealed that mortality among males is higher 

than females; this could be due to boys being 

more frail than girls. Many studies had 

confirmed this trend in mortality (19, 24) . 

Conclusions and recommendations 

There is high rate of childhood mortality 

recognized in Mosul city during the year 2007 

together with the presence of high fertility rate 

and so there is an urgent need for strategy for 

prevention of childhood mortality in Iraq 

through health services provision and 

socioeconomic development and improvement 

of family planning facilities. 

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http://image.thelancet.com/extras/04art103 

42web.pdf 7. 



Effect of amlodipine on serum lipid profile 

in hypertensive patients 

Ashraf H. Ahmed*, Rami M. A. Al-Hayali** 

*Department of Pharmacology, ** Department of Medicine, College of Medicine, University of Mosul. 


Received: 24 th Oct 2007; Accepted: 30 th Nov 2008. 

ABSTRACT 

Objectives: To assess the effect of amlodipine, as monotherapy, in hypertensive patients, on serum 

lipid profile, as assessed by serum cholesterol, serum triglyceride, high density lipoprotein cholesterol 

(HDLC), and low density lipoprotein cholesterol (LDLC). 

Subjects and methods: Thirty three hypertensive patients were included in the study, 25 of them 

were males and 8 were females. Serum cholesterol, triglyceride, HDLC and LDLC were measured 

before and after 2 months of starting treatment with amlodipine. 

Results: No significant difference could be found between the pre and post treatment levels of all 

measured parameters. 

Conclusion: Treatment with amlodipine does not produce deleterious effect on lipid profile, so it may 

be a suitable therapy in a hypertensive patient with underlying hyperlipidaemia. 


أهداف البحث:‏ أجريت هذه الدراسة لتقييم تأثير عقار الاملودبين آعلاج أحادي لمرضى ارتفاع ضغط الدم الشرياني على 

مستوى الكولسترول،‏ الدهون الثلاثية،‏ البروتين الشحمي عالي الكثافة،‏ والبروتين الشحمي منخفض الكثافة.‏ 

المشارآون وطرق العمل:‏ أجريت الدراسة على مريضا مصابا بارتفاع ضغط الدم الشرياني،‏ مريضا منهم من 

الذآور و ٨ من الإناث.‏ تم قياس مستوى الكولسترول،‏ الدهون الثلاثية،‏ البروتين الشحمي عالي الكثافة،‏ والبروتين الشحمي 

منخفض الكثافة قبل وبعد شهرين من بدء العلاج بعقار الاملودبين.‏ 

النتائج:‏ أظهرت نتائج الدراسة عدم وجود فرق معنوي في مستوى القيم المقاسة قبل وبعد العلاج.‏ 

الاستنتاج:‏ العلاج بواسطة عقار الاملودبين لايؤثر على مستوى الدهون في الدم وقد يكون علاجا مناسبا لمرضى ارتفاع 

ضغط الدم اللذين يعانون من اضطرابات في مستوى الدهون.‏ 

٢٥ 

٣٣ 

A 

rterial hypertension is one of the major 

risk factors for atherosclerosis and 

coronary artery disease, and its treatment has 

proved to be beneficial for preventing those 

pathologies. Because dyslipidaemia has been 

frequently associated with arterial hypertension, 

being also a strong risk predictor of 

coronary artery disease, one could assume 

that antihypertensive drugs should not have 

unwanted effects on lipid profile (1) . It has been 

suggested that the metabolic side effects of 

antihypertensive drugs are responsible for 

their failure to reduce cardiovascular morbidity 

in patients with hypertension. Treatment with 

some antihypertensive agents may cause 

unwanted changes in the lipid profile, 

attenuating their beneficial antiatherogenic 

effects of blood pressure reduction (2) . Beta 

blockers and thiazids may adversely affect the 

lipid profile and consequently increase the risk 

for coronary atherosclerosis (3,4) . On the other 

hand, angiotensin converting enzyme (ACE) 



inhibitors, such as captopril, seem to have a 

neutral effect, or even improve lipid profile in 

hypertensive hypercholesterolaemic individuals 

(5) . Little information is available about the 

effect of calcium channel blockers, hence, the 

present study was undertaken to evaluate the 

effect of amlodipine, a long-acting 

dihydropyridine calcium channel blocker, on 

the serum lipid profile. 

Patients and methods 

This study was conducted from April to 

August 2007 on a number of hypertensive 

patients referred from their attending 

physicians. The inclusion criteria were as 

follows: newly diagnosed hypertensive 

patients who did not previously start any 

antihypertensive therapy. They should be free 

from other organic diseases especially hepatic 

and renal diseases. Patient with history of 

heart failure, ischemic heart diseases, 

diabetes as well as smokers and alcoholic 

were excluded from the study. Their treating 

physicians should decide that they need no 

other drug apart from the antihypertensive 

agent. Out of 66 patients, 47 met the above 

inclusion criteria and were included in this 

study. 

Patients were instructed to continue the 

same diet which they were taking in the past 2 

months prior to commencement of the study. 

Careful follow up made sure that no drug was 

added during the 2 months of the study; 

especially considering the last 2 weeks. 

A total of 33 patients successfully completed 

the study. Out of these, 25 patients were 

males and 8 were females. The mean age of 

patients was 40.03 ± 7.63 years, with the 

range of 28 to 55 years. They received 

amlodipine as monotherapy in a mean dose of 

7.27 ± 2.75 mg, ranging from 2.5-10 mg/day. 

The lipid profile was done before starting the 

treatment and at the end of 2 months. The 

serum was collected in the morning after 14 

hours fasting. Serum total cholesterol, 

triglycerides, and high density lipoprotein 

cholesterol (HDLC) were directly estimated. 

The low density lipoprotein cholesterol (LDLC) 

was calculated using Freidwald formula. 

Paired t-test was used to compare the 

differences between the obtained values 

before and after treatment. 

Results 

The effect of amlodipine on the lipid profile of 

the patients has been shown in table (1). No 

significant difference could be found between 

the pre and post treatment levels. 

Table (1): Effects of amlodipine on serum cholesterol, triglycerides, HDLC and LDLC. 

Parameters 

Before treatment 

Mean ± SD 

After treatment 

Mean ± SD 

P value 

Total Cholesterol 

mg/dl 

161.72 ± 27.15 

160.45 ± 25.67 

NS 

Triglycerides 

mg/dl 

115.72 ± 28.89 

116.00 ± 28.25 

NS 

HDLC 

mg/dl 

53.93 ± 3.23 

54.06 ± 2.68 

NS 

LDLC 

mg/dl 

84.48 ± 24.32 

83.54 ± 22.60 

NS 

NS: not significant. 

Discussion 

The present study reveals no statistically 

significant alteration on either serum 

cholesterol, triglycerides, HDLC and LDLC 

levels. 

The effects of antihypertensive drugs on lipid 

profile vary with both the pharmacological 

class and the individual drugs. Because 

adverse metabolic effects probably reduce the 



benefit of blood pressure reduction therapy 

(6,7) , many studies have examined the effects 

of different antihypertensive agents on lipid 

levels. Although there is a general consensus 

that thiazide diuretics and nonselective β- 

blockers adversely affect lipid levels, many 

areas of disagreement still exist about the 

effects of other antihypertensive agents on 

lipids. Most authors agree that alpha blockers 

(8-12) 

reduce triglyceride levels, and many 

authors have concluded that ACE inhibitors do 

not affect lipids (13-15) . 

The findings of the current study are in line 

with the results of other authors (16-19) , as they 

all found that calcium antagonists as a group 

have no significant effects on lipids. This study 

prospectively evaluated the impact of 

amlodipine, as a relatively new calcium 

channel blocker, on lipid profile in hypertensive 

patients, as this drug is increasingly used in 

clinical practice. 

Drug-induced changes in lipid levels may be 

particularly important in hypertensives, since 

up to 40 percent of untreated patients with 

essential hypertension and many patients with 

borderline hypertension already have lipid 

abnormalities (20) . The relative change in blood 

pressure and lipid levels may have different 

effects on cardiovascular risk, depending on 

baseline levels. Thus, a reduction in blood 

pressure in persons with severe hypertension 

may decrease risk substantially, even if lipids 

are adversely affected. Conversely, treating 

mild hypertension with agents that increase 

cholesterol levels may be counterproductive 

(21) . For the same amount of blood pressure 

reduction, agents that adversely affect lipids 

may cause less reduction in cardiovascular 

disease. Indeed, this may partially explain why 

trials with diuretics and β-blockers failed to 

reduce cardiovascular disease as much as 

would have been expected from the degree of 

blood pressure reduction (22) . Whether newer 

agents that reduce blood pressure without 

adversely affecting lipids will more favorably 

affect cardiovascular disease remains to be 

proven in controlled clinical trials. Meanwhile, 

the result of this study provides additional 

information suggesting that amlodipine has no 

effects on serum lipid profile. 

In two similarly conducted studies (in Japan 

and Brazil), amlodipine did not influence 

plasma lipids adversely. In both studies, serum 

total, LDL, and HDL cholesterol were not 

altered, while serum triglycerides and VLDL 

cholesterol were significantly reduced. Similar 

beneficial effect on triglycerides level was not 

noticed in our study, however (23, 24) . 

Beyond the neutral effect of amlodipine on 

traditional serum lipid profile, a new study has 

shown that amlodipine significantly reduced 

oxidized LDL, an important atherogenic 

component of LDL (25) . 

Studies on rats provided additional favorable 

mechanism of amlodipine as a vasoprotective, 

beyond its blood pressure lowering effect; 

where two studies have shown that amlodipine 

does not only inhibit atherosclerotic plaque 

formation, but also regresses atherosclerosis. 

These effects are at least partly due to 

inhibition of oxidative stress and inflammatory 

response (26, 27) . 

AVALON study (28) is a recent multicentre that 

confirmed the safety, effectiveness, and 

tolerability of amlodipine and atorvastatin 

given together as a single pill for the treatment 

of coexisting hypertension and 

hyperlipidaemia. This is considered the first 

version of a polypill to treat these two common 

disorders. 

In conclusion: as far as serum lipid profile 

was concerned, amlodipine can be considered 

a safe antihypertensive drug in hypertensive 

patients with dyslipidaemia. 

References 

1. Kaplan NM. Treatment of hypertension: 

remaining issues after the Anglo- 

Scandinavian cardiac outcomes Trial. 

Hypertension 2006; 47: 10-13. 

2. Krone w, Nagele H. Effects of 

antihypertensive on plasma lipids and 

lipoprotein metabolism. Am Heart J 1988; 

116: 1729-1734. 

3. Ames RP, Hill P. Raised serum lipid 

concentrations during diuretic treatment of 

hypertension: a study of predictive 

indexes. Clin Sci Mol Med Suppl. 1978; 

4:311s-314s. 



4. Leren P, Helgoland A, Holeme I, Foss PO, 

et al. Effect of propranolol and prazocin on 

blood lipids. Lancet 1980; 2: 4-6. 

5. Ferrara LA, Marino LD, Russo O, et al. 

Doxazosin and captopril in mildly 

hypercholesterolemic hypertensive 

patients. The doxazosin- captopril in 

hypercholesterolemic hypertensive study. 

Hypertension 1993; 21: 97-104. 

6. Stokes JD, Kannel WB, Wolf PA, Agostino 

RB, et al. Blood pressure as a risk factor 

for cardiovascular disease. The 

Framingham study-30 years of follow up. 

Hypertension 1989; 13(5 Suppl): 113-8. 

7. Collins R, Peto R, MacMahon S, Hebert P, 

et al. Blood pressure, stroke, and coronary 

heart disease. Part 2, Short-term 

reductions in blood pressure: overview of 

randomized drug trials in their 

epidemiological content. Lancet 1990; 

335:827-38. 

8. Kannel WB, Carter BL. Initial drug therapy 

for hypertensive patients with 

hyperlipidemia. Am Heart J. 1989; 

118:1012-21. 

9. Lardinois CK, Neuman SL. The effects of 

antihypertensive agents on serum lipids 

and lipoproteins. Arch Intern Med. 1988; 

148:1280-8. 

10. Weidmann P, Ferrier C, Saxenhofer H, 

Uehlinger DE, et al. Serum lipoproteins 

during treatment with antihypertensive 

drugs. Drugs 1988; 35(Suppl 6):118-34. 

11. Giles TD. Antihypertensive therapy and 

cardiovascular risk. Are all 

antihypertensives equal? Hypertension 

1992; 19(1 Suppl):I124-9. 

12. Grimm RH Jr. Antihypertensive therapy: 

taking lipids into consideration. Am Heart 

J. 1991; 122:910-8. 

13. Ames RP. Antihypertensive drugs and lipid 

profiles. Am J Hypertens 1988; 1:421-7. 

14. Ames RP. The effects of antihypertensive 

drugs on serum lipids and lipoproteins. I. 

Diuretics. Drugs. 1986; 32:260-78. 

15. Black HR. Metabolic considerations in the 

choice of therapy for the patient with 

hypertension. Am Heart J. 1991; 121:707- 

15. 

16. Chait A. Effects of antihypertensive agents 

on serum lipids and lipoproteins. Am J 

Med. 1989; 86(Suppl 1B):5-7. 

17. Hunninghake DB. Effects of celipridol and 

other antihypertensive agents on serum 

lipids and lipoproteins. Am Heart J. 1991; 

121: 696-701. 

18. Raftery EG. The metabolic effects of 

diuretics and other antihypertensive drugs: 

a perspective as of 1989. Int J Cardiol. 

1990; 28:143-50. 

19. Verma RB, Chaudhary VK, Jain VK. Effect 

of calcium channel blockers on serum lipid 

profile. J Postgrad Med. 1987; 33(2): 65- 

68. 

20. Julius S, Jamerson K, Mejia A, Krause L, 

et al. The association of borderline 

hypertension with target organ changes 

and higher coronary risk. Tecumseh blood 

pressure study. JAMA 1990; 264: 354. 

21. Neaton JD, Wentworth D. Serum 

cholesterol, blood pressure, cigarette 

smoking, and death from coronary heart 

disease. Overall findings and differences 

by age for 316,099 white men. Multiple 

Risk Factor Intervention Trial Research 

Group. Arch Intern Med. 1992; 152:56-64. 

22. MacMahon S, Peto R, Cutler J, Collins R, 

et al. Blood pressure, stroke, and coronary 

heart disease. Part 1, Prolonged 

differences in blood pressure: prospective 

observational studies corrected for the 

regression dilution bias. Lancet. 1990; 

335:765-74. 

23. Sanjuliana AF, Barraso SG, Fagundes 

VGA, Rodriguis MLG, Netto JF, et al. 

Moxonidine and amlodipine effects on lipid 

profile, urinary sodium excretion and 

caloric intake in obese hypertensive 

patients. Am L Hypertes 2000;13:620-8 

24. Ahaneku JE, Sakata K, Urano T, Takada 

Y, Takada A. Lipids, lipoproteins, and 

fibrinolytic parameters during amlodipine 

treatment for hypertension. J Health Sc. 

2000;46:455-8 

25. Muda P, Kampus P, Teesalu R, Zimer K, 

Ristimäe T, Fischer K, et al. Effect of 

amlodipine and candesartan on oxidized 

LDL level in patients with mild to moderate 



essential hypertension. Blood Press 

2006;15:313-8 

26. Toba H, Nakagawa Y, Milki S, Shimizu T, 

Yoshimura A, Inoue R, et al. Calcium 

channel blockades exhibit antiinflammatory 

and oxidative effects by 

augmentation of endothelial nitric oxide 

synthase and inhibition of angiotensin 

converting enzyme in N(G)-nitro-L-arginine 

methyl ester- induced hypertensive rat 

aorta: vasoprotective effects of amlodipine 

and manidipine. Hypertens Res 

2005;28(8):689-700. 

27. Yoshii T, Iwai M, Li Z, Chen R, Ide A, 

Fukunga S, et al. Regression of 

atherosclerosis by amlodipine via antiinflammatory 

and anti-oxidative actions 

Hypertens Res 2006;29(6):457-66 

28. Messeri FM, Bakris GL, Ferrera D, 

Houston MC, Petrella RJ, Flack JM, et al. 

Efficacy and safety of co administered 

amlodipine and atorvastatin in patients 

with hypertension and dyslipidaemia; 

results of the AVALON trial. J Clin 

Hypertens (Greenwich) 2006;8(8):571-81. 



Bell’s palsy in Mosul 

Estabrak M. Alyouzbaki 

Department of Medicine, College of Medicine, University of Mosul. 


Received: 4 th Nov 2008; Accepted: 4 th Jan 2009. 

ABSTRACT 

Objective: To study the incidence, sex, age, and seasonal distribution of Bell’s palsy in Mosul. 

Methods: A prospective study of patients with Bell’s palsy from outpatient and private neurological 

clinic and Neurophysiological Unit in Ibn Sena Teaching Hospital in Mosul conducted between 

September 2001 to August 2003. The patient's age, sex and time of occurrence of Bell’s palsy were 

recorded. 

Result: the total number of the patients was 469, male patients were 207 and females were 262. The 

higher number of cases was recorded in the cold months, adult affected more than other age groups. 

Conclusion: Bell’s palsy is the commonest cause of lower motor neuron facial nerve palsy; herpes 

simplex has been claimed as a cause of the condition. 

Keywords: Bell’s palsy; facial nerve; facial nerve paralysis. 

للمرضى الذين أصيبوا بشلل العصب الوجهي ‏(القحفي 

الى آب الخلاصة 

هذه الدراسة أجريت للفترة من أيلول 

السابع)‏ والذين قاموا بمراجعة العيادات الاستشارية والخاصة لأمراض الجملة العصبية في مستشفى ابن سينا التعليمي في 

من الإناث 

منهم الموصل.‏ وقد وجد ان عدد الذين تم فحصهم ووجدوا انهم يعانون من هذه الحالة المرضية بلغ و‎٢٠٧‎ من الذآور،‏ وان أعلى نسبة من الإصابات سجلت في خلال أشهر الشتاء.‏ إلا ان هذا العدد لايمثل العدد الحقيقي 

للمرض حيث ان أعدادا آبيرة لاتراجع الأطباء بسبب بعض المعتقدات والتقاليد الخاطئة.‏ آما وجد ان أآثر الأعمار عرضة 

للإصابة بهذا الشلل هم البالغون وخصوصا مابين ٢٠-٤٠ سنة.‏ وانها قد تكون نتيجة لإصابة سابقة بفيروسHSV 

تنصح هذه الدراسة بمعالجة هذه الحالات مبكرا بعقاقير الكورتيزون ومضادات الفيروسات لتفادي تشوه في الوجه 

وخاصة في الحالات الشديدة.‏ 

. 

٢٦٢ 

٤٦٩ 

٢٠٠٣ 

٢٠٠١ 

S 

ir Charles Bell first described the anatomy 

and function of the facial nerve in the 

(1, 2) 

1800s Bell's initial description of facial 

palsy related to facial paralysis caused by 

trauma to the peripheral branches of the facial 

nerve. However, the terms "Bell's palsy" and 

"idiopathic facial paralysis" may no longer be 

considered synonymous (3, 4) . 

The onset of Bell's palsy can be frightening 

for patients, who often fear they have had a 

stroke or have a tumor and that the distortion 

of their facial appearance will be permanent. 

Bell’s palsy is the sudden onset of unilateral 

lower motor neuron dysfunction of the seventh 

cranial nerve that results in the paralysis of the 

facial muscles on the affected side of the face. 

Facial weakness is often preceded or 

accompanied by pain about the ear. 

Weakness generally comes on abruptly but 

may progress over several hours or even a 

day or so. Depending upon the site of the 

lesion, there may be associated impairment of 

taste, lacrimation, or hyperacusis. There may 

be paralysis of all muscles supplied by the 



affected nerve (complete palsy) or variable 

weakness in different muscles (incomplete 

palsy). Clinical examination reveals no 

abnormalities beyond the territory of the facial 

nerve. Most patients recover completely 

without treatment, but this may take several 

days in some instances and several months in 

others. It is generally accepted that there is 

inflammation and oedema of the nerve in the 

facial canal but, not surprisingly, there have 

been few pathological studies. A viral aetiology 

is suspected (5-6) . Although Bell’s palsy is a 

well-known and relatively common condition, 

its epidemiology is unclear. 

For this study, we estimated the numbers of 

patients who develop Bell’s palsy and their 

distribution along the year. In addition, we 

studied the independent effects of climate, and 

season on the incidence of the disease. 


Incident cases were defined as those patients 

whose first Bell’s palsy diagnosis occurred 

during the study period. 

Patients were searched to identify visits that 

resulted in a primary diagnosis of Bell’s palsy 

(International Classification of Diseases, Ninth 

Revision, Clinical Modification code 351.0) 

from outpatients and private clinics between 

September 2001 to August 2004. 

The diagnosis of Bell's palsy can usually be 

made clinically in patients with (i) a typical 

presentation, (ii) no risk factors or preexisting 

symptoms for other causes of facial paralysis, 

(iii) absence of cutaneous lesions of herpes 

zoster in the external ear canal, and (iv) a 

normal neurologic examination with the 

exception of the facial nerve. 

The Köppen system, originally developed in 

the early 1900s, is a widely recognized and 

commonly used climate classification system (7, 

8) . The system groups land areas into climatic 

categories based on characteristics (e.g., 

extremes, ranges, central tendencies) of 

temperature, rain, and aridity 

(9) . For our 

analyses, we used the Köppen classification of 

"dry climate" as our single indicator of climate, 

since it could be directly applied to Mosul area 

and was not highly correlated with other 

factors under investigation (i.e. season). 

Result 

The total number of patients that have been 

seen from September 2001 to August 2004 

and the distribution of patients during the study 

period including the number of male and 

female patients and their percentage are 

shown in the following table: 

Year 

No. of 

patients 

Males 

Females 

2001-02 168 77(45.8%) 91(54.2%) 

2002-03 141 59(41.8%) 82(58.2%) 

2003-04 160 71(44.3%) 89(55.7%) 

469 207(44.1%) 262(55.9%) 

The total number of patients was 469, 

females were affected more than males. 

The following chart (No.1) shows the 

distribution of patients during the months of 

the year which shows peak incidence during 

winter months particularly December followed 

by January, and there is clear decline of the 

incidence during hot time especially summer 

months: 



Age distributions of the incidence of Bell’s 

palsy are seen in chart (No. 2), which shows 

that peak incidence of the condition is mainly 

in adult more than young or elderly people. 

Discussion 

Although Bell’s palsy is a well-known and 

relatively common condition, its epidemiology 

is unclear. Estimates of the incidence of this 

disease in the United States range from 13 to 

34 cases per 100,000 per year (10) ; worldwide, 

estimates range from 11.5 to 40.2 cases per 

100,000 per year (11) . The number of Bell’s 

palsy patients which have been recorded in 

this study, actually it does not reflect the real 

number of the condition in our locality as large 

number of the patients doesn’t consult doctors 

because of some old religious belief. In 

addition to that nearly a similar number of 

patients are seen by GP or physicians and not 

neurologist. Most studies have found 

comparable rates between males and 

females (12) . In this study it is clear that females 

were affected more than males; this is in 

agreement with a study done in USA where 

the incidence rate of Bell’s palsy was slightly 

higher for females than for males (crude rate 

ratio=1.12) (13) . Several studies have suggested 

that Bell’s palsy is more common among 

young and middle-aged adults (5) , although 

others have documented rates that increased 

with age (12) but in our study adults affected 

more and incidence decreased in middle age 

and elderly (chart No. 2). Findings of 

associations between the risk of developing 

Bell’s palsy and seasonal (11, 14) , geographic (5) , 

racial/ethnic (11) , and environmental (15) factors 

have been inconsistent. In this study the 

geographical and racial/ ethnic factors were 

not included as they need multicenter studies 

involving all Iraq. 

In this study crude incidence rates during the 

colder months of the year (November to 

March) were consistently higher than the 

incidence rates during the warmer months of 

the year (May to September) (chart No.1). This 

is in agreement with other studies where Bell’s 

palsy rates were relatively high during cold 

seasons of the year too (13) . While results of 

other studies have been inconsistent in this 

regard (5,11, 16,17) ; when seasonal variations in 

Bell’s palsy rates were observed, they were 

generally lower in summer 

There are conflicting reports of clustering of 

cases, suggesting an infective aetiology, and 

recurring reports implicating herpes viruses (5, 

6) , and this may explain the high incidence and 

clustering of cases reported in this study in 

winter months. 

There is an agreement that most cases of 

Bell’s palsy are caused by reactivations of 

latent herpes virus type 1 (HSV–1) infections 

(11, 12, 18- 

of geniculate ganglia of facial nerves 22) . These reactivations lead to inflammation, 

swelling, compression, and ultimately, 

dysfunction of affected facial nerves. It is 

unclear what stimuli most commonly trigger 

these reactivations. 

If most cases of Bell’s palsy are indeed 

caused by reactivated herpes virus infections, 

then persons with prior HSV–1 infections 

should be at higher risk of Bell’s palsy than 

others in the same populations. In addition, 



persons with Bell’s palsy should be 

demographically similar to those with latent 

HSV–1 infections when populations are 

uniformly exposed to competent triggers of 

HSV–1 reactivation (13) ; this needs further 

evaluations and studies in the future. 

One study indicates that two physical 

stressors, residence in an arid climate and 

exposure to cold, are independent predictors 

of Bell’s palsy suggest that cold, dry air such 

as that in arid areas during winter months, may 

traumatize mucus membranes of the 

nasopharynx, which may, in turn, induce 

reactivations of herpes infections (13) .This may 

explain the increasing incidence of Bells” palsy 

in cold season in this study particularly if we 

knew that there is clear decrease in frequency 

and quantities of rains in the last decade in 

Mosul area. This needs future assessment as 

we don’t have well documented studies about 

the incidence and seasonal variations of Bells’ 

palsy in Iraq in the past where rainy seasons 

were longer and heavier. Results from other 

studies that examined relations between facial 

paralysis and climate were inconclusive (15, 16) , 

although a study reported an incidence rate in 

a desert climate was substantially higher than 

rates found in most other studies (11, 23) . 

One of the explanations of increased 

incidence of Bells’ palsy in dry cold weather is 

large variations in day-night temperatures 

(common in desert environments) and 

frequent, sudden, and/or prolonged exposures 

to cold outdoor air (common for worker 

personnel during winter months) may induce 

vasomotor changes in facial areas, initiate the 

development of edematous neuritis by reflex 

ischemia (24) , and/or provoke the reactivation of 

HSV–1 in ganglion cells (25) . 

Reactivation of latent HSV–1 infections may 

be triggered by certain psychological stress, 

and this is a well known facts. In this study 

there is clear evidence that a psychological 

stress may precede the development of Bells’ 

palsy in a good number of patients. 

Seasonal variation of mood due to the effect 

of changing weather (e.g., seasonal affective 

disorder) (26, 27) are well documented. 

Furthermore, depression has been 

associated with increased susceptibility to 

infectious illnesses such as the common cold 

(28) . It is possible that immunosuppression 

secondary to mood changes may explain 

some of the seasonal variation in risk of Bell’s 

palsy (13) . 

In conclusion Bell’s palsy is one of the 

common conditions which affect the facial 

nerve especially in late fall and early winter; 

early treatment of such condition with steroid 

and antiviral therapy in addition to 

physiotherapy will prevent permanent facial 

disfiguring particularly in those severely 

affected patients. 

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system of nerves of the human body. 

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1 in patients with Bell’s palsy. J Med Virol 

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1986; 2:228–32. 

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Effects of dairy-products' consumption on sebum 

lipids and fatty acids 

Y.Y. Al-Tamer *, A. A. Mahmood ** 

* Department of Biochemistry, Nineveh College of Medicine; ** Department of Chemistry, College of 

Education, University of Mosul. 


Received: 22 nd Jun 2008; Accepted: 25 th Jan 2009. 

ABSTRACT 

Objectives: To investigate the effect of intake of dairy-products on the sebum lipid components and 

fatty-acid composition. 

Patients and Methods: Sebaceous cysts were obtained, by simple surgery, from the scalp, face and 

neck of 21 men (aged 25-50 y) and divided into two groups. The first group included 11 cysts for 

subjects consuming dairy products and the second group included 10 cysts for subjects not 

consuming dairy products. Simple lipids, phospholipids (PLs), triglycerides (TGs), cholesterol (C), 

cholesterol ester (CE) and fatty acids (FAs) were removed by organic solvents extraction. The sebum 

lipid components, TGs and C, were determined enzymatically and PLs were determined using a 

colorimetric method based on the formation of a phosphomolybdate complex. Lipid components were 

separated by TLC. The separated components were hydrolyzed and their FAs were esterified by 

super dried-acidified methanol. Fatty-acid methyl esters were identified by capillary gas 

chromatography. 

Results: Compared to the non-consumers group, the consumers group exhibited a significant 

increase in lipid contents, viz, PLs and C. Concerning the FA composition of CE, PLs and TGs, n 6 - 

polyunsaturated FAs showed a higher percentage, viz. C 18:2 n 6 and C 9 ,t 11 CLA, while n 3 -polysaturated 

FAs showed a significant decrease, viz. C 20:5 n 3 . 

Conclusion: Consumption of dairy products affects the lipid content and the FA composition of 

sebum and C9,t11 Conjugated Linoleic Acid could be used as a marker for intake of dairy-product 

lipid. 


أهداف البحث:‏ دراسة تأثير تناول الحليب ومشتقاته على المواد الدهنية وترآيبة الأحماض الدهنية لمحتويات الأآياس 

الدهنية 

العينات وطرائق العمل:‏ تم الحصول على أآياس دهنية استئصلت بجراحة بسيطة من مناطق مختلفة من الجسم ‏(الرأس،‏ 

الوجه والعنق)‏ من من الذآور تراوحت أعمارهم بين سنة تم تقسيم العينات الى مجموعتين،‏ الأولى شملت 

آيسا دهنيا تم الحصول عليها من أشخاص يتناولون منتجات الحليب بصورة مستمرة في حين شملت المجموعة الثانية 

أآياس دهنية تم الحصول عليها من أشخاص لا يتناولون منتجات الحليب.‏ تم قياس المكونات الدهنية لمحتويات الاآياس 

‏(الكليسيريدات الثلاثية بطريقة انزيمية،‏ الدهون المفسفرة بطريقة لونية،‏ الكولستيرول الكلي والكولستيرول المؤستر بطريقة 

انزيمية)،‏ ثم تم تحليل الحوامض الدهنية لكل من هذه المكونات باستثناء الكولستيرول الحر،‏ بعد فصلها بواسطة 

آروماتوآرافيا الشرائح الرقيقة،‏ بطريقة آروماتوآرافيا الغاز السائل الشعري.‏ 

. 

٥٠ – ٢٥ 

٢١ 

. 

١١ 

١٠ 



النتائج:‏ بينت النتائج ان النماذج المأخوذة من أشخاص يتناولون منتجات الحليب تحتوي على نسب أعلى لجميع 

المكونات الدهنية.‏ أما الحوامض الدهنية فقد بينت النتائج ان نماذج المجموعة المستهلة لمنتجات الحليب آانت تحتوي على 

نسب أعلى من الحوامض الدهنية المتعددة الأواصر المزدوجة.‏ 

الاستنتاج:‏ ان تناول منتجات الحليب يؤثر على المحتويات الدهنية وترآيب الأحماض الدهنية للأآياس الدهنية ويعتبر 

حامض اللينوليك المزدوج مؤشرا على ذلك 

. 

T 

he sebaceous follicle, in which the 

sebaceous gland is greatly enlarged, is 

filled with keratinous material, sebum, bacteria 

and fungi. The sebum secreted from 

sebaceous glands keeps the skin of the 

human body soft and oily (1,2) . Sebum is a 

complex lipid mixture and its complete 

chemical nature has not been fully elucidated 

and it varies widely from species to species (2,3) . 

Free fatty acids (FAs), triglycerides (TGs), 

cholesterol (C), cholesterol ester (CE), 

phospholipids (PLs), squalene, wax esters and 

paraffins have all been identified in sebum (4) . 

The FA components have carbon chains up 

to C 25 and they are both saturated and 

unsaturated, the latter being essential and 

non-essential (3,5) . The characteristic features of 

hyperkeratosis and decreased barrier function 

in essential FA-deficiency can lead to plugging 

the follicle and it becomes distended by 

sebum, leading to the formation of sebaceous 

cysts (6,7) . Sebaceous cysts occurs most 

frequently on the scalp, face and neck, though 

they appear on any part of the body (8,9) . 

The components of sebum can be influenced 

by diet and hormones (1,4) . Dairy products 

contain a considerable amount of fat; more 

than 57% of its FAs are saturated, which is 

considered to be one of the common 

hypercholesterolemic factors (10,11) . Dairyproduct 

fat and meat from ruminants contain 

conjugated linoleic acid (CLA). The Cis 9 , 

trans 11 (c 9 ,t 11 ) is the major CLA isomer in dairy 

products (11,12) . It is formed as a result of 

biohydrogenation reactions carried out by 

bacteria in the rumen, producing the precursor 

trans-11 octadecanoic acid (trans-vaccenic 

acid, tVA) and by ∆9 desaturase, that converts 

tVA to c 9 ,t 11 CLA, primarily in the mammary 

gland (13,14) . Studies in animal models in which 

CLA intakes were increased showed antitumorigenic 

activity (15,16) , decreased 

atherogenesis (17) , decreased adiposity and 

increased lean body mass (18) . 

Concerning n 3 -polyunsaturated fatty acids 

(PUFAs), their percent in dairy-product fats are 

almost absent (19) . 

In this study, we describe the effect of 

consuming large amounts of dairy products on 

the lipid content and on incorporation of c 9 ,t 11 

CLA into sebum lipids of sebaceous cysts 

obtained from healthy men who were regular 

dairy-product consumers. 

Materials and methods 

The study was conducted on free-living 

subjects and was not strictly controlled for 

nutrient and energy intake but, in general, the 

subjects were divided into two groups. The first 

group (the consumers group) included 

subjects who usually consumed not less than 

250 g/day of milk, yogurt or other dairy 

products. The second group (the nonconsumers 

group) included subjects who 

consumed less than 250 g/week of dairy 

products. It is worth noting that meat, the 

second source of CLA, was taken a few times 

a week by most of the Iraqi population owing 

to its high cost and money was scarce in the 

period of growth of the sebaceous cysts and 

doing this study (2002) as a result of the 

economic sanctions imposed on Iraq (1990- 

2003). 

Sebaceous cysts were obtained by simple 

surgery (in Al-Jumhouri Hospital, Mosul) from 

the scalp, face and neck of 21 men, 25-50 

year old, who were non-smokers and free from 

any apparent metabolic disorders. The 

samples were divided into two groups. The 

first group included 11 cysts for consumers 

and the second group included 10 cysts for 

non-consumers. The cysts were immediately 

put into sterile screw-capped vials containing 3 

ml of methanol to limit the lipolytic and 



oxidative degradation of sebum-lipids before 

extraction (20) . 

Extraction of sebum lipids 

Based upon their solubility characteristics, 

two types of sebum lipid were described: 

simple lipids which could be removed with 

organic solvents, and complex lipids that 

required more drastic extraction procedures. 

The former contained PLs, free FAs, free 

sterols, hydrocarbons, sterol esters and TGs 5 . 

In the present research, 0.5 g was weighed 

from each sebaceous cyst and then the simple 

lipids were extracted by a chloroform / 

methanol (2:1, V/V) mixture to a final dilution 

1:20 W/V. The insoluble compounds in the 

homogenate were then removed by 

filtration (21) . The extract was mixed with 2 ml of 

distilled water and the mixture was allowed to 

separate into two phases, by standing in a 

separating funnel (22) . The lipid extract was 

evaporated (under nitrogen) to dryness, then 

the lipid was redissolved in 1 ml of methanol. 

Lipid analysis 

Sebum lipid components, TGs and C, were 

determined enzymatically using kits obtained 

from bioMeriux, France. The PLs were 

determined by a colorimetric method based on 

the formation of a phosphomolybdate 

complex (23) . Thin layer chromatography was 

applied to separate the lipid components, TGs, 

PLs and CEs using Merck silica gel G 0.25 

mm and hexane: diethyl ether: formic acid 

mixture(80:20:2 by volume). After drying, the 

plates were sprayed with 1% alcoholic solution 

of 2,7-dichlorofluorescin (a non-destructive 

agent) to visualize each band under UV-light. 

The separated components were scraped into 

separate vials and stored at – 20 °C, then their 

FAs moiety was converted to fatty acid methyl 

esters (FA-MEs) by super dried-acidified 

methanol at 90-95 °C for 2 h (20) . The 

proportional composition (%) of methylated 

fatty acids was determined by capillary gas 

chromatography. The samples were analyzed 

in the National Centre for Scientific Research 

(CNRS), the Institute of Chemistry of Natural 

Substances (ICSN), France. The capillary gas 

chromatograph was CP-3800, Varian, USA. 

The capillary column was CP-Sil 8 CB, 0.25 

mm LD × 30 m with film thickness: 0.25 mm 

and helium as carrier gas. The programme 

used a temperature gradient from 80 to 220 

°C, 5 °C for each min. The identity of 14 

individual FA-peaks was ascertained by 

comparing each peak’s retention time relative 

to the retention times of FAs in synthetic 

standards. The relative amount of each FA (% 

of total FAs) was quantified by integrating the 

area under the peak and dividing the result by 

the total area for all FAs. To minimize 

transcription errors, the data from the gas 

chromatogram were electronically transferred 

to a computer for analysis. 

Statistical Analysis 

The t-test was used to compare the means 

for the two groups in terms of the lipid 

components and FA composition of the sebum 

of sebaceous cysts. All the data were 

expressed as mean ± standard deviation. P- 

values ≤ 0.05 were considered significant. 

Results 

a. Sebum lipid components: 

Figure (1) shows the relation between the 

amount of general classes of simple lipids (C, 

PLs and TGs) in the sebum of sebaceous 

cysts of two groups of subjects, dairy-product 

consumers and non-consumers. The average 

amounts of C, PLs and TGs were 18.96 and 

26.17 mg/g, 11.61 and 15.29 mg/g and 4.35 

and 4.44 mg/g of cysts, respectively. These 

results indicate that the consumers group 

showed a significantly higher level of C and 

PLs in contrast to the non-consumers group, 

but there was no significant difference in the 

amount of TGs. 

b. Sebum fatty-acid composition: 

Fatty acid composition of sebum-lipid 

components (CE, PLs and TGs) for the two 

groups of subjects were shown in Tables a,b,c: 

i. Sebum-CE fatty acids: 

The consumers group, compared with the 

non-consumers group, (Table a) showed a 

significant decrease in saturated fatty acids 

(SFAs). Both groups, however, showed a low 

level of medium-chain fatty acids (MCFAs), 

C 10 -C 14 , and a high level of C 16 and C 18 . 

Concerning monounsaturated fatty acids 



(MUFAs), C 16:1 and C 18:1 , there was a 

significant decrease in the consumers group. 

As regards the polyunsaturated fatty acids 

(PUFAs), C 18:2 n 6 and c 9 ,t 11 CLA showed 

higher percentages for the consumers group, 

but the other PUFAs exhibited lower 

percentages. The Table showed a significant 

decrease in n 3 -FAs for the consumers group. 

ii. Sebum-PL fatty acid: 

As shown in Table (b), PLs exhibited a nonsignificant 

decrease in SFAs for the 

consumers group. The relative amount of C 18:1 

for the consumers group was significantly 

lower than that for the non-consumers group, 

while C 16:1 was nearly absent in both groups. 

As regards PUFAs, C 18:2 n 6 and c 9 ,t 11 CLA 

showed higher percentages for the consumers 

group but the other PUFAs showed lower 

percentages. There was a significant decrease 

in n 3 -FAs for the consumers group compared 

with the non-consumers group. 

iii. Sebum-TGs fatty acids: 

Table (c) showed no significant difference in 

the percentages of SFAs and MUFAs for the 

two studied groups. As regards PUFAs, the 

consumers group exhibited a decrease in their 

level except for c 9 ,t 11 CLA and, to some extent, 

C 18:2 n 6 . As in the case of CE and PLs, TGs 

showed a significant decrease in n 3 -FAs for 

the consumers group compared with the nonconsumers 

group. 

subjects non-consuming and consuming dairy 

products 

C = cholesterol, PLs = phospholipids, TGs = 

triglycerides 

* Significant difference at p ≤ 0.05 

Table: Sebum-lipid fatty acid composition of 

subjects consuming and non-consuming dairy 

products 

(a) Sebum CE-fatty acid composition (wt%) 

Fatty acid 

Saturated 

Non-consumer 

Mean ± SD 

Consumer 

10:0 0.06 ± 0.03 0.05 ± 0.03 

12:0 1.02 ± 0.01 1.14 ± 0.29 

14:0 1.56 ± 0.40 1.50 ± 0.33 

16:0 12.42 ± 0.77 12.13 ± 1.13 

18:0 6.99 ± 1.05 5.67 ± 1.06* 

Total 22.05 ± 1.07 20.49 ± 1.43* 

Monounsaturated 

16:1 1.12 ± 0.15 0.82 ± 0.11* 

18:1 20.95 ± 0.66 18.11 ± 1.39* 

Total 22.07 ± 0.63 18.94 ± 1.40* 

Polyunsaturated 

18:2 n6 45.5 ± 4.13 52.81 ± 4.41* 

Amount of lipid components (mg/1gm of cyst) 

40 

35 

30 

25 

20 

15 

10 

5 

0 

* 

* 

non-consuming 

consuming 

Sebum C Sebum PLs Sebum TG 

18:3 n6 1.45 ± 0.39 0.74 ± 0.06* 

18:3 n3 0.46 ± 0.06 0.36 ± 0.13* 

20:4 n6 6.79 ± 0.77 5.29 ± 0.78* 

20:5 n3 0.62 ± 0.07 0.33 ± 0.06* 

22:6 n3 0.62 ± 0.07 0.42 ± 0.09* 

18:2 c 9 ,t 11 0.44 ± 0.02 0.62 ± 0.04* 

n3 1.70 ± 0.13 1.12 ± 0.13* 

n6 53.74 ± 4.50 58.84 ± 4.91 

* p ≤ 0.05 = significant difference 

Fig (1): Comparison between the amount of 

sebum lipid components of sebaceous cysts of 



(b) Sebum PL-fatty acid composition (wt%) 

(c) Sebum TG-fatty acid composition (wt%) 

Fatty acid 

Mean ± SD 

Consumer 

Fatty acid 

Nonconsumer 

Nonconsumer 

Mean ± SD 

Consumer 

Saturated 

Saturated 

10:0 0.10 ± 0.04 0.13 ± 0.05 

12:0 1.64 ± 0.35 0.98 ± 0.37* 

14:0 1.38 ± 0.44 1.31 ± 0.38 

16:0 25.91 ±4.59 23.24 ±4.45 

18:0 14.95 ±1.87 14.83 ±2.54 

Total 43.97 ±5.89 40.50 ±6.19 


16:1 0.02 ± 0.02 0.02 ± 0.02 

18:1 9.31 ± 1.15 7.54 ± 1.37* 

Total 9.33 ± 1.14 7.56 ± 1.37* 


18:2 n6 27.44 ±4.18 36.02 ± 4.42* 

18:3 n6 0.18 ± 0.04 0.18 ± 0.06 

18:3 n3 0.17 ± 0.05 0.21 ± 0.06 

20:4 n6 11.43 ±3.34 9.23 ± 4.04 

20:5 n3 0.86 ± 0.16 0.45 ± 0.14* 

22:6 n3 6.11 ± 0.97 5.16 ± 1.3 

18:2 c 9 ,t 11 0.51 ± 0.03 0.69 ± 0.04* 

10:0 0.29 ± 0.04 0.38 ± 0.09* 

12:0 0.19 ± 0.03 0.38 ± 0.05* 

14:0 2.22 ± 0.61 2.25 ± 0.5 

16:0 24.46 ±4.86 21.96 ±4.04 

18:0 4.26 ± 0.51 7.01 ± 0.72* 

Total 31.42 ±5.11 31.98 ±4.32 


16:1 2.38 ± 0.48 2.35 ± 0.52 

18:1 25.26 ±5.59 23.12 ±4.46 

Total 27.64 ±5.61 25.47 ±4.59 


18:2 n6 26.01 ±5.25 30.73 ±3.89 

18:3 n6 0.71 ± 0.13 0.68 ± 0.08 

18:3 n3 0.91 ± 0.42 1.09 ± 0.33 

20:4 n6 7.32 ± 1.29 5.53 ± 1.22* 

20:5 n3 1.14 ± 0.29 0.59 ± 0.15* 

22:6 n3 4.64 ± 1.46 3.60 ± 1.35 

18:2 c 9 ,t 11 0.21 ± 0.04 0.33 ± 0.04* 

n3 7.13 ± 0.95 5.82 ± 1.31* 

n6 30.63 ±6.47 38.81 ± 6.10* 

n3 6.69 ± 1.38 5.28 ± 1.28* 

n6 34.04 ±5.32 36.94 ±7.76 





Discussion 

a. Sebum lipid components: 

As shown in the figure (1), the level of C was 

higher in the consumers-group. The increase 

in the level of sebum C might be affected by 

the increase of its level in serum since the 

habit of consuming large quantities of dairy 

products leads to increased serum-C level. 

The dairy-product lipids include the main 

cholesterolemic SFAs; C 12 , C 14 and C 16 (24) ; 

and the stratum basale is equipped with the 

LDL-receptors that allow the potential uptake 

of cholesterol. On the other hand, essentialfatty 

acid (EFAs) deficiency leads to increase 

cholesterol synthesis by affecting the activity of 

HMG-CoA reductase (cholesterol rate-limiting 

enzyme) (5,19) . 

Concerning the sebum PLs, they exhibited a 

higher level in the consumer group, which 

reflects the fact that high-fat diets, including 

dairy products, tend to increase PLs (23,24) . This 

seems to be in harmony with what Mahmood 

(2002) states about the serum PLs of subjects 

who consume dairy products. 

As figure (1) shows, there is no significant 

difference in the level of sebum TGs between 

the two groups. This indicates that the effect of 

dairy-product consumption on the level of 

sebum TGs was almost absent. Although 

about 99 wt% of human adipose tissue-lipids 

consisted of TGs (22) , the percentage of sebum 

TGs was much lower in this and other 

studies (4) . 

b. Sebum fatty-acid composition: 

The SFAs of CE of dairy-product consumers 

exhibited a decrease in their amount 

compared with that of the non-consumers 

group as shown in Table (a). This indicates 

that dairy-product SFAs do not affect the 

sebum SFAs since they are synthesized in 

situ 19,25 . The results obtained for the SFAs of 

PLs and TGs, when there was no significant 

difference in their percentage for both groups, 

seem to agree with this explanation. The Table 

shows a lower percentage of MUFAs for CE, 

PLs and, to some extent, TGs although dairyproduct 

lipid contains a high proportion of oleic 

acid (26,27) . The negative correlation may be 

attributed to either the consumption of other 

sources of the diet by the two groups or to the 

enzymatic competition for desaturases and 

elongases during the endogenous 

synthesis (24) . Generally, when analyzing the 

FA composition of tissue samples to estimate 

the FA composition of the diet, strong 

correlations have been found between EFAs 

and the estimated dietary intake. Correlations 

for nonessential unsaturated and saturated 

FAs are weaker (9,28) . 

Consumption of dairy products increases the 

level of C 18:2 n 6 in the body (19,29) and this 

mimics the result listed in the table. In addition, 

there was a negative relationship between the 

amount of MUFAs (C 16:1 and C 18:1 ) and the 

amount of C 18:2 of sebum (5) . 

The consumers group showed a significant 

decrease in C 20:5 n 3 and C 22:6 n 3 . This might be 

due to the high level of C 18:2 n 6 of this group 

which modulates the action of 5-desaturase 

under the control of hormonal factors. 

Furthermore, C 18:3 n 6 and C 20:4 were also lower 

in the consumers group probably due to the 

same effect of the high level of linoleic 

acid (25,30,31) . Dairy-product lipid seems to 

decrease n 3 -FAs and increase 

n 6 -FAs in sebum lipid as shown in the Table, 

and it is worth mentioning that the balance 

between the level of n 3 and n 6 -FAs is important 

because of the competitive nature of their 

different biological roles (5,32,33) . 

As regards CLA, the concentration of c 9 ,t 11 

which is the major CLA isomer in the diet (13) , 

probably reflects habitual intakes (12) . The 

present study showed that consuming dairy 

products naturally enriched in CLA, especially 

c 9 ,t 11 CLA, increases its concentration in all the 

studied sebum components. The positive 

association in the concentration of c 9 ,t 11 CLA 

between CE and PL might reflect the synthesis 

of CE from PL, particularly phosphatidylcholine 

by lecithin: cholesterol acyl transferase 

activity (12,19) . The FA composition of human 

adipose tissues reflects, to a great extent, the 

average distribution of the dietary FAs over a 

period of 2-3 y (22) and it has been found that 

CLA is present principally in ruminant-animal 

food products' mainly dairy products (14) . 

In conclusion, the high consumption of dairy 

products affects sebum lipid contents and fatty 



acid composition mainly c 9 ,t 11 CLA so it can be 

used as a marker for the intake of dairyproduct 

lipid. These findings are in agreement 

with a recent report (34) , which showed a dietary 

influence on the sebaceous lipogenesis. 

Acknowledgement 

We thank the French Embassy for granting a 

research fellowship for the analysis of samples 

by capillary gas chromatography, since this 

technique is not available in Iraq at the present 

time. We would also like to express our 

gratitude to Dr. Christain Marazano, Dr. 

Stephane Mons, Dr. Alice Olsker and Wafaa 

Al-Sheikh, the staff of the Laboratory of CNRS, 

France, who provided the facilities for the 

analysis performed. The cooperation of the 

volunteers and the nursing staff of Al-Jumhouri 

Hospital is sincerely acknowledged. 

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Spontaneous healing of traumatic perforations of 

the tympanic membrane 

Salim H. Al-Obiedi 

Department of Surgery, College of Medicine, Tikrit University. 


Received: 25 th May 2008; Accepted: 25 th Jan 2009. 

ABSTRACT 

Objective: To study the spontaneous healing of various types of traumatic perforations of the 

tympanic membrane in a prospective study carried out on patients with traumatic perforations of the 

tympanic membrane, presented to same author. 

Methods: Eighty patients with 84 traumatic perforations of the tympanic membrane were studied at 

Tikrit Teaching Hospital, during the period from Jan. to Dec. 2007. Diagnosis made by a history of 

trauma and otoscopic examination. Antibiotics were given to prevent or treat infections. Advice to 

keep the ear dry. Follow up the patients for a minimum of six months. 

Results: The male: female ratio was (2.6:1). Left ear perforation was more than right ear, (5%) were 

bilateral. The commonest cause was blast injury in 34 patients (43%), then hand slap in 22 patients 

(27.5%). The age of the patients was from 4-65 years, common age group affected was (21-30 

years), they were 39 patients (49%). Spontaneous healing occurred in 69 cases (82%), persistent dry 

perforation in 8 cases (9.5%), and 7 cases (8.5%) ended with chronic suppurative otitis media. Fiftysix 

cases (81%) got complete healing within six weeks. All cases due to fractures of temporal bone 

got spontaneous healing (100%), then perforation by foreign body and instrumentation (89%), ear 

syringing, and hand slap was equal (88%), then due to ear suction (80%), and the lower incidence in 

blast injury were (75%). Healing of posterior and anterior perforations about equal (92%), (91%) 

respectively, then kidney shape perforation (85%), but none of 7 cases of subtotal perforations healed 

spontaneously. 

Conclusion: Conservative care for traumatic perforations of the tympanic membrane gives excellent 

chance for spontaneous healing. The factors affecting spontaneous healing include, large size 

perforations, ear infections, type of trauma, and Eustachian tube dysfunction. 

Keywords: Traumatic perforation; tympanic membrane; spontaneous healing. 


الهدف:‏ دراسة الاندمال التلقائي ‏(الذاتي)‏ لأنواع مختلفة من الثقوب الرضية في طبلة الأذن.‏ 

الطريقة:‏ دراسة مستقبلية أجريت على مريضا مصابين بثقب رضي في طبلة الأذن،‏ قدموا إلى نفس الباحث في 

مستشفى تكريت التعليمي العراق.‏ خلال الفترة من آانون ثاني إلى آانون أول سنة تم التشخيص بواسطة تاريخ 

شدة خارجية والفحص بمنظار الأذن.‏ أعطي المريض مضادا حيويا لمنع أو علاج الالتهاب،‏ وأعطيت نصائح لحفظ الأذن 

جافة.‏ وتمت متابعة المريض لفترة لا تقل عن ستة أشهر.‏ 

النتائج:‏ ثمانون مريضا مصابين ب ثقب رضي في طبلة الأذن.‏ نسبة الرجال إلى النساء آانت ثقب الأذن 

اليسرى أآثر من اليمنى،‏ في آلا الأذنين.‏ السبب الشائع آان ضرر انفجار مريض ثم صفعة يد آان 

مريضا عمر المرضى يتراوح بين سنة)،‏ الفئة العمرية سنة)‏ آانت أآثر إصابة 

مريضا الاندمال التلقائي حصل في حالة ثقب جاف دائم في حالات و‎٧‎ حالات 

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أسابيع.‏ 

خلال أول حالة التهاب الأذن الوسطى القيحي المزمن.‏ اندمال تلقائي آامل حصل في ثم ثقب نتيجة جسم غريب أو استخدام آلات 

جميع الحالات نتيجة آسر العظم الصدغي حصل اندمال تلقائي ثم ثقب نتيجة سحب الأذن 

الاندمال لثقب نتيجة صفعة يد أو غسل الأذن آانوا متساويين آانت الاندمال للثقوب الخلفية والأمامية تقريبية 

واقل نسبة ثقب نتيجة انفجار آانت الثقوب تحت الكاملة ٧ حالات لم تندمل تلقائيا.‏ 

بالتتابع،‏ ثم الثقب المرآزي ‏(شكل الكلية)‏ آانت الاستنتاج:‏ العناية الوقائية للثقب الرضي في طبلة الأذن يعطي حظ ممتاز للاندمال التلقائي ‏(الذاتي).‏ العوامل المؤثرة على 

الاندمال التلقائي تشمل ثقب آبير الحجم،‏ التهاب الأذن،‏ نوع الضرر المسبب للثقب،‏ وعدم آفاءة قناة اوستاآي.‏ 

مفتاح الكلمات:‏ ثقب رضي،‏ طبلة الأذن،‏ اندمال تلقائي،‏ ضرر انفجار،‏ صفعة يد.‏ 

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T 

he tympanic membrane is a thin wall that 

separates the outer ear from the middle 

ear (1) . It is much more traumatized than middle 

or inner ear (2) . The incidence has been 

estimated at 6.8 per 1000 person (3) , and the 

annual incidence rates of traumatic perforation 

vary between 1.4 to 8.6 per 100.000 (2) . The 

causes of acute rupture of tympanic 

membrane, include direct trauma by 

instruments such as cotton swab, pin, and 

sticks; welding; skull fracture; foreign body. 

Iatrogenic like syringing, suction, and probing 

of the ear. Pressure changes include blast 

injury, open palm trauma (slapping), diving, 

and flying (4) . 

Most of isolated traumatic perforations of the 

tympanic membrane can be managed with 

conservative care. The ear should be kept 

clean and dry while the ear drum heals; 

insertion of cotton ball with Vaseline into the 

ear when showering or bathing, avoid blowing 

the nose, as the pressure created when 

blowing the nose can damage healing ear 

drum tissue, and causes infection (1) . 

Surgical repair includes myringoplasty, 

tympanoplasty, and ossiculoplasty, which are 

indicated if it does not heal by itself, for 3-6 

months especially if associated with significant 

conductive hearing loss, and recurrent 

drainage (4) . 


This is a prospective study which was carried 

out on patients presented to the author with 

traumatic perforations of the tympanic 

membrane, at Tikrit Teaching Hospital, during 

the period from Jan. to Dec. 2007. 

They were 80 patients. Questioning included 

type and duration of trauma, presence of 

otalgia, otorrhea, vertigo, hearing loss, tinnitus. 

Physical examination: Inspection of the auricle 

for any sign of trauma, palpation for 

tenderness, careful suctioning of blood, 

purulent discharge, and debris, from the ear 

canal if present. Diagnosis made by otoscopic 

examination; shape, size and location of the 

perforation {posterior, anterior, central (kidney 

shape) or subtotal} were recorded. Tuning fork 

tests (Renne's, Weber's, and Absolute bone 

conduction test.). The ear should be kept dry. 

An antibiotic was used to prevent or treat 

infection. Oral Amoxicillin + clavulanic acid 375 

mg/t.i.d/ for seven days, or according to C/S 

test. Aural toilet was done when indicated. 

Advice to weekly follow up was given to the 

patient if he has pain or swelling in the ear or 

discharge from his ear. Follow up period was 

for a minimum of six months. 

Results 

Eighty patients, with 84 traumatic perforations 

of the tympanic membrane; 58 patients 

(72.5%) were males, and 22 patients (27.5%) 

were females. (M:F ratio 2.6:1) (Figure 1). Left 

ear perforations were 52 patients (65%), right 

ear were 24 patients (30%), and 4 patients 

(5%) with bilateral perforations. Explosive blast 

injury of the ear was the commonest cause, 

34 patients (43%), hand slap 22 patients 

(27.5%), then foreign body and 

instrumentation 9 patients (11%), ear syringing 

8 patients (10%), ear suction 5 patients (6%), 

and fracture temporal bone 2 patients (2.5%). 

The common age group affected was (21-30 

year), 39 patients (49%), 25 patients (54%) 

were due to blast injuries. Hand slap was the 

commonest cause in the age group (11-20 

year) were 8 patients (47%), while the foreign 



bodies and instrumentation were the 

commonest causes of the perforation in the 

age group (≤10 years), 6 patients (75%) 

(Figure 2). 

The commonest site of traumatic perforation 

of tympanic membrane was posterior 

perforation which were 45 cases (54%), then 

central (kidney shape) were 20 cases (24%), 

then anterior perforation were 12 cases (14%), 

then subtotal perforation were 7 cases (8%) 

(six due to blast injury, and one due to foreign 

body button battery (Table 1). 

From 84 perforated tympanic membranes, in 

69 cases (82%) the spontaneous healing 

occurred, 8 cases (9.5%) got dry perforation 

with normal middle ear mucosa, and 7 cases 

(8.5%) having active chronic suppurative otitis 

media. (Table 2). 

Spontaneous healing of perforation due to 

fracture of temporal bone was (100%), then 

foreign body and instrumentation, ear 

syringing, and hand slap were (89%) (88%) 

(88%) respectively. Perforations due to ear 

suction was (80%), blast injury was (75%) 

(Table 2). 

Spontaneous healing of posterior and 

anterior perforation was about equal (92%), 

(91%) respectively; for central (kidney shape) 

perforation was (85%), but none of seven 

cases with subtotal perforation got 

spontaneous healing, four cases with 

continuous otorrhea ( chronic suppurative otitis 

media), and three cases ended with dry 

perforation during the follow up period (Table 

3). 

The duration of complete spontaneous 

healing was within 2 weeks in eleven cases 

(16%), 27 cases (39%) healed within 4 weeks, 

18 cases (26%) healed within 6 weeks, and 13 

cases (19%) healed within more than 6 weeks, 

so (81%) healed spontaneously within the first 

six weeks (Table 4). 

Table (1): The site and size of traumatic perforation 

Site of the 

perforation.* 

Total 

Blast 

injuries 

Hand slap 

Foreign 

body 

Ear 

syringing 

Ear 

suction 

Fracture 

temporal 

bone 

Posterior 45 (54%) 19 (42%) 16 (36%) 3 (6.6%) 3 (6.6%) 2 (4.4%) 2 (4.4%) 

Anterior 12 (14%) 5 (42%) 4 (33%) 1 (8%) 0 2 (17%) 0 

Central (kidney 

shape) 

20 (24%) 6 (30%) 4 (20%) 4 (20%) 5 (25%) 1(5%) 0 

Sub total 7 (8%) 6 (86%) 0 1 (14%) 0 0 0 

Total 84 (100%) 36 (43%) 24 (28.5%) 9 (11%) 8 (9.5%) 5 (6%) 2 (2%) 

*No attic or marginal perforations were reported. 

Table (2): Sequelae of the traumatic perforation of the tympanic membrane 

Type of trauma No. Perforated T.M Healed Dry perforation. CSOM (active) 

Blast injury. 36 27 (75%) 6 (17%) 3 (8%) 

Hand slap 24 21 (88%) 2 (8%) 1 (4%) 

Foreign body. 9 8 (89%) 0 1 (11%) 

Ear syringing. 8 7 (88%) 0 1 (12%) 

Ear suction. 5 4 (80%) 0 1 (20%) 

Fracture temporal bone 2 2 (100%) 0 0 

Total. 84* 69 (82%) 8 (9.5%) 7 (8.5%) 

* 4 patients with bilateral perforation, 2 blast injury, and 2 open hand slap. 



Table (3): Relation of site and size of perforation and healing 

Site of the perforation No.(%) Healed Dry perforation C.S.O.M 

Posterior 45 (54%) 41 (91%) 3 (7%) 1 (2%) 

Anterior 12 (14%) 11 (92%) 1 (8%) 0 

Central(kidney shape) 20 (24%) 17 (85%) 1 (5%) 2 (10%) 

Sub total 7 (8%) 0 3 (43%) 4 (57%) 

Total 84 (100%) 69 (82%) 8 (9.5%) 7 (8.5%) 

Table (4): Duration of healing of perforated tympanic membrane in relation to type of trauma 

Causes 

Duration 

Total 6 Wk 

Blast injury 27 3 (11%) 9 (33%) 7 (26%) 8 (30%) 

hand slap 21 5 (24%) 12 (57%) 2 (9.5%) 2 (9.5%) 

Foreign body 8 3 (37.5%) 3 (37.5%) 2 (25%) 0 

Ear syringing 7 0 1 (17%) 4 (50%) 2 (33%) 

Ear suction 4 0 1 (25%) 2 (50%) 1 (25%) 

Fracture 

temporal bone 

2 0 1 (50%) 1 (50%) 0 

Total 69 11 (16%) 27 (39%) 18 (26%) 13 (19%) 

Fig (1): The relation of the sex with causes of traumatic perforation of the tympanic membrane 



blast inj. 

hand slap 

foreign body 

ear syring. 

ear suction 

fr. Temp. bone 

total 

10 

9 

7 

8 8 

6 

6 

4 

4 

2 22 2 3 3 

1 2 

00 0 0100 

1 00 

100 

10 

more than 

40 years 

31‐40 

years 

39 

21‐30 

years 

21 

17 

11‐20 

years 

less or 

equal to 

10 years 

40 

35 

30 

25 

20 

15 

10 

5 

0 

Fig (2): Relation of age with traumatic perforation of the tympanic membrane 

Discussion 

The perforation of the tympanic membrane 

heals by means of epithelial migration pattern 

of tympanic membrane, and external auditory 

canal which proceeds from umbo outward (5)(6) . 

Following an acute injury, platelets gather to 

cause vasoconstriction and forming thrombus. 

An inflammatory response ensues, attracting 

neutrophils, macrophages, and bioactive 

cytokines to the wound. A matrix of 

proteoglycans and glycosaminoglycans is 

formed and allows proliferation of squamous 

epithelium layer of the tympanic membrane 

across the perforation forming a scaffold on 

which the mucosal layer can grow. The 

squamous elements responsible for bridging 

the perforation originate from 'up stream' and 

must traverse the length of the defect , so it is 

not surprising that the large perforations are 

associated with delayed healing and higher 

rate of chronicity (7) . In the experimental 

animals, proliferation of stratified squamous 

epithelium at the rim of a perforation begins 

within 12 hours, and granulation tissue growth 

begins at 36 hours (8) . Regeneration of the 

epithelium of the inner (mucosal) surface is 

more sluggish and begins only after several 

days. As long as there is suitably flat surface, 

stratified squamous epithelium grows at the 

rate of 1 mm a day (9) . Mesothelial layer does 

not regenerate. So new tympanic membrane is 

thin and has two layers, with absence of 

middle fibrous layer (6) . 

Many studies concerning healing of traumatic 

tympanic membrane perforations were 

conducted. Griffen (1979) found 90% of 

traumatic tympanic membrane perforations 

heal spontaneously within three months after 

injury (3) . Kristensen. (1992), found that the 

spontaneous healing rate appeared to be 

(78.7%) of traumatic tympanic membrane 

perforation of all sorts seen within 14 days 

after injury (10) . Chun, et al. (1999) reported 

spontaneous healing was 76%, and the mean 

duration for complete healing was 22.1 

days (11) . Bobby (2006) showed that within one 

month 68% are healed and within three 

months 94% are healed. In our study (82 %) of 

healed traumatic perforation occurs within 6 

weeks. 

The blow to the ear and instrumentation 

injuries are the common causes of traumatic 

tympanic membrane perforation. In our study 

blast injury was the commonest cause, as it is 

usually seen during war and bombing, the 

condition of our country (Iraq); they were 34 

cases (43%). The tympanic membrane is the 

structure most frequently injured by blast, 

because even at low pressure 5 Psi (pound 

per square inch) can cause tympanic 

perforation (12) , and the force required to 



rupture the tympanic membrane is equivalent 

to 195dB (5) . 

Temporary neuropraxia in the ear's receptor 

organs, manifested by deafness, tinnitus, and 

vertigo; if dynamic over pressure are high 

enough, the ossicles of middle ear can be 

dislocated (13) . Cholesteatoma formation and 

development of perilymph fistula are possible 

in blast injury (14) . Kronenberg, et al. (1993) 

evaluated healing in 147 patients with 200 

perforated ear drums, following blast. 

Spontaneous healing occurred in 155 ears 

(74%) in one year although 131 (85%) of these 

healed within the first three months (15) . Our 

result for blast injuries, spontaneous healing 

was 27 cases (75%), which is the lower rate 

of healing in relation to other causes, because 

some are large perforations (subtotal 

perforation) (Table 3), or get infection because 

of contamination by blast wind, especially 

those victims who were close to the explosion, 

and all were having shell wounds in their 

bodies. 

Open hand slap generally the second cause 

and main cause in women, due to the rise in 

domestic violence (2) and child abuse, but in 

our study the male becomes a victim of 

American military, and security officers. There 

were 13 males (59%), two of them had 

bilateral perforation, and 9 cases (41%) were 

females (Figure 1). Usually it carries better 

prognosis than blast injury, because of less 

infection rate, and moderate size perforations, 

81% of healed cases occurred within 4 weeks 

(Table 4). 

Traumatic tympanic membrane perforations 

due to ear syringing and ear suction, usually 

get infection (otitis media or otitis externa like 

otomycosis). They usually delay healing 

process, and once the infection has resolved 

most perforations healed spontaneously (16) , 

except large perforation. All cases (seven) with 

subtotal perforation did not heal spontaneously 

during at least 6 months' follow up. 

The type of trauma, the alkaline battery on 

contact with moisture results in liquefaction 

necrosis which leads to much more extensive 

injury; over time causes TMP, exposure of 

bone of the ear canal, ossicular destruction, 

sensory neural hearing loss, and facial palsy, 

so it should be removed as soon as 

possible (17) . Likewise, slag burns tend to 

cauterize the vasculature and healing 

incompletely (4) . 

The prognosis of spontaneous healing is 

poorer with persistent Eustachian tube 

dysfunction, and chronic infections, because 

they weaken the tympanic membrane and 

impair healing (4) , so prevention and promptly 

treating ear infection hasten healing. It is 

imperative to give antibiotics at presentation to 

prevent a permanent perforation (10) . Checking 

for chronic nose and sinus problems, and 

treating them, if there is no healing (16) . The 

patients that healed after 6 weeks were (15) 

patients; all having otitis media during follow 

up period. 

Histological examination of permanent 

perforation showed that stratified squamous 

epithelium grows medially over the edge of 

the perforation (18) which appears to arrest the 

subsequent closure of the perforation. The 

removal of the medialized epithelium forms 

basis of some treatment of tympanic 

membrane perforation (19) , as it will not heal 

spontaneously. However, not all people with 

unhealed perforation need treatment, many 

people have small permanent perforation with 

no symptoms or significant hearing loss (20) . 

Conclusion 

Conservative care for traumatic perforation of 

the tympanic membrane gives excellent 

chance of spontaneous healing. The factors 

affecting the spontaneous healing include 

large size perforations, ear infections, type of 

trauma, and Eustachian tube dysfunction. 

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23.2002. 

3. Griffen WL Jr. A retrospective study of 

tympanic membrane perforation in a 

clinical practice. Laryngoscope 

1979;89:261-82. 



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12. Patterson JH. Hamernik RP. Blast over 

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13. Deguine C, Pulec JL. Traumatic 

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14. Mrena R, Back L, et al. Otologic 

consequences of blast exposure .Acta 

Otolaryngol.2004;124:946-952. 

15. Kronenberg J, Ben-shosand J, Wolf M. 

Perforated tympanic membrane rupture 

after blast injury. Am J Otol 1993;14(1):92- 

4. 

16. William B. Hurst. Out come of 22 cases of 

perforated tympanic membrane caused by 

otomycosis. The Journal of Laryngology & 

otology (2001),115:879-880. 

17. Mitchell K. Ballenger's 

otorhinolaryngology Head & Neck Surgery. 

Chapter 14. Trauma to the middle ear. 

inner ear, and temporal bone.16 th Edition. 

2003. P345-356.. 

18. Somers T, et al. Growth factors in 

tympanic membrane perforation. Am J 

Otol 1998;19:428-34. 

19. Yamashita T. Histology of tympanic 

perforation and replacement membrane. 

Acta Otolaryngol (stock) 1985;100:66-71. 

20. www.privatehealth.co.UK/ diseases/ earnose 

- throat /perforated-ear drum. 



Platelet indices in the differential diagnosis of thrombocytosis 

Bashar A. Saeed*, Sana M. Taib*, Khalid Nafih** 

*Department of Pathology, **Department of Medicine, College of Medicine, University of Mosul. 


Received: 2 nd Mar 2008; Accepted: 22 nd Feb 2009. 

ABSTRACT 

Objective: To assess the role of platelet indices mainly: Mean Platelet Volume (MPV) and Platelet 

Distribution Width (PDW) for the differential diagnosis of thrombocytosis. 

Methods: A prospective case series study conducted at Ibn–Sena Teaching Hospital in Mosul during 

the period from June 2003 to January 2005. Ninety two patients with thrombocytosis were analyzed 

for platelets indices using Coulter MS-9. A control group of sixty normal subjects were also included in 

this study for comparison. 

Results: Thrombocytosis was found to be due to two main causes: 12 patients with myeloproliferative 

disorders, and 80 patients had secondary reactive causes of thrombocytosis. Patients with 

myeloproliferative disorders had significantly higher Mean Platelet Volume (MPV) than those with 

reactive thrombocytosis. Also the Platelet Distribution Width (PDW) was higher in patients with 

myeloproliferative disorders than those with reactive thrombocytosis and control group. 

Conclusion: Platelet indices especially PDW seem to be a good variable for the differential 

diagnosis of thrombocytosis. 

Keywords: Thrombocytosis; platelet indices Mean Platelet Volume (MPV); Platelet Distribution Width 

(PDW). 


أهداف البحث:‏ أجريت هذه الدراسة لمعرفة أهمية البيانات المتعلقة بالأقراص الدموية في الأجهزة المتوفرة في 

المستشفيات آجهاز آولترام ا س وخاصة الطيف التوزيعي للأقراص ومعدل حجم الأقراص للتشخيص التفريقي في 

حالات زيادة الأقراص الدموية 

طريقة البحث:‏ دراسة مستقبلية لمجموعة من الحالات.‏ تمت الدراسة في مستشفى ابن سينا التعليمي في الموصل من 

حزيران لغاية آانون الثاني أجريت الدراسة على اثنين وتسعين مريضا مصابون بزيادة تكون الأقراص 

الدموية من خلال الجهاز الالكتروني آولتر ‏(ام-‏ سا واستحصلت البيانات المتعلقة بالأقراص الدموية وشملت الدراسة 

ستون شخصا طبيعي لديه عدد طبيعي من الأقراص الدموية للمقارنة 

النتائج:‏ وجد أن المرضى المصابون بزيادة ‏(فرط)‏ الأقراص الدموية ينقسمون إلى مجموعتين رئيسيتين،‏ مجموعة 

مكونة من اثنى عشر مريضا لديهم اعتلال أولي ناجم عن اعتلال نخاعي ومجوعة أخرى تتكون من ثمانين مريضا لديهم 

أسباب ثانوية ‏(انفعالية)‏ لزيادة الأقراص 

إن المرضى الذين لديهم اعتلال أولي نخاعي آسبب لزيادة الأقراص الدموية فان الطيف التوزيعي للأقراص الدموية 

وآذلك معدل حجم هذه الأقراص اآبر من أقرانهم ذوي زيادة ‏(فرط)‏ الأقراص الدموية الثانوية أو أقرانهم الأصحاء 

الاستنتاج:‏ إن البيانات المتعلقة بالأقراص الدموية وخاصة الطيف التوزيعي للأقراص يعتبر مؤشرا ومتغيرا جيدا 

للتشخيص التفريقي في حالات فرط الأقراص الدموية بنوعيه.‏ 

. 

. 

(٩- 

.٢٠٠٥ 

. 

٩- 

. 

٢٠٠٣ 



المفتاح:‏ فرط ‏(زيادة)‏ 

للأقراص الدموية 

الأقراص الدموية ، بيانات الأقراص الدموية ، معدل حجم الأقراص الدموية ، الطيف التوزيعي 

. 

T 

hrombocytosis is the presence of 

abnormally high number of platelets in the 

circulating blood. It may result from various 

physiological stimuli and pathological 

processes. (1) Thrombocytosis can result from 

a myeloproliferative disorder, but is more 

commonly found as reactive phenomenon not 

caused by a bone marrow diseases but 

secondary to various pathological states . (2) 

Platelet size follows a log –normal distribution 

and platelet volume heterogeneity has been 

the subject of considerable investigation, 

speculation and indeed controversy in recent 

years. (3) 

Platelets from patients with myeloproliferative 

thrombocytosis may differ from those with 

reactive thrombocytosis in morphology platelet 

volume distribution pattern. (4) 

The study aims to assess the efficiency of 

Coulter MS -9 and of the derived variables; 

Mean Platelet Volume (MPV) and Platelet 

Distribution Width (PDW) for the differential 

diagnosis of thrombocytosis. 

Methods 

Ninety two patients with thrombocytosis, i.e. 

platelets count >400×10 9 /L, were included in 

this study, twelve patients with myeloproliferative 

disorders were studied; the rest were 80 

patients with reactive thrombocytosis. A 

control group of 60 people with mean platelets 

count of 255x10 9 /L with a range (162- 

388x10 9 /L) were included for comparison. 

The platelet volume analysis was made using 

a Coulter counter MS-9; particles with a 

volume between 2 and 20 FL are classified by 

this instrument as platelets by definition, a 

volume distribution histogram is generated and 

fitted to the nearest log. Normal curve 

therefrom, the platelet count , MPV and PDW 

are computed . (5) 

PDW is calculated from the volume of 16 th 

and 84 th percentile (6) ; all measurements were 

made between one and six hours after the 

blood had been collected. (7) 

Statistical analysis was done using unpaired t 

test , mean and S.D. 

Results 

Patients with thrombocytosis were classified 

according to the cause into primary (myeloproliferative) 

thrombocytosis (12) patients and 

secondary (reactive) thrombocytosis (80 

patients). 

Details of the aetiological classification were 

summarized in (Table 1) 

Table (1): Classification of patients with 

primary and secondary thrombocytosis 

Diagnosis 

1. Primary: No. (12) 

polycythaemia vera 

chronic myeloid leukaemia 

Total no of 

cases 

3 

9 

2. secondary (reactive) 

No. (80) 

Infection 25 

Non haematological 

malignancies 

23 

Iron deficiency anaemia 20 

Haemolytic anaemia 6 

Post operative including post 

splenectomy 

Collagen disease 1 

Table (2): Mean values of different platelet 

variables in normal and patient groups 

Normal 

subjects 

(control) 

Reactive 

Thrombocytosis 

Primary 

Thrombocytosis 

No of 

cases 

Mean 

platelet 

count 

(10 9 /l) 

MPV 

(fl) 

5 

PDW 

60 255 7.2 7.7 

80 537 6.7 7.4 

12 625 7.45 8.7 



The mean platelets count in the control group 

was 255×10 9 /L with a range (162-388x 10 9 /L) 

in comparison with 537x10 9 /L in reactive 

thrombocytosis, with a range (420-580x10 9 /L), 

while the mean platelet count was 625x10 9 /L 

in primary thrombocytosis with wide range 

(490-1380x10 9 /L). 

The Mean Platelet Volume (7.45) in primary 

thrombocytosis was significantly higher than in 

reactive thrombocytosis (6.7) (p


7. Gary SK, Amaros EL, Karparkin S. Use of 

megathmbocyte as an index of 

megakaryocyte number: N Engl J Med 

1971; 284:11-1. 

8. J Van Der Lelie, Aeg K R Von Dem Borne: 

platelet volume analysis for differential 

diagnosis of thrombocytosis, J. CL. Path. 

1986; 39:129-133. 

9. Cortelazzo S, Barhni T Bassan R, et al. A 

normal aggregation and increased size of 

platelets in myeloproliferative disorders. 

Thromb. Hemost. 1980; 43:127-30. 

10. Holme S, Simmonds M , Ballek R, et al 

comparative measurement of platelet size 

by coulter counter , microscopy of blood 

seems and high transmission studies . J 

Lab clin Med 1981; 97:610-22. 

11. Zalla –Z, Scott M, and Frank H. 

Microscopic platelet size and morphology 

in various haematologic disorders, blood. 

1978; 51 (3):479-485. 



Histopathological changes of decidua and decidual 

vessels of early pregnancy 

Rana A. Azooz, Noel S. Al-Sakkal 

Department of Pathology, College of Medicine, University of Mosul. 


Received: 29 th Apr 2008; Accepted: 4 th May 2009. 

ABSTRACT 

Objective: The histological examination of the decidua can provide a clue in the diagnosis of 

intrauterine pregnancy. The purpose of this study is to describe the morphologic features observed in 

the decidual blood vessels of early pregnancy loss cases prior to 20 weeks gestation, and to compare 

these findings with Arias-Stella reaction and with changes found in endometrial biopsies of nonpregnant 

women as a control group. 

Material and method: A prospective case control study done at the Department of Pathology of 

Mosul Medical College, Histopathological Laboratories of Al-Khansa and Al-Zahrawi Teaching 

Hospitals and the gynecological units of Al-Khansa and Al- Batool Teaching Hospitals in Mosul. 

The study was conducted on 161 reproductive aged women with different clinical types of abortion 

admitted for uterine evacuation. The histopathological features in the decidua and decidual vessels of 

curettage specimens were described, graded and compared with that observed in endometrial 

biopsies of non pregnant women as a control group. 

Results: Out of a total 161 abortion specimens examined,10.6% of cases showed severe degree of 

obliterative endarteritis involving one or more decidual vessels. This finding was higher than the 

frequency of Arias-Stella reaction in the same specimens and none of these features were described 

in the control group . 

Conclusion: Obliterative endarteritis of decidual vessels can be used together with other 

morphological features for the possibility of occurrence of a pregnancy in the absence of chorionic 

villi, trophoblast and other emberyonic elements. 


الهدف:‏ يمكن للفحص النسيجي للغشاء الساقط أن يؤشر لحدوث الحمل داخل الرحم.‏ تهدف الدراسة إلى وصف التغييرات 

المظهرية الملاحظة لأوعية الغشاء الساقط في حالات فقدان الحمل المبكر قبل عمر ٢٠ أسبوع ومقارنة النتائج مع تغييرات 

ارياس-‏ ستيلا ومع التغييرات الملاحظة لخزع بطانة الرحم لنساء غير حوامل آمجموعة مقارنة.‏ 

الطريقة:‏ دراسة مستقبلية أجريت في فرع علم الأمراض في آلية طب الموصل والمختبرات النسيجية ووحدات النسائية 

لمستشفيات الخنساء والزهراوي والبتول التعليمية في مدينة الموصل.‏ 

أجريت الدراسة على امرأة في سن الإخصاب يعانين من حالات إجهاض متنوعة ادخلن لتفريغ الرحم.‏ تم وصف 

وتصنيف ومقارنة التغيرات النسيجية للغشاء الساقط وأوعيته في عينات تجريف الرحم مع تلك الملاحظة في خزع بطانة 

الرحم للنساء غير الحوامل آمجموعة مقارنة.‏ 

النتائج:‏ من ضمن عينة إجهاض،‏ أظهرت من الحالات درجة شديدة من التهاب بطانة الشريان ألانسدادي 

والتي شملت واحد أو أآثر من أوعية الغشاء الساقط.‏ وآان تكرارها أآثر من تكرار تغيرات ارياس-ستيلا لنفس العينات 

بينما لم تشتمل مجموعة المقارنة على أي من تلك الصفات.‏ 

% ١٠,٦ 

١٦١ 

١٦١ 



الاستنتاج:‏ يمكن استخدام التهاب بطانة الشريان ألانسدادي لأوعية الغشاء الساقط مع التغيرات المظهرية الأخرى آمؤشر 

لحدوث الحمل في حالة عدم وجود الزغابات المشيمية،‏ الطبقة الغاذية والعناصر الجنينية الأخرى.‏ 

T 

he histopathological diagnosis of a 

pregnancy is usually dependent upon 

finding of fetal parts, gestational sac, viable or 

necrotic chorionic villi or trophoblast (1,2) . 

During implantation the trophoblast invades 

into capillaries and veins within the superficial 

endometrium and aggregates of 

cytotrophoblast cells occlude the distal 

segments of the spiral arteries until a direct 

utero-placental circulation is established at 

around ninth to tenth weeks of gestation as a 

result of loosening of some of these arterial 

plugs (3, 4, 5, 6) . 

In the absence of fetal parts, trophoblast or 

chorionic villi, the presence of dilated vascular 

channels of placental beds are features helpful 

in distinguishing the true decidua of 

intrauterine pregnancy from the deciduoid 

changes secondary to hormonal therapy (1,2) . 

Furthermore, the presence of enlarged 

hyalinized spiral arterioles and a fibrinoid 

matrix are also features suggestive of 

intrauterine pregnancy (1) . 

The morphological changes observed in the 

spiral arteries during early pregnancy are not 

fully understood (7) . Obliterative changes 

involving one or more of the decidual spiral 

arteries have been well described in 

endometrial curettage biopsies (8) and were 

attributed in part to the interaction of the 

trophoblast with the arterial wall during their 

migration into these vessels (7) . 

The Arias-Stella reaction is the histological 

glandular feature that was originally described 

with the presence of intrauterine pregnancy, 

(9,10,11) 

ectopic pregnancy as well as in 

association with administration of exogenous 

hormones (12) . It is marked by hypersecretory 

gland with large cells, abundant clear to 

eosinophilic cytoplasm and irregularly 

protruded nuclei which exhibit hyperchromasia 

and marked pleomorphism (12) . 

The present study is designed to describe 

the morphological changes in the decidual 

vessels among abortion specimens prior to 

twenty weeks' gestation and to compare these 

features with those observed in the 

endometrial biopsies of non-pregnant women 

as a control group and with Arias-Stella 

reaction as a possible marker of viable 

pregnancy. 

Patients and method 

Patients 

During the period of study between October 

2004 to June 2005, products of conception 

were collected from 161 reproductive aged 

women with different clinical types of abortion 

prior to 20 weeks' gestation. The age of 

women varied from 17-45 years. They were 

admitted for uterine evacuation at both Al- 

Khansa and Al-Batool Teaching Hospitals in 

Mosul City. The occurrence of a pregnancy 

was confirmed by a pregnancy test and/ or 

ultrasonography. An obstetric history of preeclampsia, 

diabetes, and Rhesus 

incompatibility were excluded. The evacuation 

of the uterus was performed by either D & C 

or sponging curettage. Endometrial tissues 

were fixed in 10% neutral formalin, embedded 

in paraffin blocks, cut at 5µ sections and 

stained by H & E. 

Histopathological Examination 

On microscopical examination, obliterative 

endarteritis of decidual blood vessels were 

described and classified depending upon the 

severity of luminal narrowing and the degree of 

intimal proliferation (8) , as follow: 

Grade 0: Normal arterioles. 

Grade I: Arterioles with slight thickening of 

their walls and minimal intimal proliferation. 

Grade II: Arterioles with moderately severe 

wall thickening with a lumen –to-wall ratio 2:1 

or 1:1 or with eccentric intimal proliferation and 

intimal foamy cells. 

Grade III: At least one or more of the vessels 

is showing a near total obliteration of the 

lumen due to marked intimal hyperplasia and 

intimal foamy cells with surrounding edema. 



Results 

The mean age of the sampled women was 

26.5 years. The results obtained from 161 

endometrial biopsies examined are illustrated 

in table (1). Mild arteritis of decidual vessels 

(grade I) (figure 1) was elicited in only five 

cases (3.1%), whereas the majority of the 

observed arteritis are associated with 

moderate intimal proliferation with moderate 

and severe luminal reduction and fell within 

grade II (figure 2) and grade III (figure 3) .They 

include 17 cases representing 10.6% (table 1). 

The percentage of obliterative endarteritis 

was compared with that of Arias-Stella 

reaction in the same 161 curettage specimens 

and with twenty endometrial biopsies obtained 

from non pregnant women as a control group. 

The total number of arteritis observed in 161 

abortion specimens is 22 (13.7%) while 

arteritis associated with moderate and severe 

luminal reduction is observed in 17 cases 

(10.6%) (table 1 & 2). The Arias-Stella reaction 

was only described in 11 cases among the 

same 161 abortion specimens representing 

6.8% of all cases (table 2), figure 4 shows 

Arias-Stella reaction. 

Vascular changes were also compared with 

twenty endometrial biopsies obtained from 

non-pregnant women who served as a control 

group. Table (3) shows that only one case of 

proliferative endometrium of the control group 

elicits mild degree of obliterative endarteritis 

while none of these changes were described 

in cases with secretary endometrium. 

Table (2): Frequency of vascular changes and 

Arias-Stella reaction in 161 endometrial 

biopsies of early pregnancy. 

Histopathological 

changes 

Number of positive 

cases 

Number of 

negative cases 

Total 

Arteritis 

22 

139 

161 

% 

13.7 

86.3 

100 

Arias- 

Stella 

reaction 

11 

150 

161 

Table (3): Vascular changes in control material 

Degree 

of 

vascular 

changes 

Grade 0 

Grade I 

Grade II 

GradeIII 

Total 

Proliferative 

endometrium 

9 

1 

0 

0 

10 

% 

90 

10 

0 

0 

100 

Secretory 

endometrium 

10 

0 

0 

0 

10 

% 

6.8 

93.2 

100 

% 

100 

0 

0 

0 

100 

Table (1): Frequency of vascular changes in 

161 endometrial biopsies of early pregnancy. 

Degree of 

vascular 

changes 

Number of 

cases 

Percentage 

Grade 0 

139 

86.3 

Grade I 

5 

3.1 

Grade II 

13 

8.1 

Grade III 

Total 

4 

161 

2.5 

100 

Figure (1): Grade I: mild thickening of the wall 

of the vessel (H & E) 



Figure (2): Grade II Arterioles with moderately 

severe wall Thickening (H & E). 

Figure (3): Grade III : marked thickening of the 

wall of the vessel with foam cells and severe 

narrowing of the lumen (H & E) 

Figure (4): Arias-Stella reaction (H & E) 

Discussion 

The finding of characteristic histological 

features that can be used to confirm the 

diagnosis of intrauterine pregnancy in the 

absence of fetal parts, villi or trophoblast has 

been the subject of previous works particularly 

when such a diagnosis is important as in 

cases of infertility with the possibility of 

abortion following hormonal therapy (8) . A 

recent field in which the diagnosis of 

pregnancy is necessary are cases in whom the 

conception was attempted by in vitro 

fertilization with subsequent abortion. 

Many endometrial patterns have been found 

to be helpful in suggesting that a gestation has 

occurred although some of these changes 

have been also described in the decidua of 

cases with extra uterine pregnancy or following 

hormonal therapy such as the Arias-Stella 

reaction. Nevertheless, it is still regarded as a 

possible physiological response to viable 

trophpblastic tissue (1) . 

In the present study, the frequency of 

obliterative endarteritis among abortion 

specimens was compared with that of Arias- 

Stella reaction in the same specimens. The 

frequency of arteritis in curettage specimens 

was 13.7% and was 10.6% for vessels with 

more severe lumen reduction. This percentage 

was higher than that of Arias-Stella reaction 

(6.8%), these results were remarkably 

comparable with that observed by Lichtig C et 

al (8) . On the other hand, only one case of 

proliferative endometrium of the control group 

showed a mild degree of arteritis, this finding 

might be explained by the over interpretation 

of histopathological features, or it could be 

related to an associated medical illness like 

hypertension or diabetes . 

Arias-Stella reaction was detected at a 

relatively low frequency among abortion 

specimens. This marker is less specific for 

intrauterine pregnancy and could also occur in 

extra uterine pregnancy or following hormonal 

therapy (1,9,12) . 

In conclusion, obliterative endarteritis was 

suggested to be due to the result of interaction 

of the trophoblast with the vessel wall and 

hence necessitating the occurrence of a 

pregnancy for this change (8) . They could be 



used with other histological and 

endocrinological parameters as suggestive 

marker of intrauterine pregnancy in the 

absence of chorionic villi, trophoblast, or other 

embryonic fragments. 

References 

1. Rosai J: Ackerman’s Surgical Pathology, 

9 th edition. Elsevier, 2004: 1737-1761. 

2. Barson AJ: Fetal and Neonatal Pathology: 

Perspectives for the General Pathologist, 

Praeger Publishers, 1982 : 27-64. 

3. Jauniaux E, Watson AL, Hempstock J, et 

al. Onset of maternal arterial blood flow 

and placental oxidative stress: A possible 

factor in human early pregnancy failure. 

Am J Pathol 2000 ; 157: 2111-2122. 

4. Hempstock J, Jauniaux E, Greenwold N, 

et al. The contribution of placental 

oxidative stress to early pregnancy failure. 

Hum Pathol 2003; 34:1265-1275. 

5. Jauniaux E, Hempstock J, Greenwold N, 

et al. Trophoblastic oxidative stress in 

relation to temporal and regional 

differences in maternal placental blood 

flow in normal and abnormal early 

pregnancies. Am J Pathol 2003; 162: 115- 

125. 

6. Kliman HJ. Uteroplacental blood flow. The 

story of decidualization, menstruation, 

and trophoblast invasion. Am J Pathol 

2000; 157(6):1759-1768. 

7. Lichtig C, Deutch M, Brandes JM. 

Vascular changes of endometrium in early 

pregnancy. Am J Clin Pathol 1984;81:702- 

707. 

8. Lichtig C, Korat A, Deutch M, et al. 

Decidual vascular changes in early 

pregnancy as a marker for intrauterine 

pregnancy. Am J Clin Pathol 1988 ; 90(3) : 

284-288. 

9. Kokawa K, Shikone T, Nakano R. 

Apoptosis in human chorionic villi and 

decidua in normal and ectopic pregnancy. 

Mol Hum Reprod 1998; 4 (1) : 87-91. 

10. Tam KF. Atypical glandular cells in 

cervical smear during pregnancy and 

postpartum period. Clin Med & Res 

2005;3(1):1-2. 

11. Thomas P, Connolly DO, Evans AC. 

Atypical Papanicolaou Smear in Pregnancy. 

Clin Med & Res 2005;3(1):13-18. 

12. Sternberg S, Antonioli DA, Carter D, et al : 

Diagnostic Surgical Pathology, 3 rd Edition. 

Lippincott Williams & Wilkins, 1999; 2182- 

2220. 



Seasonal variation of glycated hemoglobin A 1c % among diabetic 

patients in Mosul 

Nabeel N. Fadhil *, Omar A. Jarjees ** 

* Department of Medicine, Nineveh College of Medicine;** Department of Biochemistry, College of 

Medicine, University of Mosul. 


Received: 7 th Oct 2008; Accepted: 4 th May 2009. 

ABSTRACT 

Objective: To determine the seasonal variation of glycemic level among diabetic patients in Mosul, 

and to define the seasons where blood glucose may surge or decline. 

Patients and methods: An observational retrospective case series study of seven hundred HbA 1c % 

results pertaining to 653 randomly enrolled type 2 (96%), and type 1 (4%) diabetic patients which 

were collected over 28 consecutive months. The HbA 1c % mean of each month separately, and the 

HbA 1c % means of the months whose HbA 1c reflects the glycemic control of the preceding season 

were estimated, plotted, and statistically compared. 

Results: The monthly HbA 1c % means throughout the study period comprised a sinusoidal curve with 

higher values between early spring (March) to early summer (June) and lower values between early 

autumn (September) to early winter (January) of each year. Throughout the study period, the mean 

HbA 1c % of all early springs (8.87% ± 1.57% SD) was the maximal, while the mean HbA 1c % of all early 

autumns (7.81% ± 0.94% SD) was the minimal. 

Conclusion: Glycemic levels among diabetic patients in Mosul, as reflected by early spring's peak, 

and early autumn's trough of HbA 1c %, are highest during winter and lowest during summer. 


هدف البحث:‏ يهدف هذا البحث إلى بيان تأثير الفصول على مستوى آلوآوز الدم لدى السكريين في الموصل وتعيين 

الفصول التي قد يرتفع فيها مستوى آلوآوز الدم أو ينخفض.‏ 

مريض 

فحص مختبري لنسبة خضاب الدم الكلوآوزي تعود ل طريقة البحث:‏ اشتملت هذه الدراسة على شهراً‏ متتابعاً.‏ ولقد تم حساب معدل نسبة خضاب الدم الكلوآوزي لكل 

و‎١‎ خلال سكري عشوائي الاختيار من النمط شهر من أشهر فترة البحث على حده،‏ وللأشهر التي يمثل معدل خضاب الدم الكلوآوزي فيها مستوى سكر الدم خلال 

الفصول السابقة لها.‏ آما تمت جدولة النتائج ومقارنتها إحصائيا.‏ 

النتائج:‏ شكلت المعدلات الشهرية لنسبة خضاب الدم الكلوآوزي منحنىً‏ جيبياً‏ يرتفع ما بين بداية الربيع ‏(آذار)‏ وبداية 

وبداية الشتاء ‏(آانون ثاني)‏ من آل عام.‏ وآان معدل نسبة خضاب 

الصيف ‏(تموز)،‏ وينخفض ما بين بداية الخريف هو الأعلى خلال فترة البحث،‏ فيما آان معدل نسبة خضاب الدم 

الدم الكلوآوزي لبدايات الربيع آلها 

هو الأوطأ.‏ 

الكلوآوزي لبدايات الخريف آلها 

الاستنتاج:‏ إن مستوى سكر الدم لدى السكريين في الموصل،‏ آما يعكسه ارتفاع نسبة معدلات خضاب الدم الكلوآوزي في 

بدايات الربيع وانخفاضه في بدايات الخريف،‏ يبلغ مستواه الأعلى في فصل الشتاء والأوطأ في فصل الصيف.‏ 

S 

٦٥٣ 

easons affect body physiology in health 

and disease. Seasonal variation of 

sleeping metabolic rate, thyroid activity (1) , 

٧٠٠ 

٢٨ 

© 2009 Mosul College of Medicine 42 

٢ 

) بآ ( 

(١,٥٧ ± %٨,٨٧) 

(٠,٩٤ ± %٧,٨١) 

serum cholesterol, free testosterone, 

prolactin (2) , and hypertension (3,4) had all been 

reported. Studies on diabetes, generally


agreed on the finding that glycated 

hemoglobin A 1c % (HbA 1c %) vary seasonally; 

however, there were inconsistency in the 

results. 

Garde et al (in 2000) found that HbA 1c % 

increases in autumn and in spring and 

decreases in winter and in summer (1) , while 

Nordfelds and Ludrigsson (in 2000) showed 

that HbA 1c % of type 1 diabetes peaks in 

autumn and in winter and declines in spring 

and in summer. (5) Ishi et al (in 2001) found that 

the mean HbA 1c % is higher in winter compared 

with autumn. (6) Sohmiya et al (in 2004) 

reported higher levels of HbA 1c % in autumn 

and winter and lower level in spring and 

summer. (7) The last research in this regard 

was Tseng's et al (in 2004) at US that reported 

increasing values of HbA 1c in late winter to a 

peak in March-April, and decreasing values in 

late summer to a trough in September- 

October. (8) Seasonal variation in the last study 

was more marked at locations where wintersummer 

temperature difference is more than 

50F°, and among those who had higher 

glycemic levels. (8) 

Because of its clinical and therapeutic impact, 

seasonality of glycemic level among diabetic 

patients should be evaluated everywhere it is 

expected to be found in the world. Mosul, 

according to online Weather Reports 

Company, occurs at a latitude of 36°18´ N, a 

longitude 43° 12´ E, and an elevation of 732 ft. 

During winter (December-February) the 

average temperature is 6.6 C° (°F 44), with a 

light duration as short as (9.5) hours. During 

summer (June-August) the average 

temperature is 32.6° (°F 91), with a light 

duration as long as (14.5) hours. 

The objective of this study is to determine the 

seasonal variation of glycemic level among 

diabetic patients of Mosul, and to define the 

seasons where blood glucose surges or 

declines. 


An observational retrospective case series 

study design was used to analyze data 

collected over 28 consecutive months between 

the 1 st of December 2005 and the 31 st of 

March 2008. It enrolled 700 HbA 1c % test 

results that pertain to 653 randomly enrolled 

diabetic patients. Ninety six per cent of the 

patients were type 2 (n 626), and 4% were 

type 1 (n 27). Males (n 268) constituted 41% 

and females (n 385) were (59%). The mean 

age (±SD) was 22 (±10.7) years for type 1, 

and 55.4 (±6.8) years for type 2. All of the 

enrolled patients were on oral hypoglycemic 

drugs and/or insulin. There were no exclusion 

criteria apart from evident hemoglobinopathies 

or uremia. All of HbA 1c % tests were primarily 

done for the sake of assessment and 

management of the patients, however, 

patients' consent was formally obtained. 

Hemoglobin A 1c % of non fast intravenous 

blood samples, was colorimetrically 

quantitated, using standard solution as a 

reference (Stanbio laboratory, Texas USA). 

The tests were all conducted at one civil 

laboratory, and the data were all registered at 

one private clinic in Mosul. Most of HbA 1c % 

tests (n 621) were once achieved in the first 

visit of the patients, but 79 of them were 

repetitions of the test belonging to 32 patients. 

Because of the limited number of the study 

samples per month, sub grouping of the 

enrolled patients into sex, age, and disease 

duration was unfeasible. 

Method of electing the months whose 

HbA 1c % best represents glucose levels of 

the preceding seasons: 

Hemoglobin A 1c , a fraction of hemoglobin A, 

is glycated by non-enzymatic combination of 

ambient serum glucose to the terminal valine 

of beta chains. (9) Once glycated, HbA 1c will 

remain so all through the RBC life span (120 

days), hence HbA 1c % testing at any time 

reflects the mean blood glucose of the 

preceding 8-12 weeks. 

The RBC mass at any month can be 

arbitrarily divided into four generations. The 

oldest quarter is the one that has been 

synthesized about four months ago and going 

to vanish soon. The second is the one that has 

been synthesized about three months ago and 

will stay further one month. The third has been 

synthesized about two months ago and going 

to stay two months more, and the fourth is the 

one that has been thrown into the circulation 

about one month ago and going to survive for 

further 3 months. 



Considering the above concept, it was 

concluded that March’s mean HbA 1c % is the 

best representative of winter glycemia, as 75% 

of March's RBC mass has been synthesized, 

and glycated, during the preceding winter 

months (December, January, and February). 

Next to it in significance is the mean HbA 1c % 

of March and April together, as 68.75% of 

winter months' RBCs were synthesized in 

these two months, i.e. March and April. 

June, accordingly, is the best representative 

of spring season, followed by June and July, 

September is the best representative of 

summer, followed by September and October, 

and December is the best representative of 

autumn, followed by December and January. 

Because of the larger number of HbA 1c % 

tests in two months than in one month, that 

gives better statistical results, we elected the 

mean HbA 1c % of March-April, of June-July, of 

September-October, and of December- 

January, as representatives of winter, spring, 

summer, and autumn glycemic levels 

respectively. These months have been used 

for the same purpose in serious similar 

study. (8) The mean HbA 1c % of patients 

attending in each month, and the mean HbA 1c 

of patients attending in the representative 

months were estimated (±one SD). A t-test 

analysis was used to compare the numerical 

results and a P value


plasma cortisol, for example, had been found 

to be higher in winter than in summer. (18) 

Hansen and others, in this regard, also 

reported higher levels of cortisol during 

December-January in comparison to other 

months of the year. (18,19) . In respect to 

catecholamine role, adrenal medullectomized 

rats were shown to die faster than normal 

controls when exposed to cold stress. (20) 

Thyroid stimulating hormone (TSH), in its turn, 

is increased in laboratory animals by cold and 

decreased by heat. (20) Middle-aged and older 

men and women were proved to have 

significantly higher TSH levels in winter (21) . No 

studies were seen on glucagon or growth 

hormone seasonal variation. 

Whatever the homeostatic purpose behind 

the winter rise of these hormones, and 

whatever the other functions they exert during 

winter, glucose level elevation during this 

season seems to be beneficial in serving heat 

production (thermogenesis) to combat winter 

cold, we speculate. 

When the environmental temperature is lower 

than body temperature, the temperature 

control system institutes heat conserving 

procedures and increases thermogenesis .(22,23) 

Thermogenesis in human is achieved by 

muscle contraction, assimilation of food, and 

vital processes of basal metabolic rate 

(BMR). (21) 

Shivering, an involuntary muscle contraction, 

is promoted during winter to provide heat, in 

addition to semiconscious increase of motor 

activity. (20) The energy in the muscles is 

liberated from hydrolysis of the compounds 

adenosine triphosphate (ATP), and, to a lesser 

extent, phosphoryl creatine (PC) (24) . After 

hydrolysis and energy liberation, ATP and PC 

are regenerated using energy provided by the 

breakdown of glucose to CO2 and H2O. (24) 

Glucose involvement in the regeneration of 

ATP and PC highlights the essential role of 

glucose in muscular thermogenesis during 

winter. 

Basal metabolic rate, the other major 

thermogenic process, also increases in winter. 

Eskimo have been shown to have elevated 

BMR relative to predicted values. This 

elevation, has been postulated, to be a 

physiological adaptation to chronic and severe 

cold stress (25) . Sleeping metabolic rate was, as 

well, shown to be maximal in winter and 

minimal in summer (2) . Glucose role in 

promoting metabolic thermogenesis seems to 

be as essential as in the muscular 

thermogenesis. Hepatic glucose release was 

reported to positively correlate with BMR both 

in type 2 diabetes and in control subjects (26) . 

Inefficient thermogenesis in diabetes: 

In diabetes, especially type 2, thermogenesis 

frankly looks inefficient for many reasons. 

First: insulin resistance reduces glucose 

uptake and energy expenditure irrespective of 

obesity (27) . Insulin resistance in diabetes is, as 

well, associated with a decreased sensitivity 

and responsiveness to norepinephrine in lab 

animals suggesting a reduced thermogenic 

capacity among diabetic patients (28) . Second: 

autonomic neuropathy that complicates 

uncontrolled diabetes, further contributes to 

thermogenic failure. Patients whose ß- 

adrenergic receptors are blocked by ß- 

adrenergic blockers had been found to have a 

lower BMR (29) , suggesting the importance of 

autonomic nervous system in the metabolism, 

thence the thermogenesis. Young diabetic 

patients with autonomic neuropathy have, 

also, showed impaired thermoregulation to 

external cooling, even during metabolic 

stability, which may predispose to 

hypothermia (30) . Moreover, shivering, the 

involuntary autonomic activity that greatly 

contributes to thermogenesis during winter is 

expected to be hindered in diabetes. Tseng's 

finding of greater seasonal variation of blood 

glucose among the higher HbA 1c (>9%) 

subgroup (8) could be due to the higher 

prevalence of autonomic neuropathy among 

subjects of this subgroup. The depressed 

thermogenesis in diabetes, also, interprets the 

higher risk of hypothermia among elderly 

diabetic patients (31) . 

In conclusion, we believe that glucose rise in 

winter is a part of a normal thermoregulatory 

strategy in human, but, the depressed 

thermogenesis in diabetes leads to 

accumulation rather than making use of the 

winter rise of glucose, producing a marked 

winter glycemic surge. 



Whatever the underlying mechanism, Mosul's 

diabetic patients and health providers should 

seriously consider glycemic rise in winter, and 

be aware of a reciprocal summer 

hypoglycemia. 

Figure (1): Monthly HbA 1c % mean (±SD) throughout the study period. The first three letters of each 

month represent the months’ name during the study period. 

Table (1): HbA 1c % mean of the season representing months all through the study period, the number 

of patients (n), and the P value. 

Season representing months 

of the assigned years 

Mean HbA 1c % 

(±SD) 

n 

P value 

Decembers - Januaries 

2005, 2006, 2007, 2008 

Represent autumns 

Marches - Aprils 

2006, 2007 

Represent winters 

Junes - Julies 

2006, 2007 

Represent springs 

Septembers - Octobers 

2006, 2007 

Represent summers 

8.52% ± 0.89 113 

8.87% ± 1.57 111 

8.55% ± 0.78 43 P


Table (2): The monthly, and the season representing months' HbA 1c % mean in each year separately, 

the number of patients (n), and the P values. 

Year Month n Mean HbA 1c % 

2005 December 10 7.97 ± 2.2 

January 18 10.53 ± 2.7 

February 36 8.84 ± 1.9 

March 27 8.64 ± 1.7 

April 27 8.86 ± 1.4 

May 20 8.7 ± 1.8 

Mean HbA 1c % of season 

representing months 

8.75% ± 0.15 

P value 

2006 

June 13 8.61 ± 0.59 

July 10 8.49 ± 1.5 

August 6 8.42 ± 1.5 

September 32 8.15 ± 1.1 

P


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The prevalence of fatty liver disease among diabetics in Mosul 

Dhaher J. S. Al-Habbo*, Younise A. Khalaf**, Nabeel Alkhiat***, Ali K. Habash*** 

*Department of Medicine, College of Medicine, University of Mosul; ** Diabetes clinic, Dohuk Directorate 

of Health, Dohuk; ***Nineveh Directorate of Health, Mosul. 


Received: 26 th Nov 2008; Accepted: 4 th May 2009. 

ABSTRACT 

Objectives: To examine the occurrence of fatty liver disease in diabetic patients type 1 and 2 disease 

and to focus the attention in our locality about this serious condition. 

Method: This prospective study of one hundred ten diabetic patients and one hundred patients as 

control was conducted in Ibn-Sena Teaching Hospital. Patients and control were referred from Al- 

Wafa Diabetic Center in Mosul, the outpatient department, and from the Medical Center of Mosul 

Medical College University of Mosul. All were referred for clinical assessment and for ultrasound 

examination of their abdomen. 

Results: The patients include 34 patients with type 1 and 76 patients with type 2 diabetes. Of the 110 

patients examined, 52.7% proved to have fatty infiltration in the liver by ultrasonography with no 

statistically significant difference between male and female. 

Patients with type 2 diabetes mellitus were more vulnerable to develop fatty infiltration of the liver 

than type 1 diabetes mellitus, with statistically significant difference between them. Eighty six percent 

of patients with NAFLD were type 2 diabetes and 13.7% were type 1 diabetic disease. The control 

group have NAFLD in 8% only. 

The age of the patients shows positive correlation and fatty infiltration in the liver increased with age. 

The longer the duration of diabetes mellitus makes the patients more likely to develop fatty infiltration 

in the liver. 

The postprandial blood sugar level correlates significantly with the presence of fatty infiltration in the 

liver while the fasting blood sugar level does not. 

Conclusion: Nonalcoholic fatty liver disease is common in our diabetic patients, occurs in both type1 

and type 2 diabetes. Ultrasound may be used for epidemiological studies for detection of NAFLD in 

diabetics. 

Keywords: Diabetes mellitus; fatty infiltration; Ultrasound. 


تم اجراء دراسة للتحري عن وجود ترسبات الشحوم في الكبد من عدمه في المرضى المصابين بداء السكر.‏ 

أجريت الدراسة في مستشفى ابن سينا التعليمي بالموصل على مريض مصاب بداء السكر،‏ منهم مصاب بداء 

السكر المعتمد على الأنسولين و‎٧٦‎ مريض مصاب بداء السكر المعتمد على المعالجة بالحبوب المخفضة للسكر في الدم.‏ 

وتم آذلك فحص مجموعة ضابطة من ١٠٠ شخص لايعانون من داء السكر.‏ 

أخذت عينة من دم مرضى السكر لفحص نسبة السكر في الدم وهم صائمون وآذلك بعد الأآل.‏ تم اجراء فحص الأمواج 

فوق الصوتية للمرضى وللعينة الضابطة للتحري عن وجود ترسبات الشحوم في الكبد.‏ 

٣٤ 

١١٠ 



النتائج:‏ تبين ان 52.7% من العينة المفحوصة من مرضى السكر يعانون من وجود ترسبات الشحوم في الكبد،‏ وتبين ان 

منهم مصابين بداء السكر المعتمد على المعالجة بالحبوب المخفضة للسكر و‎13.7%‎ منهم مصاب بداء السكر 

المعتمد على الانسولين.‏ آذلك تبين ان عمر المريض ومدة الاصابة بالسكر تتناسب طرديا مع درجة الاصابة بترسبات 

الشحوم في الكبد.‏ نسبة الاصابة بترسبات الشحوم في الكبد في العينة الضابطة آانت %٨ فقط.‏ 

٨٦% 

N 

onalcoholic fatty liver disease (NAFLD) 

was described first by Ludwig in 1980 (1) . 

Most patients with nonalcoholic fatty liver 

disease are asymptomatic, but some may 

complain of fatigue and right upper quadrant 

abdominal fullness or pain with or without 

hepatomegaly (2) . The prevalence of NAFLD in 

the general population is estimated to be 20% 

(3) . Nonalcoholic fatty liver disease now refers 

to a spectrum of diseases of the liver ranging 

from steatosis (i.e., fatty infiltration of the liver) 

to nonalcoholic steatohepatitis (NASH) (i.e., 

steatosis with inflammation and hepatocyte 

necrosis) to cirrhosis. The prevalence of 

nonalcoholic steatohepatitis (NASH) in the 

United States is 2-3% , which makes NASH 

the potentially most common hepatic 

disease (4) . 

Diabetes is an important independent 

predictor of severe hepatic fibrosis in NASH (5) . 

Up to one third of patients with NAFLD have 

diabetes or fasting hyperglycemia at the time 

of diagnosis with NASH (6-7) . Nonalcoholic fatty 

liver disease if untreated, will progress to 

NASH and end up by cirrhosis, because of that 

some of them will die in few years time (8) .The 

fibrosis of the liver may progress to cirrhosis, 

hepatocellular cancer and liver-related death 

(9,10) . The most frequent association of NASH 

is type 2 diabetes, although difficult-to-control 

insulin-dependent diabetes may also be 

affected (11) . 

In type 2 diabetes mellitus and in obesity, 

insulin resistance plays a fundamental role 

and is the most predisposing and reproducible 

factor in NASH (12) . 

Ultrasonography of the liver has a sensitivity 

of 82 to 89 percent and a specificity of 93 

percent for identifying fatty liver infiltrate (13,14) . 

As it is known that nonalcoholic fatty liver 

(NAFL) is a medical condition that may 

progress to end-stage liver disease with the 

consequent development of portal hypertens- 

ion and liver failure (8) , this study aimed to 

examine the occurrence of fatty liver disease 

in diabetes mellitus type 1 and 2 disease and 

to focus the attention in our locality about this 

serious condition. 

Methods 

This was a prospective study for one hundred 

ten (110) diabetic patients and one hundred 

(100) patients as control group referred mainly 

from Al-Wafa Center in Mosul, the outpatient 

department, and from the Medical Center of 

Mosul Medical College University of Mosul, for 

clinical assessment and for ultrasound 

examination. The patients' agreements were 

taken by their verbal consent. The control 

group was selected randomly from patients 

consulting the radiology department for 

ultrasound of the abdomen. 

The inclusion criteria and the clinical 

assessments of the patients and the control 

group were mainly to exclude the presence of 

obesity (Body Mass Index (BMI) more than of 

>30 Kg/m 2 ) and to exclude any history of 

alcohol intake. There must be no evidence of 

chronic liver diseases, this specifically for 

history of hepatitis B (HBsAg) and hepatitis C. 

Furthermore there must be no history of 

chronic renal diseases. 

All the ultrasound examinations were done in 

Ibn-Sena Teaching Hospital. 

The age of the patients ranged from 11 to 73 

years, 47 male and 67 female, the duration of 

diabetes was from 8 to 32 years. While the 

age of the control group patients ranged from 

13 to 75 years, 52 males and 48 female with 

their age group distribution . 

The patients include 34 patients with type 1 

and 76 patients with type 2 diabetes mellitus, 

43 patients on insulin therapy and 67 on oral 

hypoglycemic drugs. All the patients had their 

fasting and postprandial blood sugar done, 

HbA1c done only for 69 patients who agree to 

do the test in a private laboratory. 



The statistical calculations were done for all 

parameters and the different variables by 

using the means, SD, cross-tabulation, the chi- 

Square test (Fishers exact test). 

Results 

Of the 110 patients examined 58 (52.7%) 

proved to have fatty infiltration in the liver by 

ultrasonography and 52 (47.2%) patients had 

no fatty infiltration in the liver. There was no 

statistically significant difference between male 

and female with p-value >0.05 (NS) when 

tested by the cross-tabulation and the chi- 

Square test as in table (1): 

Table (1): Fatty liver changes in correlation with the sex of the patients 

Sex 

Non-fatty liver 

Fatty liver 

No. % No. % 

Male 24 51.1 23 48.9 

Female 28 44.4 35 55.6 

Total 52 58 

p-value 

>0.05 (NS) 

As it was expected, our study indicates that 

the type of diabetes mellitus correlates very 

well with the frequency of fatty infiltration in the 

liver and was found to have positive correlation 

with p-value < 0.001 by using the crosstabulation 

and the chi-Square test (Fishers 

exact test) as in table (2): 

Table (2): Fatty liver changes in correlation with the type of diabetes mellitus 

DM 


Fatty liver 

No. % No. % 

Type 1 26 76.5 8 23.5 

Type 2 26 34.2 50 65.8 

Total 52 58 

p-value 


Table (4): Fatty liver changes according to age distributions 

Age groups (year) 


Fatty liver 

No. % No. % 

11-20 9 81.8 2 18.2 

21-30 8 66.7 4 33.3 

31-40 8 81.8 3 18.2 

41-50 11 52.4 10 47.6 

51-60 11 29.7 26 70.7 

>60 5 27.8 13 72.2 

Total 52 58 

p-value 

15 14 33.3 28 66.7 

Total 52 58 

p-value 

0.05 (NS) 

HbA1c (%) 9.51 ± 1.59 9.25 ± 1.52 >0.05 (NS) 

Of the 100 patients of the control group 

examined only 8 (8%) proved to have fatty 

infiltration in the liver by ultrasonography, 5 

female and 3 male patients as in table (7): 

Table (7): Age distributions of the control 

group and the NAFLD among them. 

Age 

groups 

(year) 

Numbe 

r of 

patients 

Fatty 

liver 

Female 

positive 

Male 

positive 

11-20 8 0 5 3 

21-30 11 0 

31-40 22 0 

41-50 27 2 

51-60 16 3 

>60 16 3 

Total 100 8 (8%) 



Discussion 

Typical patient with NAFLD as had been 

described by Powell EE and coauthors, is a 

middle-aged woman (15) . In our studied sample 

58 patients were labeled to have NAFLD by 

ultrasound, 23 male and 35 female patients 

with no statistically significant difference 

between male and female. 

Males generally have greater abdominal 

visceral fat mass, which has a lipolytic nature 

and is in close proximity with the portal 

system. Furthermore, visceral fat and therefore 

free fatty acids, exposing the liver to large 

amounts of oxidizing substances or 

triglycerides which may either get stored 

(steatosis) or secreted into the circulation (16) . 

This phenomenon may explain our finding. 

Furthermore, epidemiologic studies of NAFLD 

suggest that men are at least as likely as 

women to have NAFLD or even higher 

(6,17,18,24) . All these findings are similar and 

support our results. 

Fatty liver disease was found in (52.7%) of 

our patients with diabetes, this result is the 

same as in other studies, where they found 

that NAFLD occurs in about 50 percent (range, 

21 to 78 percent) of patients with diabetes 

(6,7,19) . 

Fifty out of the fifty eight diabetic patients with 

fatty liver disease, were type 2 diabetes 

mellitus (86%) of all patients with NAFLD and 

form (65.789%) of patients with type 2 

diabetes mellitus. Furthermore, 44 patients on 

oral hypoglycemic therapy have NAFLD which 

makes 75.9% of the patients with NAFLD, this 

difference in the number is because some of 

our patients on insulin therapy were originally 

type 2 diabetes, these findings were similar to 

others (6,7,20) . 

Type1 diabetes is less likely to cause NAFLD 

but in our patients 13.7% of those with NAFLD 

were type 1 diabetes, which form nearly 

(23.5%) of our patients with type 1 diabetes. 

These findings are different from our control 

group where NAFLD are found in 8% only. 

Although our control group is not big enough 

to represent the Iraqi population, our control 

group had a lower figure of NAFLD if we 

compare it with other studies 

(3) . The 

prevalence of NAFLD in type 1 diabetes in our 

study is in agreement with other studies where 

they found even children with type 1 diabetes 

mellitus may develop NAFLD, although our 

figure is somewhat higher probably due to the 

older age group among our adult patients and 

even among the children in our patients 

(11,21,22) . The established risk factors for NAFLD 

in children include obesity, insulin resistance, 

and diabetes (23) . Although the evidence of 

insulin resistance is common among type 2 

diabetic in youth, it is also seen in 30% of 

youth with type 1 diabetes (35) . These findings 

may explain the prevalence of fatty liver in our 

studied patients with type 1 diabetic disease . 

The postprandial blood sugar (PPBS) level 

correlates significantly with the presence of 

NAFLD, while the fasting blood sugar (FBS) 

level and the HbA1c value showed no 

significant correlation with the development of 

NAFLD. The PPG is a marker of glycemic 

burden and is as predictive or more predictive 

of the risk for complications of diabetes when 

compared with FPG (36) .The positive correlation 

between fatty liver and the level of 

postprandial blood sugar may indicate the 

presence of insulin resistance in this group of 

patients. Insulin resistance is a major feature 

of NAFLD that, in some patients, can progress 

to steatohepatitis (37) . The HbA1c level was 

done only in about 62% of our patients, 

therefore its value may be not truly 

representative of the its real correlation with 

the NAFLD. 

Ultrasonography as a diagnostic test had 

been found to have a sensitivity of 89 percent 

and a specificity of 93 percent in detecting 

NAFLD (13,25) . 

Nonalcoholic fatty liver disease is usually 

diffusely distributed or occasionally focal. 

Consequently, CT scans may be 

misinterpreted as malignant liver masses (26) . 

Few studies compare ultrasound and CT 

scans for diagnostic accuracy in NAFLD and 

they were nearly the same with a sensitivity of 

75%, 80% respectively (27) . 

The histopathological diagnosis by liver 

biopsy is logically the golden standard method 

for detection of NAFLD, but this requires the 

equipments, laboratory investigations, 



preparation of the patients by doing blood 

group and cross match , the expertise in doing 

liver biopsy and the patient's consent because 

of the expected complication of this rather 

invasive and sometimes harmful procedure. 

Furthermore, recent studies have questioned 

its reliability because it may frequently miss 

the diagnosis. More than 24% of proven 

NAFLD may be missed if only one biopsy 

sample had been taken (28) . 

For all the above reasons we decided that 

our radiologist should examine our patients by 

using the new version of ultrasound 

(MEDISON 8000 LIVE KOREA) which is 

available in Ibn-Sena Teaching Hospital, as 

this procedure is available and affordable free 

off charge to all our patients. 

Hepatic magnetic resonance spectroscopy 

imaging is more sensitive than ultrasound for 

detecting minor degrees of steatosis and 

allows a quantitative assessment of fatty 

infiltration of the liver (29,30) . 

This rather small study indicates that NAFLD 

is present in our diabetic patients involving 

more than 50% of them. These findings should 

raise the alarm for the problem of NAFLD in 

our diabetic patients and to look for all the 

available means to prevent and/or to treat the 

high risk group patients. Furthermore, 

increased prevalence of liver disease occurs in 

both type 1 and type 2 diabetic patients, 

resulting in an increased prevalence of 

cirrhosis, portal hypertension, liver failure, 

steatosis, iron overload, and even hepatoma 

(31) . Nonalcoholic fatty liver disease some 

times follows a relatively benign course and 

remains stable (32) . However NAFLD is the 

most common cause of elevated liver enzymes 

in adults in the United States and the most 

common cause of cryptogenic cirrhosis (33,34) . 

Conclusion 

Nonalcoholic fatty liver disease is common in 

our diabetic patients, occurs in both sexes and 

in type 1 and type 2 diabetes mellitus. 

Ultrasound may be used for epidemiological 

studies for detection of NAFLD in diabetics, 

general population and obese people. 

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4753-4761 



Diagnostic laparoscopy in female infertility 

Raida M. Al-Wazzan*, Entessar Abdel Jabbar ** 

* Department of Obstetric and Gynecology, College of Medicine, University of Mosul;** Al-Batool 

Teaching Hospital, Mosul. 


Received: 31 st Dec 2007; Accepted: 3 rd Jun 2009. 

ABSTRACT 

Objective: To highlight the importance of laparoscopic evaluation in the etiology of infertility and to 

evaluate the etiology in primary and secondary infertility. 

Methods: This retrospective study included 1233 patients complaining of infertility, 919 patients had 

primary infertility and 314 patients had secondary infertility. All had been subjected to diagnostic 

laparoscopy at the Infertility Center in Al-Batool Teaching Hospital, Mosul. 

Results: Laparoscopy diagnosed pelvic abnormality in 87.27% of infertile patients which was 

statistically significant difference comparing to no abnormality detected in 12.73%. The ratio of 

positive findings in secondary infertility was significant in comparison with the positive findings in 

primary infertility. Single pelvic abnormality detected during laparoscopy among infertility patients was 

seen in 75.09% of cases and it was statistically different from multiple pelvic abnormality: 24.91%, 

and it was highly significant among primary infertility patients (77.24%) and among secondary 

infertility patients (30.87%). Among all infertile patients, ovarian factor was the most common 

(66.83%) followed by tubal factor (22.03%), endometriosis (4.46%), pelvic inflammatory disease 

(2.85%), pelvic adhesion (2.10%) and uterine fibroid (1.73%). Ovarian factor was highly significant in 

primary infertility while tubal factor and pelvic inflammatory disease were the highly significant in 

secondary infertility. 

Multiple pelvic pathology identified by laparoscopy showed the tubal factors associated with poly 

cystic ovary in 29.49% of cases (31.66% in primary infertility and 25% in secondary infertility with no 

significant statistical difference). Pelvic inflammatory disease associated with other pelvic abnormality 

34.09% was highly significant among secondary infertility patients. Congenital uterine abnormalities 

was not seen alone, it was seen associated with other causes among primary infertility patients (9 

cases 0.72%). 

Conclusion: Diagnostic laparoscopy is a valuable technique and is a mandatory invasive 

investigation for complete assessment of female infertility before the couple progresses to infertility 

treatment especially where assisted reproductive techniques were not available. 

Keywords: Infertility; primary infertility; secondary infertility; diagnostic laparoscopy. 


الهدف:‏ لتبيان أهمية الناظور التشخيصي في معرفة سبب العقم عند النساء في حالات العقم الأولي والثانوي.‏ 

الطريقة:‏ دراسة أستعادية ل مريضة لديها حالة عقم من اللواتي راجعن مرآز العقم في مستشفى البتول التعليمي في 

مريضة تعاني من العقم الأولي و ٣١٤ مريضة تعاني من العقم الثانوي.‏ 

النتائج:‏ أظهرت النتائج بان الناظور شخّص وجود سبب في الحوض في من الحالات وان وجود سبب واحد 

في الحوض هو الأآثر في حالات العقم الأولي بينما وجود عدة أسباب في الحوض آانت الأآثر بين حالات 

العقم الثانوي.‏ المبيض ومشاآله السبب الرئيسي في حالات العقم وهو السبب الأآبر في العقم الأولي بينما مشكلة الأنابيب 

%٨٧,٢٧ 

%٧٥,٠٩ 

١٢٣٣ 

الموصل.‏ ٩١٩ 



والتهابات الحوض آان السبب الأآبر في حالات العقم الثانوي.‏ وفي حالات العقم عامة التي وجد فيها أآثر من سبب وجد 

مشكلة الأنابيب وحالة تكيس المبيض في ووجد أن مشكلة التهاب الحوض مع أسباب أخرى أآثر حدوثا في 

حالات العقم الثانوي.‏ 

الاستنتاج:‏ الناظور التشخيصي فحص له قيمة لإآمال فحوصات النساء اللواتي لديهم حالة عقم قبل العلاج المتقدم خاصة 

في حالة عدم توفر وسائل العلاج 

%٢٩,٤٩ 

. 

I 

n Iraq (like some other countries), infertility 

and uncontrolled fertility are two major 

problems affecting women’s health and quality 

of life leading to social and psychological 

upsets (1) . Infertility is defined as the inability to 

conceive after one or two years of unprotected 

intercourse. It may be primary or secondary in 

nature (2,3) . It is one of the most prevalent 

chronic health disorders involving young 

adults (4) . Major causes of infertility include 

male and female factors (5) . Female factors 

include: ovarian dysfunction, tubal disease, 

endometriosis, and uterine or cervical factors. 

In approximately one fourth of couples, the 

cause is uncertain and is referred to as 

unexplained infertility and the etiology is 

multifactorial for some couples (5) . 

The appropriate selection of investigations 

based on problem areas identified by history 

and physical examination would guide the 

physician in the management of the infertile 

couple (6) . Diagnostic laparoscopy is not 

recommended as a first line screening test, 

however, it should be considered in patients 

with a history suggestive of endometriosis, 

previous pelvic inflammatory disease or 

previous pelvic surgery. Furthermore, if the 

hysterosalpingography reports an abnormal 

result, verification should be carried out with 

diagnostic laparoscopy. Some clinicians hold 

the view that to diagnose unexplained 

infertility, both peritoneal factor and 

endometriosis should be excluded, even in 

patients with normal hysterosalpingography, 

by carrying out laparoscopic examination (3) . As 

a result, diagnostic laparoscopy is a valuable 

technique and is a mandatory invasive 

investigation for complete assessment of 

female infertility in many clinics before the 

(1, 7-11) 

couple progresses to infertility treatment 

and making a decision to go to assisted 

reproductive technology (12,13) . 

On visual laparoscopic inspection, the 

appearances of the ovaries are suggestive of 

certain clinical conditions (1) . Most ovarian 

abnormalities can be managed 

laparoscopically and often a laparoscopic 

examination of the adnexa will enable the 

gynecologist to decide if laparotomy is 

indicated. Laparoscopy is an ideal procedure 

for diagnosing and staging endometriosis, 

because the magnification offered by the 

laparoscope (14) . It is generally accepted that it 

is the gold standard in diagnosing tubal 

pathology (15,16) and its etiology (15) . It is superior 

in evaluation of proximal tubal 

obstruction (3,4,14) , and other intra-abdominal 

causes of infertility, as pelvic adhesions and 

endometriosis (1,3,5,8,9,12,14,15,17,18) . It also allows 

the identification of peritubal adhesions either 

of inflammatory origin or due to 

endometriosis (7,19) . For these reasons, the cost 

and associated surgical morbidity of 

laparoscopy have traditionally been justified (7) . 

This study was carried out to highlight the 

importance of laparoscopic evaluation in the 

etiology of infertility and to obtain an idea 

about the etiology of primary and secondary 

infertility in our locality. 

Methods 

This 5 years retrospective study was done at 

the Infertility Center in Al-Batool Teaching 

Hospital where files of infertile women who 

have undergone diagnostic laparoscopy from 

January 2001 to January 2005 were recorded 

and included in the study. 

One year or more of regular unprotected 

sexual intercourse without conceiving is the 

definition of infertility considered in this center. 

All infertile patients underwent evaluation with 

history from male and female and clinical 

examination, as well as evaluation of 



ovulation, tubal patency (most cases) and 

male factor by seminal fluid analysis. 

Diagnostic laparoscopy was decided to the 

infertile patient who had one or more of the 

following: history suggestive of endometriosis, 

previous pelvic inflammatory disease, previous 

pelvic surgery, abnormal hysterosalpingography 

or there was greater than 36 months 

period of infertility. 

Diagnostic laparoscopy was done using the 

same method and the same principle in 

reporting the result by the four gynecologists 

who work in this center (at study time) who 

had approximately same experience level in 

doing laparoscopy. 

Laparoscopy was done as a day case under 

general anaesthesia. Pneumoperitoneum was 

created by CO 2 gas through varess needle. 

During the procedure, pelvis was inspected, 

visualizing uterus, fallopian tubes, ovaries, 

round ligaments, uterovesical pouch, 

uterosacral ligaments and pouch of Douglas. 

The tubes were visualized and any 

abnormalities were noted. Both ovaries were 

examined regarding their size, shape, 

evidence of ovulation. Peritubal, periovarian 

and omental adhesions, tubo-ovarian masses, 

endometriotic deposits, fibroid, presence of 

free fluid in the pouch of Douglas or any other 

pathology of the appendages if present was 

noted. 

The patency of the fallopian tubes was 

ascertained by injecting methylene blue into 

the uterine cavity and observing it as it spilled 

through the fimbrial ends. 

The statistical analysis was performed using 

statistical program (Minitab version 11) and 

Fisher test (sometimes). P value


Ovarian factor (66.83%, n=540) was the 

highest abnormality seen among infertility 

patients followed by tubal factor (22.03%, 

n=178), endometriosis (4.46%,n=36), pelvic 

inflammatory disease (PID) (2.85%, n=23), 

pelvic adhesion (2.10%, n=17) and uterine 

fibroid (1.73%, n=14). Bilateral tubal blockage 

diagnosed in 74.43% of tubal factor cases. 

Although ovarian factor was the most 

common cause identified in both primary 

(n=445, 72.83%) and secondary infertility 

(n=95, 48.22%) but it was highly significant in 

primary infertility (p value=0.000). Tubal factor 

(39.09%) and pelvic inflammatory disease 

(5.08%) were significantly different (p value 

0.000, 0.03 respectively) in secondary infertility 

than primary infertility (16.53%, 2.13%). Other 

causes showed no significant difference 

between them. Table (3). 

Most tubal factor cases of primary and 

secondary infertility were diagnosed to have 

bilateral blockage (69.306% and 81.33% 

respectively) with no significant difference 

between them. 

Table (3): Distribution of causes among primary and secondary infertility. 

Causes 

Primary infertility 

Secondary infertility 

No. % No. % 

P-value 

Chi sq 

Ovarian 445 72.83 95 48.22 0.000 40.695 

Tubal 101 16.53 77 39.09 0.000 25.903 

Pelvic inflammatory 

disease (PID) 

13 2.13 10 5.08 

0.037 4.360 

Endometriosis 30 4.91 6 3.04 0.289 1.123 

Pelvic adhesion 13 2.13 4 2.03 0.934 0.007 

Uterine Fibroid 9 1.47 5 2.54 0.319 0.993 

Total 611 197 

Polycystic ovary was the common finding 

among infertility patients (97.2% (primary 

97.3% and secondary 96.84% of ovarian 

factors) while ovarian cyst and tumour 

constitute 2.7%; table (4). There was no 

significant statistical difference between 

primary and secondary infertility. 

Table (4): Ovarian pathologies seen in laparoscopy 

Pathology 

infertility 

Primary 

infertility 

Secondary 

infertility 

No. % No. % No. % 

P-value 

Chi sq 

Poly cystic ovary 

(PCO) 

Ovarian cyst and 

tumour 

525 97.22 433 97.3 92 96.84 0.976 0.001 

15 2.78 12 2.7 3 3.16 0.809 0.058 

Total 540 445 95 

In the study multiple pelvic abnormalities 

identified by laparoscopy showed the tubal 

factor associated with poly cystic ovary (PCO) 

in 83 cases (39.71%), (61 cases primary 

infertility (44.52%) and 22 cases secondary 

infertility (30.55%)) with no significant 

statistical difference. 



Among patients with tubal blockage with 

other apparent pelvic pathology, 71 cases 

(76.34%) due to pelvic inflammatory disease 

(PID), 17cases (18.28%) due to endometriosis, 

5 cases (5.38%) due to pelvic adhesion. 

Pelvic inflammatory disease associated with 

other abnormality seen in 71 cases (26.49%) 

with statistical difference between secondary 

infertility (n=30, 34.09%) and primary infertility 

(n=41, 22.77%). 

All cases of uterine abnormality(9 cases, 

0.72%) were seen in primary infertility 

associated with other abnormality (7cases with 

polycystic ovary and 2 with tubal blockage). 

Other associations between multiple pelvic 

abnormalities show no significant difference 

between primary and secondary infertility. 

Discussion 

According to the criteria followed in this study 

for choosing infertile patients for diagnostic 

laparoscopy, 74.53% had primary infertility and 

25.47% had secondary infertility. It is nearly 

similar to the laparoscopic study conducted in 

Bahawal Victoria Hospital (1) where (72.19%) of 

infertile women had primary infertility and 

(27.81%) had secondary infertility and to the 

result of Krishna et-al study (20) where 70.44% 

primary infertility and 29.55% secondary 

infertility, as well as to Cairo study (14) where 

primary and secondary infertility affected 

70.7% and 29.3% of the couples respectively . 

Pelvic abnormalities were diagnosed in this 

study in 87.27% of infertility cases which is 

higher than other studies where seen in 

61.03% in Bitzer et-al study (17) , 62% in 

Oxford (7) and 58.58% in Mehmood study (1) . 

This can be explained by the design of most 

other studies which include unexplained 

infertility only. 

pelvic abnormality in primary infertility was 

seen in 73.51% and in secondary infertility in 

26.49% in this study which is nearly similar to 

the result seen in Bahwall study (1) where 

73.73% of primary infertility and 26.26% of 

secondary infertility, But it differs from Bitzer 

et-al study (17) which showed the same 

percentage of abnormal findings in primary 

and secondary infertility. The positive findings 

in secondary infertility were significantly higher 

than primary infertility which conforms with 

Hovav et-al study (21) . 

During evaluation of infertility causes in this 

study, the ovarian factor (66.83%) was the 

most common cause followed by tubal factor 

(22.03%) which differ from Mehmood study (1) 

and Usmani et-al study (22) where the tubal 

factor was the most common cause and 

constituted 35.85%, and 37.6% of cases 

respectively while ovarian factor was seen in 

32.83%, and 26.08% of cases respectively. 

These difference can be explained by the 

omission of diagnostic curettage as a routine 

investigation which was done by different 

category health personnels during evaluation 

of infertile patient in Mehmood study as well as 

lower incidence of sexually transmitted 

disease . 

Pelvic endometriosis (4.46%) was seen less 

frequently than in other studies (16.16% (1) , 

5.35% (22) ) due to the difference in racial and 

environmental factor as well as to the practice 

of avoiding sexual intercourse at time of 

menstruation. But it is seen more than in 

Otolorin et-al study (23) (1.8%) which may be 

due to difficulty in diagnosing mild cases in 

early use of laparoscopy as it was done in 

1987. 

Pelvic inflammatory disease (2.85%) and 

pelvic adhesion (2.1%) in our study was seen 

less frequently than in other studies (23,24) ; it 

may be due to low incidence of sexually 

transmitted diseases in our locality. 

Uterine fibroids (1.73%) diagnosed in 

infertility patients in this study was much lower 

than in other studies where was seen in 

7.14% (22) and 15.15% (1, 23) which could be 

explained by the difference in racial and 

environmental factors between the studies. 

Polycystic ovary seen in 97.22% of cases 

among ovarian factor of infertility which is 

somewhat similar to Usmani et-al study (22) 

where it accounted for all cases. Bilateral tubal 

blockage constituted 74.43% of patients with 

tubal blockage which is higher than Vasiljevic 

et-al study (25) where was seen in 50.94% of 

cases and lower than 78.57% seen among 

infertile Nigerian women (23) . 

While comparing the most significant cause 

among primary and secondary infertility, the 



result showed ovarian factor (72.38%) among 

primary infertility group and tubal factor 

(39.09%) among secondary infertility group, 

which differ from other studies (24,26) where all 

showed the tubal factor was the significant 

cause among primary and secondary infertility. 

This could be explained by the fact of low 

occurrence of pelvic infection in primary 

infertility and the high occurrence of post 

partum and post abortal infection and pelvic 

inflammatory disease in secondary infertility. 

During laparoscopy multiple pelvic 

abnormalities were seen and the association 

of tubal factor with polycystic ovary (PCO) was 

seen in 39.71% of cases which is lower than 

Kousta et al study (27) where was seen in 50% 

of cases. 

In this study, among patients with tubal 

blockage, it appears mainly due to pelvic 

inflammatory disease, endometriosis and 

pelvic adhesion, while in Jamal study (28) the 

cause was mainly due to pelvic inflammatory 

disease, tuberculosis and endometriosis. 

The higher incidence of pelvic inflammatory 

disease associated with other abnormality in 

secondary infertility can be explained by 

higher incidence of pelvic inflammatory 

disease among secondary infertility and its 

sequela of tubal blockage and pelvic adhesion 

which is seen later. 

All cases of uterine abnormality 0.72% seen 

on laparoscopy among infertility patients were 

diagnosed among primary infertility and all 

associated with other pelvic abnormality, which 

is less than in other studies where it was seen 

in 2.9% (25) and 5% (26) . 

Conclusion 

The diagnostic laparoscopy is a valuable 

technique and is a mandatory invasive 

investigation for complete assessment of 

female infertility. 

Recommendation 

As the high cost of In Vitro Fertilization (IVF) 

needed and its unavailability in our locality, it is 

a good practice for infertile women to complete 

all investigations of infertility including 

laparoscopy before referral of patient to In 

Vitro Fertilization. 

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laparoscopies for infertility. JSP Journal of 

surgery Pakistan International 2003;8(3): 

8-10. 

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of obstetrics and gynaecology,7 th ed, 

India, 2007; 440-60. 

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obstetric and gynecology -An evidencebased 

text for MRCOG. 1 st ed, India, 2004; 

566-73. 

4. Smith S , Pfiefer M , Collins J. Diagnosis 

and management of female infertility. 

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Infertility. American Family Physicians 

2007;75(6) :849-56. 

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couple. Ann Acad Med Singapore 

2003;32(5) :611-3. 

7. Ayida G, Chamberlain P, Barlow D, 

Koninckx P, Golding S, Kennedy S. Is 

routine diagnostic laparoscopy for infertility 

still justified? A pilot study assessing the 

use of hysterosalpingocontrast 

sonography and magnetic resonance 

imaging. Human Reproduction 1997;12 

(7):1436–39. 

8. Tanahatoe S, Hompes P, Lambalk C. 

Investigation of the infertile couple Should 

diagnostic laparoscopy be performed in 

the infertility work up programme in 

patients undergoing intrauterine 

insemination?. Human Reproduction 

2003;18(1):8-11. 

9. El-Yahia AW. Laparoscopic evaluation of 

apparently normal infertile women. Aust N 

Z J Obstet Gynaecol 1994;34(4):440-2. 

10. Donnez J, Langerock S, Lecart C, Thomas 

K. Incidence of pathological factors not 

revealed by Hysterosalpingography but 

disclosed by laparoscopy in 500 infertile 

women. Eur J Obstet Gynecol Reprod Biol 

1982;13(6):369-75. 

11. Malinowski A, Nowak M, Podciechowski L, 

Kaminski T, Szpakowski M. The cost of 

laparoscopy in the diagnosis of female 

infertility. Ginekol Pol 1998;69(12):1198- 

202. 



12. Corson SL, Cheng A, Gutmann JN. 

Laparoscopy in the normal infertile patient: 

a question revisited. J Am Assoc Gynecol 

Laparosc 2000; 7 (3): 317- 24. 

13. Komori S, Fukuda Y, Horiuchi I,Tanaka H, 

Kasumi H, Shigeta M, Tuji Y, Koyama K. 

Diagnostic laparoscopy in infertility: a 

retrospective study. J Laparoendosc Adv 

Surg Tech A 2003; 13(3):147-51. 

14. EL-Tabbakh M, Amin A. Diagnostic 

laparoscopy in gynecological problems: A 

retro-spective study. OBGYN.net, 

laparoscopy and hysteroscopy.WEB SITE: 

http:// 64.4.18.250/cgi-bin/linkrd 

15. Yang Y, Hao M, Zhu Y. Laparoscopic 

diagnosis of tubal infertility and fallopian 

tube lesions. Zhonghua Fu Chan Ke Za 

Zhi 1996; 31(6):327-9. 

16. Ismajovich B, Wexler S, Golan A, Langer 

L, David MP. The accuracy of hysterosalpingography 

versus laparoscopy in 

evaluation of infertile women. Int J 

Gynaecol Obstet 1986; 24(1): 9-12. 

17. Bitzer J, Korber HR. Laparoscopy finding 

in infertile women. Geburtshilfe 

Frauenheilkd 1983; 43 (5) : 294 - 8. 

18. Bacevac J, Ganovic R. Diagnostic value of 

hysterosalpingography in examination of 

fallopian tubes in infertile women. Srp Arh 

Celok Lek 2001; 129 (1-2):18 - 21. 

19. Forti G, Krausz C. Evaluation and 

treatment of the infertile couple. The 

Journal of Clinical Endocrinology & 

Metabolism 1998 ; 83 (12) : 4177 - 

88. 

20. Krishna UR, Sathe AV, Mehta H, Wagle S, 

Purandare VN. Tubal factors in sterility: 

alaproscopic study of 697 cases of 

sterility. J Obstet Gynaecol India 1979; 

29(3):663-7. 

21. Hovav Y, Hornstein E, Almagor M, Yaffe 

C. Diagnostic laparoscopy in primary and 

secondaey infertility. J Assist Reprod 

Genet 1998; 15(9):535-7. 

22. Usmani A, Shaheen F, Waheed N. 

Laparoscopic evaluation of female 

infertility. Pak Armed Forces Med J 

1995;45(2):63-5. 

23. Otolorin EO,Ojengbede O, Falase AO. 

Laparoscopic evaluation of the 

tuboperitoneal factor in infertile Nigerian 

women. Int J Gynaecol Obstet 

1987;25(1):47-52. 

24. Ashraf V, Baqai S. Laparoscopy; 

diagnostic role in infertility. Professional 

Med J Mar 2005;12(1):74-79. 

25. Vasiljevic M, Ganovic R, Jovanovic R, 

Markovic A. Diagnostic value of 

hysterosalpingography and laparoscopy 

in infertile women. Srp Arh Celok Lek 

1996;124(5-6):135-8. 

26. Kanal P. Sharma S. Study of primary 

infertility in females by diagnostic 

laparoscopy. IJMU 2006;1(2):6-8 

27. Kousta E,White D, Cela E, McCarthy 

M,Franks S. The prevalence of polycystic 

ovaries in women with infertility. Human 

Reproduction 1999;14(11):2720-23. 

28. Jamal T. Tubal factor in Infertility. J 

Postgrad Med Inst 2004;18(2):255-60. 



Coronary angiographic findings among diabetic 

and non-diabetic patients 

Dhiyaa A. Alhamadani, Fakher Y. Husain, Mahmood A. Abbo 



Received: 26 th Oct 2008; Accepted: 12 th Jul 2009. 

ABSTRACT 

objectives: Atherosclerotic coronary artery disease (CAD) is a major cause of death all over the 

world. Among patients with CAD there are many of them having diabetes mellitus which is regarded 

as a major additive risk factor. Diabetic patients who developed CAD carry high morbidity and 

mortality rates. 

The objective of this study was to analyze the coronary angiographic outcome of patients with type 

two diabetes mellitus suspected to have coronary artery disease and comparing these results with 

non-diabetic patients. 

Methods: Patients referred to Mosul Cardiac Catheterization Unit of Ibn-Sena Teaching Hospital for 

coronary angiography were serially included until obtaining a total of 75 diabetic and 75 non-diabetic 

patients with predicted coronary artery disease and with different ischemic heart disease risk factors 

including obesity, smoking, hypertension and dyslipidemia. All of them underwent coronary 

angiography. 

Result: Diabetic patients showed more significant stenotic lesions. Moreover the lesions in the 

coronary artery were more diffuse with higher incidence of multivessel involvement in comparison to 

non-diabetic patients. Also diabetic patients show increasing incidence of the left main stem artery 

involvement which carry very high mortality rate. 

Conclusion: Diabetes mellitus is an independent risk factor for coronary artery disease associated 

with more advanced, serious and extensive obstructive atherosclerotic lesions in the coronary 

arteries. 


مقدمة:‏ تصلب الشرايين التاجية العصادية هو أحد أآثر أسباب الوفاة انتشارا في العالم.‏ ويعتبر السكري عامل خطورة 

مستقل إضافة للعوامل المعروفة في حدوث عملية تصلب الشرايين التاجية العصادية مسببا نسبة أعلى من الأمراض 

والوفاة والتي ممكن أن تكون بسبب طبيعة التغيرات العصادية للشرايين التاجية المنتشرة والشديدة في داء السكر.‏ 

الهدف من الدراسة هو دراسة تحليلية لنتائج القثطرة القلبية لمرضى السكري من النمط الثاني والمصابين بقصور 

الشرايين التاجية ومقارنة هذه النتائج مع غير مرضى السكري.‏ 

طريقة البحث:‏ شملت هذه الدراسة التحليلية المستقبلية مريض أجريت لهم عملية قثطرة تشخيصية للشرايين القلبية 

في وحدة قثطرة القلب في مستشفى ابن سينا التعليمي في الموصل.‏ لاحتمال إصابتهم بقصور الشرايين التاجية ممن لديهم 

عوامل خطورة متعددة مثل السمنة والتدخين والضغط واختلال دهون الدم وتم تقسيم المرضى إلى مجموعتين بالاعتماد 

على وجود السكري أو عدمه.‏ 

النتائج:‏ أظهرت الدراسة بأن السكري يعمل على تضييق الشرايين بشكل ملحوظ وتبين أن قصور الشرايين التاجية 

منتشر أآثر وأشد في مرضى السكر.‏ 

(١٥٠) 



الاستنتاج:‏ أثبتت الدراسة بان داء السكر عامل خطورة مهم لمرض شرايين القلب التاجية بغض النظر عن وجود بقية 

عوامل الخطورة الأخرى مسببا نسبة أعلى وأشد من المرض وقد يؤدي الى زيادة في نسبة الوفاة 

. 

D 

iabetes mellitus is a chronic disease with 

approximately 150 million people 

worldwide are suffering from this condition and 

the number is expected to rise to 300 million 

by 2025 (1) . With the increasing prevalence, 

diabetes is rapidly growing into a global public 

health problem. For many years, 

cardiovascular diseases and especially 

coronary heart disease (CHD) have been the 

main cause of premature death in many 

countries. In addition to the other classical risk 

factors (age, male sex, smoking, hypertension 

and hypercholesterolemia, etc.), diabetes is 

recognized as an important risk factor for 

cardiovascular disease (2) . A previous study (3) 

showed that patients with diabetes mellitus are 

at an increased risk for the development of 

coronary artery disease. The cardiovascular 

disease is a major consequence of this chronic 

condition and is regarded as the leading cause 

of death in type two diabetes mellitus (T2DM), 

(4,5,6) . Although there has been considerable 

improvement in managing patients with 

coronary artery disease, unfavorable events 

remained heightened among patients with 

diabetes; in other words, diabetes 

independently worsens long-term prognosis for 

medically treated patients (7,8) . Epidemiological 

data from the Framingham Study 

demonstrated a two- to fourfold increase in 

atherosclerotic disease in diabetic patients and 

the risk of death from cardiovascular disease 

is much higher for patients with diabetes 

compared with those without diabetes (9) . Also 

diabetic patients who have had myocardial 

infarction have a higher mortality rate in the 

acute phase of myocardial infarction and in 

long-term follow-up even when they were 

treated with fibrinolytic regimen. (10-12) 

The aim of this work is to study the impact of 

diabetes mellitus on coronary arteries (the 

characters of coronary artery lesion and its 

extent), and comparing the angiographic 

findings between diabetic and non diabetic 

patients. 


Patients referred to Mosul Cardiac 

Catheterization Unit of Ibn-Sena Teaching 

Hospital for coronary angiography were 

serially included until obtaining a total of 75 

diabetic and 75 non-diabetic patients between 

February 2007 and August 2007. All of them 

predicted to have coronary artery disease 

and with different ischemic heart disease risk 

factors including obesity, smoking, 

hypertension and dyslipidemia. All of them 

underwent coronary angiography. Written 

informed consent was obtained from all 

patients before the study. Some patients had 

previously known clinical evidence of CHD 

confirmed by typical history of disease and by 

the presence of classical electrocardiographic 

ischemic changes; not all of them have 

positive exercise electrocardiographic test. 

The diabetic patients were classified as 

having diabetes if it was documented on their 

medical reports, if they were taking insulin or 

oral hypoglycemic agents, or on the basis of 

the national Diabetes Data Group and WHO 

criteria for diagnosis of DM 

* Symptom of DM plus RBS > 11.1 mmol/L 

(200 mg /dL) or 

* FBS > 7.0 mmol/L (126 mg/dL) or 

* Two –hour plasma glucose > 11.1 mmol/L 

(200 mg/dL) during an OGGT (13) . The nondiabetic 

patients were considered as the 

control group. Preliminary evaluation of all 

patients included the clinical characteristics of 

the patients, age, sex, duration of CHD, history 

of myocardial infarction, history of 

hypertension and/or if the measured systolic 

blood pressure was ≥ 140 mmHg and/or 

diastolic blood pressure ≥ 90 mmHg at day of 

admission with the presence or absence of the 

evidence of target organ involvement, 

smoking, (current or prior). Dyslipidemia was 

considered as a risk factor if the patient has 

any one of the following abnormalities: total 

cholesterol > 5.17 mmol/L (200 mg /dL) , low 

density lipoprotein > 2.6 mmol/L (100 mg /dL) , 

high density lipoprotein men < 1.15 mmol/L (< 



45 mg /dL). Women < 1.4 mmol/L (< 55 

mg/dL), and triglyceride > 1.7 mmol/L (> 150 

mg/dL). (16) 

The criteria for the metabolic syndrome have 

been looked for in both groups (16) . As shown 

in Table (1). Coronary angiography was 

performed at the cardiac catheterization unit 

of (Ibn-Sena Teaching Hospital) using 

Siemens' *AXIOM Artis equipment (Germany). 

We routinely perform angiography in at least 

four projections. These projections are 

recorded in our data base. Qualitative 

angiographic assessment regarding the 

presence or absence of significant coronary 

artery lesion was done by at least two expert 

interventional cardiologists during or 

immediately after the procedure. The 

angiogram was assessed for the presence or 

absence of significant vessel occlusion. 

The degree of luminal narrowing was 

recorded in percentage of prestenotic 

diameter. Internal luminal narrowing of 70% 

was considered significant, except for the left 

main coronary artery, in which 50% stenosis 

was regarded as significant. Based on the 

results of coronary angiography, the character 

of the lesion was defined as diffuse by the 

presence of more than one significant lesion in 

the culprit artery or if the obstructed lesion was 

more than 20 mm in length (17) . Statistical 

analysis was performed using Student’s t test 

between two proportions and Chi square test. 

Data are expressed as means ± SD or n(%). 

P ≤ 0.05 was considered statistically 

significant. 

Table (1): clinical identification of metabolic 

syndrome. 

Central obesity: waist circumference > 102 

cm(M), > 88 cm(F) 

Hpertriglyceridemia: Triglycerides > 1.7 m 

mol/L 

Low HDL cholesterol: 130 mm Hg 

systolic or >85 mm Hg diastolic 

Fasting plasma glucose > 6.0 m mol/L or 

previously diagnosed type 2 diabetes 

Results 

Risk Factor Characteristic 

Baseline characteristics were comparable 

between the patients with T2DM and those 

without diabetes mellitus as shown in Table 

(2). The results of the analysis of the baseline 

clinical characteristics showed that patients 

with diabetes were older (mean age was 56.3 ± 

7.4 years) than non-diabetic patients (mean 

age 53.9 ± 8.8 years). There was an equal 

proportion of men and women (48 men 64%) 

and (27 women 36%) in both groups. The 

current smoking habit was more frequent in 

the diabetics 18 (24%) than non-diabetics 10 

(13.3%) (p=0.70). Patients with diabetes 

more often had arterial hypertension 44 

(58.7%) (p=0.05) with a higher incidence of 

previous attack of acute myocardial infarction 

23 (30.7%). The prevalence of obesity and 

metabolic syndrome were higher in diabetics 

group (46.7%), (p=0.002) when compaired 

with other group as shown in Tables (3) and 

(4). 

There was no statistically significant 

differences in the atherogenic index (the ratio 

of TC to HDL lipoprotein cholesterol) between 

two groups as shown in Table (5). The mean 

duration of DM was 6.33 ± 4.9 y. Most of 

diabetic patients seem to have poor control of 

their diabetes as the mean FBS for the studied 

group was 9.64 ± 3.5. 

Angiographic Characteristics 

Regarding the angiographic characteristics of 

the studied groups, the non-significant lesions 

on angiography were more commonly 

detected in non-diabetics compared with those 

with diabetes (42% versus 12.0% respectively) 

(p < 0.001). On the other hand, 19 diabetic 

patients (24%) had a smaller vessel size and 

more diffuse lesion when compared with nondiabetic 

patients (p= 0.009). Multivessel 

disease {(two vessel disease p= 0.05) and 

(three vessel disease p


Table (2): Clinical characteristics of diabetic and non-diabetic patients. 

NS = Not significant 

Table (3): Obesity parameters of the studied groups. 

BMI 

Diabetes (n=75) 

Non-diabetes (n=75) 

No. % No % 

p-value 

< 25 (Normal) 5 6.6% 11 14.6% 0.05 

25 – 30(over wt) 26 34.6% 25 33.4% NS 

30 -35 18 24.0% 21 26.7% NS 

35 -40 17 22.7% 11 14.7% NS 

>40 9 12.0% 7 9.3% NS 

Total 75 100% 75 100^% -- 

Waist circumference of studied groups 

Men>102 

Women>88 

NS= not significant. 

Variables Diabetics (n=75) Non-diabetics (n=75) p-value 

Male 48(64.0%) 48(64.0%) 

Sex 

NS 

Female 27(36.0%) 27(36.0%) 

Mean age ± SD (yr) 56.3 ± 7.4 53.99 ± 8.8 NS 

Duration of DM (yr) 6.33 ± 4.9 -- -- 

Duration of IHD (yr) 3.2 ± 3.67 3.21 ± 4.71 NS 

FBS (mmol/L) 9.64 ± 3.5 5.0± 0.5 -- 

Prior MI 23(30.7%) 16(21.3%) NS 

HT 44(58.7%) 32(42.7%) 0.05 

Smoking 

Current 18(24.0%) 16(21.3%) NS 

Prior 10(13.3%) 11(14.7) NS 

Table (4): Metabolic syndrome in the studied groups. 

53 70.7% 46 61.3% NS 

Metabolic syndrome 

Patients 

Total 

No. % 

Diabetes 75 35 46.7% 

Non-diabetics 75 17 22.7% 

p-value 

0.002 

Table (5): Lipid profile in the studied groups. 

Lipid 

Target 



No. % No. % 

p-value 

TC (mmol/L) >5.17 15 20.0 12 16.0 NS 

LDL (mmol/L) >2.6 14 18.7 12 16.0 NS 

HDL (mmol/L) 

men 1.7 16 21.3 14 18.7 NS 

Atherogenic index > 5 30 40.0 28 37.3 NS 

NS = Not significant 



Table (6): Angiographic data of the studied groups. 

Extent of Coronary disease 



No. % No. % 

p-value 

No significant lesion 9 12.0 32 42.7


strong indication for coronary angiography for 

confirmation of the disease, determine the 

choice of therapy and assess the prognosis. 

The angiographically significant atherosclerotic 

coronary lesion among patients with 

diabetes was more diffuse than non-diabetics, 

as found in another study (19) which showed 

that diabetic patients were associated with 

more extensive and diffuse coronary 

atherosclerosis. (20) In addition, the prevalence 

of multi-vessel disease was higher among 

diabetics similar to the other studies (21) . 

The incidence of the left main stem lesion 

was higher in diabetics as in another study (22) . 

These finding probably may explain why 

diabetic patients with CHD have worse 

prognosis with higher mortality rate than nondiabetic 

patients (7-11) . 

There are many mechanisms that explain 

the higher incidence of stenosis and occlusion 

rate in diabetic patients. These mechanisms 

include: 

1. Haemostatic abnormalities; that predispose 

them for increased risk of vascular 

thrombosis. Platelet aggregation is 

increased with enhanced synthesis of 

(23) 

thromboxane A 2 and platelet activation 

(platelet factor 4 and ß-thromboglobulin) 

can be elevated (24) . 

2. A relative hypercoagulability state may be 

present in diabetic patients. Procoagulant 

factors include fibrinogen, factor VII, and 

von Willebrand factor may be increased in 

diabetics while the synthesis of prostacyclin 

is reduced (25) . While fibrinolysis may be 

attenuated because of increases in 

plasminogen activator inhibitor type 1 and 

lower levels of urokinase-type plasminogen 

activator (26) . 

3. Functional abnormalities of the vascular 

endothelium; diabetic patients have some 

vascular endothelial dysfunction which may 

further enhance the tendency to vasospasm 

and coronary thrombosis as hyperglycemia 

causes endothelial dysfunction by 

decreasing the production of endotheliumderived 

relaxing factor (27) , increasing 

oxidative stress by vascular protein 

glycation (28) and free radical formation (29) , 

and decreasing prostacyclin production (30) . 

Moreover; lipoprotein abnormalities (31) may 

impair endothelium- dependent relaxation (32) 

and a greater growth factor stimulation 

occurs in diabetics (33) . These factors are 

likely to produce a prothrombotic state in 

patients with diabetes, and may account for 

more aggressive coronary artery lesion. All 

these mechanisms, the prothrombotic state, 

imbalance of fibrinolytic systems and 

endothelial dysfunction may contribute and 

explain the problem of coronary stenosis 

with poor angiographic outcome in patients 

with diabetes mellitus. In this study the 

incidence of previous myocardial infarction 

{23 (30.7%)} was more in diabetic patients 

when compared with non-diabetics {16 

(21%)} and this is probably due to the more 

advanced coronary artery disease in 

diabetic patients. 

Over-weight and obesity are associated with 

insulin resistance and metabolic syndrome. 

However the presence of abdominal obesity is 

more highly correlated with metabolic 

syndrome than the elevated BMI. The clinical 

significance of insulin resistance is gaining 

prominence, and has been associated with 

several medical conditions such as polycystic 

ovarian syndrome and syndrome X. While 

insulin resistance may precede the onset of 

type 2 diabetes, its presence portends a 

heightened risk of occurrence of myocardial 

infarction (34) and stroke (35) . Indeed, the United 

Kingdom Prospective Diabetes Study 

(UKPDS) showed a reduction in 

macrovascular events by improving insulin 

resistance with Metformin in obese patients 

with type 2 diabetes. (36) Although the precise 

mechanisms for the deleterious effects of 

insulin resistance remain uncertain, excessive 

free fatty acids is likely to be a major 

contributor. They reduce production of the 

nitric oxide and other vasodilatory substances 

mediated through reactive oxygen radicals (37) . 

Conclusion 

Two major clinical implications may derive 

from our findings. 

* First: diabetes is often associated with other 

risk factors that predispose to coronary heart 

disease and may influence the outcome. 



* Second: diabetic patients will have a worse 

angiographic outcome. Diabetic patients with 

suspected CHD are strong indication for 

coronary angiography which provide the 

clinician valuable information regarding the 

confirmation of the presence or absence of 

coronary artery disease, the prognosis of the 

patients with CHD and it determines the choice 

of therapy whether drug therapy, coronary 

stenting or surgical by pass graft depending on 

the type and the number of the coronary 

arteries involvement. 

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Renin – angiotensin system (RAS) and hypertensive disease 

"From the link in pathophysiology to the outcomes of inhibition" 

Asim M. Al-Chalabi 

Consultant Physician, Ninaveh Private Hospital. 


Received: 15 th Nov 2009; Accepted: 2 nd Dec 2009. 

SUMMARY 

The renin – angiotensin system is a major contributor to both hypertension and associated 

pathophysiologic changes in the heart and cardiovascular wall (The target organ). Major basic and 

clinical trials have shown that ACE inhibitor and ARB are the main renin- angiotensin system blockers 

in use assist in controlling hypertension and reducing target organ damage, thus they should be used 

as a first-line treatment for hypertension. Moreover, ARBs specifically reduces the frequency of atrial 

fibrillation and stroke, thus it has emerged as a new preventive and therapeutic strategy for these 

conditions. 

In theory, combining ACE inhibitor and ARBs maximizes benefits because it offers more complete 

RAS blockage but this expectation was not confirmed by most recent clinical trials and was not 

translated into real patients benefits. Renin inhibition was introduced as a better step for reducing 

angiotensin II, because it offer complete blockage of the whole system. Early studies confirmed that 

renin inhibitors reduced blood pressure better than ACE inhibitors but further large clinical trials have 

been started and therefore in the near future, further clinical evidences will be available to confirm the 

antihypertensive, anti-inflammatory and antiatherosclerotic effects of renin inhibitor. 

List of abbreviations: RAS (renin – angiotensin system), ACE (angiotensin converting enzyme), 

ARB (angiotensin receptor blocker), AT 1 (angiotensin II receptor type 1), AT 2 (angiotensin II receptor 

type 2), AT 4 (angiotensin II receptor type 4), LVH (Left ventricular hypertrophy), AF (atrial fibrillation), 

CCF (Congestive heart failure). 


نظام الرنين انجيوتنسين هو عامل رئيس لكل من فرط ضغط الدم والتغيرات المرضية في القلب وجدار الأوعية الدموية 

‏(العضو المستهدف).‏ لقد بينت الكثير من الأبحاث الأساسية والسريرية ان موانع أنزيمات محولات الانجيوتنسين ومحصر 

مستقبلات الانجيوتنسين هما أهم موانع نظام الرنين انجيوتنسين المستعملة حاليا تساعد للسيطرة على فرط ضغط الدم 

وتقليل تلف العضو المستهدف وعليه يجب استعمالهما آخط أول لعلاج فرط ضغط الدم.‏ اضافة الى ذلك فان محصر 

مستقبلات الانجيوتنسين خاصة تقلل تكرار حدوث ارتجاف الأذينين والسكتة الدماغية وعليه فقد برزت آطريقة وقائية 

وعلاجية جديدة لهذه الأمراض.‏ 

نظرياً،‏ الجمع بين موانع أنزيمات محولات الانجيوتنسين ومحصر مستقبلات الانجيوتنسين يزيد الفائدة لأنها تعمل على 

منع النظام منعاً‏ تاماً،‏ ولكن هذا التوقع لم يؤآد بأآثر الأبحاث السريرية حداثة ولم ينعكس آفوائد حقيقية للمرضى.‏ موانع 

الرنين قدمت آخطوة أفضل لتقليل الانجيوتنسين لأنه يعمل على المنع الكلي للنظام بأآمله.‏ الأبحاث الأولية أثبتت ان 

موانع الرنين خفضت فرط ضغط الدم أفضل من موانع أنزيمات محولات الانجيوتنسين ولكن الأبحاث السريرية الموسعة 

التي بدأت ستطلعنا في المستقبل القريب عن تأآيد نتائج تأثيرها على فرط ضغط الدم ومضادات الالتهابات وتصلب 

الأوعية الدموية.‏ 

(٢) 



A 

direct, continuous and independent 

relation between blood pressure and the 

incidence of various cardiovascular events, 

such as stroke and myocardial infarction is 

well accepted. This increase in risk can be 

attributed to structural and functional changes 

in target organs. Central to many of these 

pathophysiologic process is the renin – 

angiotensin system "RAS" specifically 

angiotensin II. In fact, the RAS is a major 

regulatory system of cardiovascular and renal 

function, and is a major contributor to both 

hypertension and associated pathophysiologic 

changes in the heart and vascular wall. 

Accordingly, the renin – angiotensin system 

has been at the center of intensive research 

activities for several decades. 

Accordingly, in the last twenty years, growing 

evidence has clearly pointed out that RAS 

activity may represent an ideal target for 

pharmaceutical treatment in a number of 

cardiovascular diseases, including 

hypertension, atherosclerosis, congestive 

heart failure, renal diseases, stroke, 

myocardial infarction and others. In fact, 

evidences provided by major clinical trials and 

the continuously increasing use of ACE 

inhibitors in the clinical practice as well as of 

RABs has confirmed the value of inhibiting the 

RAS as an effective approach to reduce 

cardiovascular risk and cardiovascular and 

renal complications associated with major 

diseases (1) . 

Thus, blockade of RAS is now evidence 

based strategy for the protection of 

cardiovascular, cerebrovascular and renal 

systems. This article reviews the current views 

on the biophysiology of RAS, its link to 

pathophysiology of hypertensive disease, and 

discuss the outcomes of its inhibition in this 

condition. 

Biophysiology of RAS 

The RAS comprises a cascade of enzymatic 

reactions resulting in the formation of 

Angiotensin II, which is the effective molecule 

of the RAS and can act as a systemic 

hormone "Endocrine" or as a locally generated 

factor "paracrine". Figure 1 (2, 3) . Renin is a 

proteolytic enzyme that is produced and stored 

in the granules of the juxtaglumerular cells 

surrounding the afferent arterioles of the 

glomeruli in the kidney. Renin acts on the 

basic substrate angiotensinogen (a circulating 

α2-globulin made in the liver) to form the 

decapeptide angiotensin I (figure1). 

Angiotensin I is then enzymatically 

transformed by angiotensin converting 

enzyme "ACE", which is present in many 

tissues particularly pulmonary vascular 

endothelium, to the octapeptide angiotensin II 

by removing of the two c-terminal amino acids. 

Figure (1): Simplified overview of RAS 

pathway. Reproduced with permission from 

Prof. T. Unger, the role of the reninangiotensin 

system in the development of 

cardiovascular disease. AMJ card. (31) . 

Regardless of the pathway by which it is 

formed, angiotensin II is a potent pressor 

agent and mediate its physiologic effects by a 

final common step: binding to highly specific 

receptors located on the cell membrane. In 

humans two main types of angiotensin II 

receptor subtypes have been characterized: 

angiotensin II type 1 (AT 1 ) and angiotensin II 

type 2 (AT 2 ) which differ markedly in their 

biological activities (4, 5) . 

The angiotensin type -1 receptor (AT 1 ) 

The AT 1 receptor is a 7-transmembrane 

domain receptor, coupled to a guanosine 

triphosphate – binding protein "G-protein". It is 

located primarily in the adrenal glands, 

vascular smooth muscle cells, kidney, and 

heart (4) . 



Virtually all of the known regulatory actions of 

angiotensin II on blood pressure and 

osmoregulation have been attributed to AT 1 

receptor. These include vasoconstriction, 

aldosterone and vasopressin release, renal 

tubular sodium reabsorption, and decreased 

renal blood flow (table 1). Although these 

effects on blood pressure and electrolytes 

homeostasis played an essential physiologic 

role at an earlier point in human evolution to 

maintain adequate organ perfusion at times of 

acute volume loss, they are now largely 

redundant in modern civilization. More 

important are the pathophysiologic 

consequences arising from AT 1 receptor 

activation. 

Table (1): Differential effects mediated by AT 1 

and AT 2 receptors. 

AT 1 receptor 

• Vasoconstriction 

• Aldosterone synthesis and 

secretion 

• Renal tabular sodium 

reabsorption 

• Increased vasopressin secretion 

• Decreased renal blood flow 

• Renal renin inhibition 

• Cardiac hypertrophy 

• Cardiac contractility 

• Vascular smooth muscle cell 

proliferation 

• Augmentation of peripheral 

noradrenergic activity 

• Modulation of central 

sympathetic nervous system 

activity 

• Central osmocontrol 

• Extracellular matrix formation 

AT 2 receptor 

• Fetal tissue 

development 

• Inhibition of cell 

growth/proliferation 

• Vasodilation 

• Modulation of 

extracellular matrix 

• (Neuronal) 

regeneration 

• Cell differentiation 

• Apoptosis 

Reproduced with permission from Prof. T. 

Unger, the role of the renin-angiotensin system 

in the development of cardiovascular disease. 

AMJ card. (31) . 

In this regard AT 1 , receptor stimulation has 

been shown to mediate cell growth and 

proliferation of vascular smooth muscle cells (6) 

cardiomyocytes (7) , and coronary endothelial 

cells (8, 9) . Accordingly, the AT 1 receptor has 

been implicated in various cardiovascular, 

renal and cerebral pathologies, such as left 

ventricular hypertrophy, vascular media 

hypotrophy, cardiac arrhythmias, 

atherosclerosis, glomerulosclerosis, stroke and 

dementia (9, 10) . Inhibition of these effects by 

specific AT 1 receptor blockade can be 

expected to offer therapeutic benefit in certain 

pathologic condition e.g. hypertension, to 

inhibit vasoconstriction and prevent vascular 

and cardiac hypertrophy. 

The angiotensin type -2 receptor (AT 2 ) 

The AT 2 receptor is also a 7-transmembrane 

glycoprotein and has approximately 34% 

amino acid sequence homology to that of the 

AT 1 receptor. Less is known about its signaling 

pathways. They are present at a high density 

in all tissues during fetal development, but 

they are much less abundant in adult tissue, 

being expressed at high concentration only in 

the adrenal medulla uterus, ovary, vascular 

endothelial and specific areas of brain (11) . 

Expression is also upregulated under certain 

condition, such as in heart failure, post 

infarction repair, and skin and nervous system 

lesions (12, 13) . 

AT 2 receptors thus appear to be involved in 

the control of cell proliferation, cell 

differentiation and development, angiogenesis, 

wound healing, tissue regeneration, and even 

apoptosis (table 1), namely, biologic processes 

that counteract the trophic responses 

mediated through AT 1 receptors i.e. AT 2 

receptor opposes AT 1 receptor – mediated 

effects (14-15) . 

Speculation suggests that, in a milieu of 

selective AT 1 receptor blockade, circulating 

angiotensin II would act only at unopposed 

AT 2 receptors, thereby amplifying the 

vasodilator component of the biphasic arterial 

blood pressure response to angiotensin II. By 

the same inference, AT 1 receptor blockade 

would be expected to preserve "or even 

augment" the favorable effects of angiotensin 

II on cell growth and proliferation mediated 

through the AT 2 receptor. 

Other enzymes and receptors 

In 2000, a new enzyme associated with the 

generation of angiotensin peptides was 

identified ACE2, a carboxy peptidase similar to 

ACE (16) . ACE2 does not generate angiotensin 

II but increases the formation of angiotensin 

(1-7) (figure 2). This heptapeptide causes 

vasodilatation and growth inhibition (17) but 



ACE2 has several function that are not yet fully 

understood (18, 19) . 

The effects of all angiotensin peptides are 

mediated through specific cell surface 

receptors (table 2). AT 1 & AT 2 already has 

been mentioned. An AT 4 receptor for 

angiotensin IV was found recently to affects 

kidney tubular function and improves the 

memory of Rodents (20) . A renin - prorenin 

receptor was described by Nguyen and 

colleagues in 2002 

(21) . Work in animals 

support notion that over expression of the 

renin - prorenin receptor increase blood 

pressure (22) , but the role of this receptor in 

human beings remain to be established (23) , 

but might of particular importance for the 

effects of renin inhibitors. 

Figure (2): Expanded overview of RAS 

pathway. Reproduced with permission from 

Prof. R. F. Schmieder. Renin–angiotensin 

system and cardiovascular risk. Lancet 

2007 (65) . 

Table (2): Cell surface receptors of the RAS. 

AT 1 

Full name Ligand(s) Function 

Angiotensin II type 1 receptor 

Angiotensin II, 

Angiotensin III 

Vasoconstriction, stimulation of aldosterone release 

and sympathetic nerve activity, promotion of cell 

growth, matrix deposition, inflammation 

AT 2 Angiotensin II type 2 receptor Angiotensin II 

AT 4 

Angiotensin IV receptor 

Angiotensin IV, 

LVV-haemorphin 7 

R/P-R Renin/prorenin receptor Renin and prorenin 

mas mas oncogene Angiotensin (1-7) 

Antagonism of the effects of AT 1 , promotion of 

apoptosis, protection of neural tissue, possible 

synergism with AT 1 in promoting inflammation 

Vasodilatation, decrease tubular sodium transport, 

improved memory, possibly promoting inflammation 

Increase of angiotensin generation, further 

independent promotion of matrix deposition 

Antagonism of the effects of AT 1 , antidivretic, inhibits 

cell growth. Not yet clear whether or not all actions 

of angiotensin (1-7) are mediated by mas oncogene 

Reproduced with permission from Prof. R. F. Schmieder. Renin – angiotensin system and 

cardiovascular risk. Lancet 2007 (65) . 

Angiotensin II and atherosclerosis 

At the beginning of the nineties, Dzau and 

Braunwald proposed the concept of the 

cardiovascular continuum in humans (figure 3) 

(24) . Accordingly, the onset and progression of 

cardiovascular disease can be regarded as a 

continuum of events, according to this 

concept, the presence of risk factors, such as 

hypertension, dyslipidemia, or diabetes 

mellitus and smoking, initially predisposes to 

the development of endothelial disfunction, 

atherosclerosis and target organ damage. 



Progression to overt coronary artery disease 

can cause clinical syndrome of myocardial 

ischaemia, whereas thrombus formation at the 

sites of an atherosclerotic plaque may occlude 

a coronary artery and results in myocardial 

infarction. Sequelae of myocardial infarction 

include cardiac arrhythmias and loss of cardiac 

muscle, potentially culminating in sudden 

death. However, if the individual survives the 

acute event, post infraction remodeling will 

occur, leading to ventricular dilatation, heart 

failure, and ultimately, end-stage heart 

disease, and eventually death. 

Figure (3): The cardiovascular continuum. 


Unger, the role of the renin-angiotensin system 

in the development of cardiovascular disease. 

AMJ card. (31) . 

Central to all these pathways is the activation 

of the renin – angiotensin system with 

angiotensin II binding to AT 1 receptor as a 

major effector, producing acute 

vasoconstriction, leading to an increase in 

blood pressure and independently to chronic 

disease pathology by promoting vascular 

growth and proliferation, and endothelial 

dysfunction, i.e., atherosclerosis 

(25) . 

Experimental evidence clearly suggests a key 

role of the RAS and the induced inflammatory 

processes at all stages of this continuum and 

consequently a strong rational for its blockade 

in order to prevent cardiovascular events. 

Inhibition of the system has a potent anti 

atherosclerotic effect which is mediated by 

their antihypertensive, anti-inflammatory, 

antiproliferative, and oxidative stress lowering 

properties. The possibility of a positive effect of 

the RAS blockade at the early stages of 

cardiovascular continuum, that is, the 

endothelial dysfunction was specifically 

addressed by some clinical studies (26) . 

Inhibition of the RAS 

Because angiotensin II has a pivotal role in 

the sequence of events constituting the 

cardiovascular continuum, and the implication 

of chronic RAS activation as a major factor 

contributing to progressive dysfunction of 

target organs, it would seems logical to target 

the RAS in therapeutic strategies aimed at 

reducing the overall cardiovascular risk-factor 

profile of an individual. Identification of this link 

between angiotensin II and the 

pathophysiologic changes associated with 

various cardiovascular conditions prompted 

the development of pharmaceutical agents, 

capable of blocking the actions of angiotensin 

II and reducing the associated pathologies. 

Firstly, the ACE inhibitors were available, and 

more recently, the selective AT 1 receptor 

antagonists. 

Proven cardiovascular benefit from 

angiotesin-converting enzyme (ACE) 

inhibitions is a cornerstone of evidence–based 

medicine (27) . The first study to show dramatic 

benefits from ACE inhibition was the 

Cooperative North Scandinavian Enalpril 

Survival Study (CONSENSUS-1), in which a 

31% decrease in the rate of death was 

observed in patients with severe heart failure 

at the end of 1 year of enalpril treatment (28) . 

(figure 4). 



Figure (4): Kaplan-Meier curve from the 

Cooperative North Scandinavian Enalapril 

Survival Study (CONSENSUS-1). Reproduced 

with permission from Prof. T. Unger, the role of 

the renin-angiotensin system in the 

development of cardiovascular disease. AMJ 

card. (31) . 

Other studies SAVE & AIRE (29) verified that 

ACE inhibition decrease heart failure, 

myocardial infarction, and mortality, and that 

striking benefit could be observed within 30 

days. The Heart Outcomes Prevention 

Evaluation (HOPE) study conclusively 

demonstrated that ramipril angiotesinconverting 

enzyme (ACE) inhibitor reduces the 

risk of a primary cardiovascular event (death, 

stroke, or acute M I) in high-risk patients by 

22% (30) . (figure 5) 

Theoretically, AT 1 receptor antagonists might 

offer even greater improvements in clinical 

outcomes than ACE inhibitors because they 

selectively block the negative actions of 

angiotensin II that are mediated through AT 1 

receptors yet preserve (and potentially amplify) 

the favorable effects mediated by through AT 2 

receptors (31) . A growing body of data indicates 

that ARBs can improve cardiovascular 

outcomes in patients with hypertension as well 

as in patients with related conditions such as 

heart failure (31, 32) . Accordingly it has been 

used in patient intolerant to ACE inhibitor with 

equal efficacy and of course with fewer side 

effect (cough and angioedema). 

Figure (5): Kaplan-Meier estimates of the 

primary composite outcome of my myocardial 

infarction , stroke or death from cardiovascular 

causes from the Hypertension Outcomes 

Prevention Evaluation (HOPE) study. 


Unger, The Role of thr renin-angiotensin 

system in the development of cardiovascular 

disease. AMJ card. (31) . 

In theory also, more complete RAS blocked 

using a combination of an ACE inhibitor and 

an AT 1 receptor antagonist should provide 

even greater attenuation of the deleterious 

angiotensin II-induced local tissue effects (31) , 

because it produces more complete blockade 

of the RAS, while preserving the beneficial 

effects mediated by AT 2 receptor stimulation 

and increased bradykinin levels which 

possesses vasodilatory and tissue – protective 

properties. (table 3). The randomized 

evaluation of strategies for left ventricular 

dysfunction (RESOLVD) study indicated that 

combining an ACE inhibitor with an ARB 

decreases blood pressure and improved the 

ejection fraction more than treatment with 

either drug alone in patient with heart failure 

(34) , and the valsartan in heart failure trial (Val- 

Heft) showed that the combination of an ACE 

inhibitor and an ARB reduces hospitalization 

for heart failure in patients with CCF by 27.5% 

(35) . 



Table (3): The Potential Overall Effects of ACE inhibitors and ARBs Combination. 

ACE Inhibitor 

AT 1 Receptor 

Antagonist 

AT 1 stimulation ↓ ↓↓ ↓↓ 

AT 2 stimulation ↓ ↑↑ ↑ 

Plasma rennin activity ↑ ↑ ↑ 

Angiotensin II levels ↓ ↑ =/↑ 

Bradykinin levels ↑ = ↑ 

ACE Inhibitor + AT 1 

Receptor Antagonist 

Reproduced with permission from Prof. T. Unger, the role of the renin-angiotensin system in the 

development of cardiovascular disease. AMJ card. (31) . 

But, unfortunately, these theoretical 

expectations could not be confirmed by the 

most recently published clinical trials. In 

(36) 

TRANSCEND study which compared 

(telmisartan) an ARB to placebo, the result 

have shown that the active treatment 

(telmisartan) was not superior to placebo in the 

prevention of cardiovascular events, primary 

composed end point represented by 

cardiovascular death MI, stroke, or admission 

to the hospital for heart failure events. The 

ONTARGET trial (published recently, a very 

large multicenter randomized trial) in which the 

patients were treated with an ACE inhibitor 

(ramipril), an ARB (telmisartan), or the 

combination of the two drugs (37) . After a 

medium follow up of 56 months the occurrence 

of the primary outcomes, consisting of death 

from cardiovascular causes, MI, stroke, or 

hospitalization for heart failure, was not 

significantly different in the ramipril and 

telmisartan groups, though the ARB was better 

tolerated. However, there were trends slightly 

favoring the ACE inhibitor for MI prevention 

and the ARB for stroke prevention, but these 

differences did not reach statistical 

significance. The other important issue 

addressed by the trial, the clinical role of the 

combined renin-angiotensin blockade, brought 

a word of caution about this strategy since 

more adverse events were observed. Ripley & 

Harison suggested that these unexpected data 

could be explained by the differences in 

patients number, event rate and the use of 

other life saving drugs between these studies 

and HOPE studies (38) . However, these results 

confirmed the difficulty to the demonstrate a 

significant effect of the renin-angiostensin 

blockade in the cardiovascular prevention 

beyond the blood pressure control. 

In addition, Skeggs et al., suggested another 

possible approach to inhibit the RAS which is 

renin inhibition (39) . Renin inhibitors are under 

investigation and phase III trials have shown 

their effectiveness at lowering blood pressure 

(40, 41) . Compared with the ACE inhibitors, renin 

inhibitors have few side effects and may be 

indicated in combination of drugs such as 

diuretics, ACE inhibitors, and ARBs which 

increase plasma renin through feed-back 

loops. They are illuminated via the liver with 

little interaction with other drugs and may be 

useful in patient with concomitant renal 

disease (42) . Of course, renin inhibitors offer the 

potential to inhibit the entire cascade of the 

system. Although the results from AGELESS 

study showed the first – in – class direct renininhibitor 

aliskiren provides significantly greater 

blood pressure reduction compared to ACE 

inhibitor ramipril (43) , but at present, the effects 

independent of antihaypertensive activity of 

aliskiren have been shown by one clinical trial 

focused on end – organ damage. In aliskiren 

in the evaluation of proteinuria in diabetes 

(AVOID) trial, the treatment with aliskiren 

reduced proteinuria independently of blood 

pressure (44) . Other clinical trials have been 

started to investigate the possible benefit of 

aliskiren in cardiac remodeling after 

myocardial infarction (AVANT GARDE- 

ASPIRE) and diabetic nephropathy 

(ALTITUTE) (45) . Therefore, in the next future, 

further clinical evidence will be available to 

confirm these preliminary anti-inflammatory 

and anti-atherosclerotic effects of renininhibitors 

in humans. 



RAS and hypertensive disease 

Patients with hypertension die prematurely, 

the most common cause of death is heart 

disease, followed by stroke and renal failure. 

The excess morbidity and mortality related to 

hypertension are progressive over the whole 

range of systolic and diastolic blood pressures, 

the risk approximately doubles for each 6 

mmHg increased in diastolic blood pressure 

(46) . Cardiac complications are the major 

causes of morbidity and mortality due to target 

– organ damage caused by hypertension and 

prevention of this damage should be a major 

goal of therapy. The most important 

cardiovascular target-organ damage caused 

by hypertension are: left ventricular 

hypertrophy, atrial fibrillation and stroke. 

Left ventricular hypertrophy 

It is one of the early organ damage caused 

by hypertension which by itself increases the 

risk of major cardiovascular event 2-5 folds (47) . 

Angiotensin II, acting through the AT 1 receptor, 

is involved in virtually every step along the 

cardiovascular continuum. Consequently, any 

intervention that specifically blocks these 

actions can be expected to have a significant 

impact on cardiovascular morbidity and 

mortality by retarding the succession of events 

(figure 4). Evidences for an association 

between the RAS and L. V. H. stem from: 

1. Left ventricular hypertrophy has been 

shown to be high in patient with renal 

artery stenosis, a stage characterized by 

the system activation compared with 

patients with primary hypertension at 

similar levels of blood pressure (48) . 

2. In a study cohort of untreated hypertensive 

(49) 

people high "angiotensin II 

concentrations were closely associated 

with high left ventricular mass (figure 6) 

subsequent analysis revealed that 

increased activity and insufficient 

suppression of the RAS corresponds to 

inadequately high left ventricular mass in 

relation to the 24 hr ambulatory blood 

pressure load (50, 51) . 

Figure (6): Box plot of left ventricular mass in 

never treated patients, according to 

angiotensin 11 concentrations in relation to 

urinary sodium excretion. Reproduced with 

permission from Prof. R. F. Schmieder. Renin 

– angiotensin system and cardiovascular risk. 

Lancet 2007 (65) . 

3. Further evidence of an association 

between RAS and LVH stem from 

therapeutic trials of the five 

antihypertensive agents recommended as 

first – line treatment, calcium antagonists, 

ACE inhibitors, and ARBs reduce left 

ventricular mass to a greater extent than 

do B-blockers and diuretics (figure 7) (52, 

53) . 

Figure (7): Reduction of left ventricular mass 

stratified according to various antihypertensive 

regimens. Reproduced with permission from 

Prof. R. F. Schmieder. Renin – angiotensin 

system and cardiovascular risk. Lancet 2007 

(65) . 



In addition, in a prospective trial "LIFE study" 

(54) with hypertensive patients who had L.V.H. 

at baseline the investigators consistently 

reported that reduction of L.V.H. was greater 

with the ARB Losartan than with the β-blocker 

atenelol, and this effect was maintained at 

similar blood pressure levels throughout the 

whole follow-up of 5 years (55) . Thus, it is not 

only a question of treatment duration or 

achieved blood pressure, but the choice of 

drug is also of clinical relevance to the 

treatment of L.V.H. In addition many clinical 

trials (56) have clearly shown that reduction of 

L.V.H. translates in to a reduced rate of 

cardiovascular complications and improved 

prognosis. Accordingly, reduction of L.V.H. 

appears as a therapeutic goal in primary 

hypertension that should be taken seriously. 

Atrial fibrillation 

Atrial fibrillation is the most common 

sustained cardiac arrhythmia, affecting roughly 

1% of people younger than 65 years. The 

incidence and prevalence of atrial fibrillation 

steeply rises with advancing age affecting 5% 

of individuals older than 65 years (57) and 9% 

of those aged over 80 years of note, 70% of 

atrial fibrillation patients are aged between 65 

and 85 years, and overall 84% are older than 

65 years (58) . Atrial fibrillation increases the risk 

of cardiovascular mortality by two-fold and it is 

the cause of up to 15% of all strokes (59, 60) . 

Hypertension is the most important risk factor 

for atrial fibrillation on a population basis, and 

in hypertensive patients, age, left atrial 

chamber diameter, and left ventricular mass 

have been identified as independent risk 

features for the development of atrial fibrillation 

(61) . 

The rule of renin-angiotensin system in the 

pathogenic mechanism of atrial fibrillation 

stemmed from many therapeutic trials. In 

hypertensive patients with atrial fibrillation at 

baseline, the LIFE study findings suggested 

that treatment based on ARBs was more 

effective than that based on B-blockers in 

reducing the risk of the composite 

cardiovascular endpoint, stroke and death (62) . 

Similarly, treatment with ARBs reduced the 

frequency of atrial fibrillation in patients without 

atrial fibrillation at baseline by 21% (63) , and in 

VALUE study, new atrial fibrillation onset was 

less frequent in those on ARBs than in those 

on calcium antagonists (64) . Accordingly, reninangiotensin 

system blockade has emerged as 

a new preventive and therapeutic strategy for 

atrial fibrillation (65) . 

Stroke 

Stroke is the third most common cause of 

death in the developed world after cancer and 

ischemic heart disease, and is the most 

common cause of severe physical disability 

(66) . About one-fifth of patients with an acute 

stroke will die within a month of the event, and 

at least half of those who survive will be left 

with physical disability (66) . The incidence and 

prevalence of stroke increases linearly with 

age and blood pressure (67) , accordingly the 

most crucial factor in stroke prevention is best 

possible blood pressure control (68) . 

Meta-analysis suggest that ARBs (but not 

ACE inhibitors) are effective in stroke 

prevention beyond blood pressure control (68) . 

The explanation of this result came from 

animal studies 

(69) , treatment with ARBs 

improved neurological outcome of focal central 

ischemia and protected brain tissue against 

ischemic injury. Stimulation of the AT 2 receptor 

induces vasodilatation because it potentiates 

locally synthesized nitric oxide and 

prostacycline, which in turn could improve 

cerebral blood flow by collateral circulation (70) . 

In the brain region adjacent to the infarct area, 

AT 1 receptor density remained unaltered but 

AT 2 -receptors were upregulated in neurons (70, 

71) 

and selective blockade of central AT 2 

abolished the neuroprotective effect of ARBs 

(70) . Thus experiments have shown that 

cerebral AT 2 receptors exert neuroprotective 

effects in response to ischemia induced 

neuronal injury (70) . 

These new experimental findings helped to 

explain the results of several clinical trials. In a 

trial of hypertensive patients aged 35-64 

years, diuretics that activate the RAS 

prevented substantially more stroke than did 

β-blockers, which suppress the system activity 

by equal blood pressure reductions (72) . In 

hypertensive patients with stroke, the PPARS 

(73) 

study showed that the ACE inhibitor 

resulted in 5% stroke reduction, compared with 



a 43% stroke reduction if the diuretic 

indapamide was added. In hypertensive 

patients with LVH but without previous stroke, 

the LIFE study showed a 25% reduction in 

strokes with ARB based regimen that the β 

blocker one (41) similar results were reported in 

patients with isolated systolic hypertensive 

(40% & 24% stroke reduction) in LIFE study 

and SCOPE respectively (74, 75) . In these trials 

with ARBs, control of blood pressure was 

much the same, suggesting that the recorded 

difference in stroke frequency could be 

attributed specifically to treatment with ARBs. 

Finally in a meta-analysis, calcium antagonists 

that do not affects the RAS reduced the risk of 

stroke better than did ACE inhibitors (58) . 

In summary, the most important factor in 

stroke prevention is good blood pressure 

control, and the control of systolic blood 

pressure might be of particular importance (76) 

and the cerebroprotective effects of the AT 2 

(77) 

receptor stimulation by ARBs have 

emerged as an important clinical means to 

reduce the serious target-organ damage of 

hypertension namely the ischemic stroke. 

Conclusion 

The renin-angiotensin system (RAS) is a 

major contributor to both hypertension and 

associated pathophysiologic changes in the 

heart and vascular wall (the target organ). 

Major clinical trials have shown that 

angiotensin converting enzyme and 

angiotensin receptor blockers assist in 

controlling hypertension and reducing target 

organ damage. 

To advance clinically, it is important to 

optimize treatment directed at the RAS, i.e., 

more complete RAS blockade using a 

combination of an ACE inhibitors and RABs to 

maximize patients benefit. Theoretically, it 

seems logical but, results of the recent clinical 

trials did not confirm this expectation and 

appear to be associated with little more 

adverse effect. Renin inhibitors are other 

advances because they offer the potential of 

inhibiting the entire cascade of the system. 

Clinical trials have been started to investigate 

this possibility and the results are awaited in 

the near future. 

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Case report: 

Accidental cooking gas intoxication 

Dhaher J. S. Al-Habbo 



Received: 23 rd Apr 2008; Accepted: 4 th Jan 2009. 

ABSTRACT 

The primary component of natural gas is methane (CH 4 ). It also contains ethane (C 2 H 6 ), propane 

(C 3 H 8 ), butane (C 4 H 10 ), and other sulfur containing gases, in varying concentrations. 

Suicide by domestic gas was forming more than 40 percent of the annual number of suicides in 

England and Wales in 1963. 

Jarvis et al. reported that women using gas stoves had double the respiratory problems of women 

cooking on electric stoves. I am reporting three cases of accidental cooking gas intoxication, with 

history of unconsciousness, with or without convulsion. The two males among our patients presented 

were ended up with neurological deficits like abnormal movements, disorientation and irritability. The 

3 rd patient recovered more or less completely but still she was complaining from mild weakness in the 

lower limbs. Natural gas carries an important cause of respiratory and neurological illnesses if the 

patients are exposed to it for enough time. 


إنّ‏ المكوّنات الأساسية للغاز الطبيعي هي:‏ الميثان بصورة أساسية وآذالك يحتوي على الإيثان،‏ البروبان،‏ البيوتان،‏ 

وغازات تحتوي على الكبريت.‏ وآمية هذه الغازات بنسب متفاوتة..‏ 

الانتحار بالغاز الطبيعي آان يشكل أآثر من ٤٠ بالمائة من العدد السنوي لحالات الانتحار في إنجلترا وويلز في ١٩٦٣. 

جار فيس وجماعته توصلوا إلى أن النساءِ‏ اللواتي يستعملن الطباخات الغازية آان عندهن نسبة الإصابة بالآفات الرئوية 

آالربو ضعف ما آان يصيب النساءِ‏ اللواتي يستخدمن الطبّاخات الكهربائية.‏ 

أردت تسجيل ثلاثة حالات تسمّم عرضي بالغاز المستخدم في الطبخ:‏ ثلاثة مرضى أحيلوا إلى وحدة العناية المرآزة 

والتنفسية في مستشفى ابن سينا التعليمي بالموصل،‏ رجلان وامرأة وآانوا جميعا في حالة فقدان الوعي،‏ مع الإصابة 

بنوبات صرع متكرر.‏ اثنان من مرضانا انتهوا بخلل في الجهاز العصبي المرآزي مثل الحرآات غير الإرادية في الجذع 

والأطراف مع تشوش الذاآرة خصوصا في تحديد المكان،‏ أما المريض الثالث ‏(الأنثى)‏ فقد تعافت تقريباً‏ بالكامل ولكنها 

بقيت تشتكي من ضعف بسيط في الأطراف.‏ 

الغاز الطبيعي مسبب رئيسي للأمراض التنفسية والعصبية إذا تعرّض له المرضى واستنشقوا الغاز لفترة طويلة مناسبة.‏ 

T 

he primary component of natural gas is 

methane (CH 4 ); the shortest and lightest 

hydrocarbon molecule. It also contains heavier 

gaseous hydrocarbons such as ethane (C 2 H 6 ), 

propane (C 3 H 8 ), and butane (C 4 H 10 ), as well as 

other sulfur containing gases, in varying 

amounts as in (Table 1) (1) . 

Suicide by domestic gas was accounting for 

more than 40 percent of the annual number of 

suicides in England and Wales in 1963. At the 

year 1975 this number showed a sudden, 

unexpected decline from 5,714 to 3,693 at a 

time when suicide continued to increase in 

most other European countries. This appears 

to be the result of the progressive removal of 

carbon monoxide from the public gas supply 

(1) . 



In 1996 Jarvis et al. reported that, in the UK, 

females who used gas cookers had an 

increased risk of wheeze and other asthma 

symptoms, as well as lower lung function 

(FEV 1 and FEV 1 /FVC) than females not using 

gas cookers. (2) 

Furthermore they found that women using 

gas stoves had double the respiratory 

problems of women cooking on electric stoves. 

When natural gas is burned, the chemicals 

byproducts create nitrogen dioxide, carbon 

monoxide, fine particulates, polycyclic 

aromatic hydrocarbons, volatile organic 

compounds (including formaldehyde) and 

other compounds (2) . Among the top10 leading 

sources of fatal work-related inhalations in the 

United State of America are coal, natural gas, 

and petroleum fuels and its products; they 

form about (11.8%) of the total number of 

dead patients (3) . Butane is a derivative of 

natural gas which is used in gas lighter refills; 

its abuse by inhalation of cigarette lighter refills 

and aerosol propellants can cause many 

health hazards (4). 

I am reporting three cases of accidental 

cooking gas intoxication referred to the 

Respiratory and Intensive care Unit (RICU) at 

Ibn-Sena Teaching Hospital in Mosul during 

the cold weather period from November 2004 

to early January 2005.The three patients had a 

history of collapse while they were in the 

bathroom, discovered by their families 30-45 

minutes after their entrance to the bathroom. 

Their families managed to open the door of the 

bathroom by force after 30-40 minutes where 

they found them unconscious, with or without 

convulsion and there was a leaking cooking 

gas heater (locally made) that were used by 

the patients to warm the bathroom and the 

water for bathing. 

Case report (1): A 23 -yearold male patient 

referred to the RICU at Ibn-Sena Teaching 

Hospital from the casualty department on the 

30 th of November 2004. The patient was 

brought to the casualty department where he 

developed a convulsion and then referred to 

the RICU. The on arrival examination details in 

the RICU are as in (Table 2). 

The various laboratory investigations as in 

(Table 3). The CT scan brain and MRI brain 

are useful investigation for unconscious 

patient with convulsion, but the CT scan was 

not working in our hospital at that time and the 

MRI brain was impossible to be done for our 

patients because the patients were not 

cooperative and the anesthetist in the MRI unit 

refuses to give adult patients anesthesia as 

they use anesthesia for children only and this 

applies for the other two patients. 

The immediate physical signs were similar to 

increased intracranial pressure, so we started 

him on dexamethazone ampl.4mg 6 hourly, 

mannitol 200mL during 30 minutes twice daily 

and ampicillin-cloxacillin 500mg IV 6hourly. 

The patient was given high oxygen 

concentration and to be mechanically 

ventilated if the SpO 2 remain low. 

The patient was monitored hourly as usual in 

the RICU with continuous SpO 2 monitoring. 

Arterial blood gas analysis was not available. 

On the 2 nd of December the patient became 

conscious but irritable with slurred speech and 

abnormal chorioathetosis-like movements of 

his upper and lower limbs, slightly disoriented 

for place .The respiration was normal and his 

SpO 2 on room air was 98%. Neurological 

consultation confirmed the diagnosis of 

chorioathetosis, and the patient neurological 

abnormality was treated accordingly. 

The patient continues to be slightly 

disoriented for place with the same abnormal 

movement but it was less than before even 

two months later when he was seen for followup. 

Case (2): A 24 years male patient referred to 

the RICU at Ibn-Sena Teaching Hospital from 

the casualty department on the 26 th of 

December 2004. The patient was brought to 

the casualty department and then referred to 

the RICU. The on arrival examination details in 

the RICU are as in (Table 2). The laboratory 

investigations as in (Table 3). 

The immediate physical signs and treatments 

of the patient were similar to case number one. 

The patient monitored hourly as usual in the 

RICU with continuous SpO 2 monitoring. 

On the 27 th of December the patient regained 

his consciousness although he was 

disoriented for place with slurred speech; he 

became irritable with abnormal 



chorioathetosis-like movements of the trunk 

and the extremities. The patient was treated 

accordingly. The SpO 2 became 98% with 

normal respiration. 

The patient was brought for follow up three 

weeks later with the same disorientation for 

place, irritability and mild abnormal 

chorioathetosis-like movements. 

Case (3): An 18-year-old female patient 

referred from Telafar Hospital directly to the 

Respiratory and intensive care unit at Ibn- 

Sena Teaching Hospital on the 23 rd of January 

2005. The on arrival examination details in the 

RICU were as in (Table 2). The immediate 

treatments of the patient were similar to the 

first and second patients. The ordinary 

laboratory investigations as in (Table 3). The 

patient monitored hourly as usual in the RICU 

with continuous SpO 2 monitoring. 

On the 24 th of January 2005 the patient was 

fully conscious but unable to walk. 

Neurologically there was generalized 

weakness in both lower limbs; all reflexes were 

intact and the plantar reflex was flexor with no 

localizing sign . 

By the 26 th of January the patient was able to 

walk for a short distance alone and she felt 

weak in both lower limbs and she was happy 

to be discharged home. The patient failed to 

come for follow up. 

Table (1): The Components of Natural Gas 

Component wt. % 

Methane (CH 4 ) 70-90 

Ethane (C 2 H 6 ) 5-15 

Propane (C 3 H 8 ) and Butane (C 4 H 10 ) < 5 

CO 2 , N 2 , H 2 S, etc. 

balance 

Table (2): The physical signs and symptoms during examination in the RICU 

Symptoms and Signs Case 1 Case 2 Case 3 

Pulse Tachycardia Tachycardia Tachycardia 

SpO 2 58% 62% 70% 

Blood Pressure Normal Normal Normal 

Breathing 

Tachypnoea and 

Periodic 

Tachypnoea 

Tachypnoea 

Cyanosis Present Present Mild Cyanosis 

Conscious Level 

(GLASGOW COMA 

SCALE) 

GCS=5 GCS=6 GCS=10 

History of Convulsion Present Present Present 

Pupils 

Normal in size and 

reacting to light 





Plantars Equivocal Normal Normal 

Auscultation of the Chest 

Chest x-ray 

Diffuse crackles 

bilaterally 

Increased lung 

markings 

Harsh Vesicular 

Breathing with 

scattered crackles 

Normal 

Harsh Vesicular 

Breathing 

Normal 

ECG Sinus Tachycardia Sinus Tachycardia Sinus Tachycardia 



Table (3): The investigations done for the three patients 

Cases 

Hb 

g/L 

WBC 

FBS 

or 

random 

mmol/L 

B.UREA 

mmol/L 

S.CREATININE 

µmol/L 

S.Na. 

mmol/L 

S.K 

mmol/L 

Case-1 139 8.6 R(9.2) 5.5 109 140 4.4 

Case-2 90 9.7 6.4 5.0 100 135 4.0 

Case-3 120 7 6.0 7.0 80 136 3.5 

Discussion 

Natural gas brings harmful chemicals into 

homes through the methane and other 

components it contains. Methane (which gives 

the flame its blue colour as it does in propane) 

is an asphyxiant chemical. 

The natural gas typically contains radon and 

other radioactive materials, BTEX (Benzene, 

Toluene, Ethylbenzene and Xylene), 

organometallic compounds such as 

methylmercury, organoarsenic and 

organolead. Mercaptan, an odorant, is also 

added to natural gas so that it can be detected 

by smell before reaching the toxic or explosive 

levels (5) . 

The patients presented in this paper were 

intoxicated accidentally by inhalation of 

cooking gas rather than due to abuse. The 

intoxication developed due to the use of the 

only available cooking gas stoves for heating 

the bathrooms and to have hot water for 

bathing. 

The intoxication with asphyxiant gases 

usually started clinically as euphoria, 

excitation, blurred vision, slurred speech, 

nausea, vomiting, coughing, sneezing and 

increased salivation. If the intoxication 

continues then disinhibition, confusion, 

perceptual distortion, hallucinations, delusions, 

tinnitus and ataxia develop. If the dose 

increased, the patient will start to have 

nystagmus, dysarthria, tachycardia, central 

nervous system depression, drowsiness, coma 

and sudden death which may result from 

anoxia, vagal inhibition of the heart, respiratory 

depression, cardiac arrhythmias (6,7) . 

There is no typical clinical finding of 

inhalation poisoning apart from possible 

unconsciousness, the diagnosis is usually 

made depending on the history of exposure to 

the gas in badly ventilated space (4, 8) . 

The three patients I am presenting were 

unconscious at presentation and it was 

impossible to take history from them and they 

were in severe hypoxic state as they were 

centrally cyanosed with their SpO 2 58%, 62% 

and 70% (case 1, 2 and 3 respectively). 

Furthermore all the three patients presented 

with convulsion as an indication of cerebral 

anoxia due to the long period of intoxication 

which the three patients sustained and these 

findings are in accord with previously 

mentioned studies (6,7) . 

Patients with loss of consciousness are at 

high risk of developing delayed 

neuropsychiatric symptoms, which vary from 

mild intellectual impairment or personality 

changes to specific neurological deficits such 

as deafness, blindness, and Parkinsonism (9) . 

The previously mentioned neurological deficits 

occurred in our case number one, case 

number two and to a lesser extent in case 

number three. 

In the United Kingdom during 1988-1990, 

398 people mainly teenagers died due to 

abuse of fuel gas. Butane (as a derivative of 

natural gas) inhaled from lighter refill canisters 

has accounted for three times as many deaths 

as any other abuse of fuel gas products (10) . 

Gunn et al., 1989 reported a boy aged 15 

years with a habitual inhalation of butane by 

spraying it on his towel and then inhaling it to 

get euphoria where he developed ventricular 

fibrillation followed by apnea and he was 

ventilated for 36 hours due to cerebral oedema 

and made complete recovery (11) . Furthermore 

Bauman et al., 1991 reported a myocardial 



infarction in a boy aged 15 years; the boy was 

found unresponsive and cyanosed after 

inhaling butane from a plastic bag. The patient 

developed generalized tonic clonic seizures. 

The patient's ECG indicates anterolateral 

myocardial infarction. The patient was 

ventilated for 13 days, on discharge the patient 

left with memory and personality problems (12, 

13) . 

Gray and Lazarus in 1993 reported rightsided 

hemiparesis in a 15 year old boy after 

inhalation of a half a can of butane. The 

patient was left with pronounced proximal 

muscle weakness of the upper limbs and 

hemiplegic gait and his CT scan was normal 

(14) . 

Adgey et al reported in UK, that fuel gases 

appeared to be responsible for about 30% of 

deaths due to solvent abuse and aerosol 

propellants responsible for 20% 

(15) . 

Furthermore Chaudry in the year 2002 

reported 64 deaths from volatile substance 

misuse, more than 50% of them were 

attributed to fuel gas inhalation (16) . 

The patients presented in this paper were 

intoxicated accidentally by Fuel gas and none 

of them were suffering from cardiac problem at 

presentation apart from the sinus tachycardia. 

Our three patients were presented with 

neurological problems like convulsion and loss 

of consciousness, these findings are in accord 

with the finding by Doring et al as they 

reported severe encephalopathy in a 15 yearold 

girl due to abusive butane inhalation (17) . 

Furthermore two of our patients presented 

ended up with neurological deficits like 

abnormal movements, disorientation and 

irritability; the 3 rd patient recovered more or 

less completely but still she was complaining 

from mild weakness in the lower limbs. Similar 

abnormalities were reported in the USA by 

Bowen et al during the period 1987-1996. 

They reported 39 cases in Virginia who likely 

died as a direct consequence of exposure to 

an abused inhalant with definite CNS effects 

like behavior changes, slow speech, elated 

mood, hallucinations and illusionary 

experiences (18) . 

It is fair to say that acute carbon monoxide 

poisoning may cause similar clinical picture, 

but we assume that our cooking gas brand 

was from the new generation i.e. carbon 

monoxide free cooking gas, due to the 

progressive removal of carbon monoxide from 

the public gas supply which was carried out by 

the Petrol companies starting from the early 

sixties (1) . Furthermore the pulse oximeter 

measures both carboxyhaemoglobin and 

oxyhaemoglobin, therefore it may indicate a 

normal value in carbon monoxide poisoning 

which were not the case in our patients . The 

pulse oximeter measure of our patients 

returned to normal in nearly the 2 nd or 3 rd day 

without using the hyperbaric oxygen therapy 

which is usually required in carbon monoxide 

poisoning although its use is controversial now 

a days (19) . 

Conclusion 

Natural gas carries an important cause of 

respiratory and neurological illnesses if the 

patients exposed to it for enough time, 

especially in those who use the open flame 

gas cook stoves, hot water heaters, and 

furnaces. 

There are good medical evidences indicating 

clearly that natural gas should be restricted to 

generating electrical energy; this kind of 

legislation is now approved in Canada. 

References 

1. Ronald V. Clarke, Pat Mayhew. The British 

Gas Suicide Story and Its Criminological 

Implications. Crime and Justice 1988; Vol. 

10: 79-116. 

2. Jarvis D, Chinn S, Luczynska C, Burney P. 

Association of respiratory symptoms and 

lung function in young adults with use of 

domestic gas appliances. Lancet 

1996;347:426–431. 

3. Francesca Valent, Gerald McGwin, Jr. 

Massimo Bovenzi, and Fabio Barbone. 

Fatal Work-Related Inhalation of Harmful 

Substances in the United States. Chest. 

2002;121:969-975. 

4. Ellenhorn MJ and Barceloux DG. 

Diagnosis and treatment of human 

poisoning. Medical Toxicology. New York: 

Elsever.1988:964-968. 

5. Agnes Malouf and David Wimberly . The 

Health Hazards of Natural Gas. Nova 



Scotia Allergy and Environmental Health 

Association, Canada. Update Summer 

2001; 1-2. 

6. Ramsey J, Anderson HR, Bloor K and 

Flanagan RJ. Mechanism of Sudden 

Death Associated with Volatile Substance 

Abuse. Human Toxicol.1989; 8:261-69. 

7. Sheferd RT. Mechanism of Sudden Death 

Associated with Volatile Substance Abuse. 

Human Toxicol 1989; 8:287-92. 

8. Ashton CH. Solvent abuse: Little progress 

after 20 years. BMJ 1990; 300:135-36. 

9. Choic IS. Delayed neurologic sequelae in 

carbon monoxide intoxication. Arch Neurol 

1983; 40,433-435. 

10. Russell J. Fuel of the Forgottten Deaths. 

New Scientist. 1993;1859(137):21-23. 

11. Gunn J, Wilson J and Mackintish AF. 

Butane Sniffing Causing Venticular 

Fibrillation. Lancet 1989 i:617. 

12. Bauman JE, Dean BS and Krenzelok EP. 

Myocardial Infarction and 

Neurodevastation following Butane 

inhalation. Vet. Hum Toxicol. 1991; 4:150. 

13. Aviado DM and Beley MA. Toxicity of 

Aerosol Propellants on the Respiratory and 

Circulatory System. Cardiac arrhythmias in 

the Mouse Toxicology 1974;4:150. 

14. Gray MY and Lazarus JH. Butane 

inhalation and Hemiparesis. Clinical 

Toxocology. 1993;31(3):483-485. 

15. Adgey, A.A.J, P.W. Johnston, and S. 

McMechan. Sudden cardiac death and 

solvent and aerosol propellants abuse in 

UK.Resuscitation.1995;29:219-221. 

16. Chaudry, S. Deaths from volatile 

substance misuse fall. BMJ 2002;325:112. 

17. Doring, G,F.A.M. Baumeister, J. Peter, and 

J.von der Beek. Butane abuse associated 

encephalopathy. Klin. Paediatr 2002; 

214:295-298. 

18. Bowen, S.E, J. Daniel, R.L. Balster. 

Deaths associated with inhalant abuse in 

Virginia from 1987 to1996.Drug Alcohol 

Depend. 1999;53:239-245. 

19. Jonse Al, Dargan Pl. Churchill's text book 

of toxicology. Edinburgh: Churchill 

Livingston; 2001. (Reviewed: Med J Aust 

2002; 176: 291). 


@@Ý–ì¾a@k @òÜª 

الد ٣٥ حزيران ٢٠٠٩ العدد ١ 

@@‹í‹znÛa@ò÷îç@@@@@@@@@@@@@@ @@ @@@@@@@ 

رئيس هيئة التحرير 

ألأستاذ الدكتور طاهر قاسم الدباغ 

نائب رئيس التحرير 

ألأستاذ الدكتور هشام أحمد الأطرقجي 

أعضاء هيئة التحرير 

ألدكتورة بدور عبد القادر الارحيم 

ألأستاذة الدكتورة إلهام خطاب الجماس 

ألدكتور قحطان بشير إبراهيم 

ألدكتورة سحر خطاب عمر 

ألدكتور رامي محمد عادل الحيالي 

مدير التحرير 

الشؤون الإدارية:‏ الآنسة فائزة عبيد آغا 

@òÜª@@@@@@ Ý–ì¾a@k مجلة دورية طبية علمية تصدرها كلية الطب في جامعة 

الموصل.‏ وهي مدرجة في الفهرس 

الطبي لمنظمة الصحة العالمية لمنطقة شرق المتوسط وأنظمة الإيداع العالمية في فرنسا.‏ رقم الإيداع ١٢ 

لسنة ١٩٩٠. 

تحتفظ الة بحقوق الطبع والنشر،‏ والمعلومات المنشورة فيها تعبر عن رأي أصحاا وهي لا تمثل وجهة نظر 

هيئة التحرير.‏ ترسل جميع المراسلات وطلبات الاشتراك إلى:‏ مكتب سكرتارية مجلة طب الموصل،‏ كلية طب الموصل،‏ 

محافظة نينوى-‏ جمهورية 

العراق .E-mail: annalsmosul@yahoo.com 

تمت طباعة هذا العدد في آذار/‏ ٢٠١٠ في كلية طب الموصل.‏

@@Ý–ì¾a@k @òÜª 

@@òíŠb“nüa@ò÷îa@@@@@ 

@@ 

طب اتمع - كلية طب الموصل 

الكيمياء الحياتية - كلية طب الموصل 

– كلية الصيدلة 

كلية طب الأسنان 

جامعة الموصل 

جامعة الموصل – 

الكيمياء الحياتية - كلية طب الموصل 

– الأحياء اهرية 

كلية طب الموصل 

طب اتمع - كلية طب دهوك 

الكيمياء الحياتية - كلية العلوم/‏ جامعة الموصل 

الطب الباطني - كلية طب الموصل/‏ متقاعد 

الفسلجة - 

الأطفال - طب 

الأدوية - 

كلية طب الموصل/‏ متقاعد 

كلية طب نينوى 

الشركة العامة لصناعة الأدوية 

والمستلزمات الطبية/‏ نينوى 

الأدوية - 

الأستاذة الدكتورة أسماء أحمد الجوادي 

الأستاذ الدكتور أكرم جرجيس أحمد 

الأستاذ الدكتور باسل محمد يحيى 

الأستاذة الدكتورة اني عبد العزيز الصندوق 

الأستاذ الدكتور رعد يحيى الحمداني 

الأستاذ الدكتور زين العابدين عبد العزيز 

الأستاذ الدكتور صميم أحمد الدباغ 

الأستاذ الدكتور طارق يونس 

الأستاذ الدكتور عبد الإله أحمد الجوادي 

الدكتور عبد الخالق رشيد الملاح 

الأستاذ الدكتور فارس بكر الصواف 

الأستاذ الدكتور فرج محمد عبد االله 

الأستاذ الدكتور فؤاد قاسم 

الأستاذ الدكتور مزاحم قاسم الخياط 

الدكتور نزار مجيد قبع 

الأستاذ الدكتور يسار يحيى التمر 

كلية الطب البيطري 

الجراحة الناظورية - كلية طب الموصل 

الطب الباطني - كلية طب الموصل 

الكيمياء الحياتية - كلية طب نينوى

Volume 35 June 2009 Number 1 - University of Mosul

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