January 2007 Vol 7 correct A.indd


ABSTRACT Objective: To evaluate  the impact of the National Cholesterol Educational Program Adult Treatment Panel III (ATP 
III) and the Framingham Offspring Study on Omani diabetic subjects. Methods: 22 subjects with type 2 diabetes (86 females and 
35 males) and 56 non-diabetic subjects (70 females and 86 males) aged 30-70 years attending Sultan Qaboos University Hospital 
between 999-2002 were recruited. Lipid profile, glucose, %HbAc, apoproteinA- and apoproteinB were measured. Low density lipo-
protein was calculated using the Friedwald formula. ATP-III and Framingham Offspring Study guidelines were used to classify lipid
parameters into coronary heart disease-risk categories. Results: Diabetic compared to non-diabetic subjects had significantly higher
triglycerides of >.7 mmol/L  (p=0.0) and lower low density lipoprotein cholesterol of >4.2 mmol/L (p=0.02 ) and, in female subjects 
only, lower high density lipoprotein cholesterol of <.5 mmo/L for ( p<0.000).  In addition, 57% of diabetic subjects had abnormal 
aplipoproteinB of >.2 g/L compared to 49% of non-diabetic subjects.  Combined raised levels of triglycerides, apolipoproteinB and 
low levels of high density lipoprotein were found in 42% of diabetic compared to 26% of the non-diabetic subjects (p=0.05). Diabetic 
subjects had significantly higher (p=0.008) NCEP risk-score for coronary artery disease, however, only 34% conformed to a NCEP 
0-year-risk score of >0%. Conclusion: A substantial proportion of the Omani diabetic subjects were dyslipidaemic according to the 
ATP III guidelines. This study recommends the implementation of a lower cut-off threshold for starting lipid-modifying agents for
Omani diabetics when using the 0-year Framingham Risk Scoring equation. 

Key words:  Lipids, Lipoproteins, diabetes mellitus, Oman, and NCEP risk score. 

Abbreviations: TC, total cholesterol; LDL-C, Low Density Lipoprotein cholesterol; HDL-C, High Density Lipoprotein cholesterol; 

Lipids-Risk Categories in Omani Type 2 Diabetics
Impact of the National Cholesterol Educational Program

Ali I Al-Bahrani, Riad Bayoumi, *Said A Al-Yahyaee

 SULTAN QABOOS UNIVERSITY MEDICAL JOURNAL
DECEMBER 2006 VOL 6, NO. 2
SULTAN QABOOS UNIVERSITY©

Department of Biochemistry, College of Medicine and Health Sciences Sultan Qaboos University. P.O. Box 35, Al-Khoud 123, Sultanate of Oman

*To whom correspondence should be addressed. Email: syahyaee@squ.edu.om

O R I G I N A L  S T U D Y

الثاني النوع - السكر العمانيني املصابني بداء عند الشحوم خطورة تصنيف
الكوليستيرول حول التربوي البرنامج أهمية

ــل ــة فرمنجهام لنس (NCEP - ATP III) و دراس للبالغني العالجي التوعوي الوطني ــترول الكوليس تطبيق برنامج ــر تأثي ــص: الهــدف: تقييم امللخ
و135 رجال 86 امرأة بينهم الثاني) – من (النوع السكر بداء مصابا 221 شخصا هذه الدراسة ــملت الطريقة: ش . ــكر الس بداء املصابني العمانيني
السطان جامعة ــفى مبستش ، 30-70 عاما بني أعمارهم تتراوح 86 رجال) ، و (70 امرأة ــكري الس بداء مصاب غير ــخصا 156 ش من ضابطة وعينة ،
(أ1-)  نوع البروتيني ميمٌ والصَ الدم خلضاب املئوية والنسبة واجللوكوز ، الدم في ــحوم الش لَة شاكِ ــتوى مس مت قياس .2002-1999 بني عامي قابوس
مقادير الشحوم لتصنيف لألنسال فرامنجهام دراسة وارشادات فرايدوالد طريقة حسب الكثافة قليل الشحمي البروتني ــتوى ــاب مس مت حس و(ب).
الغليسيريد ثالثي 0.01) من (احصائيا- أعلى مستوى السكر بداء املصابني ألنتائج: كان لدى القلبية. الشرايني في االصابة بأمراض خطورتها حسب
1.15 ملي مول/ل) (  من (أكثر الكثافة قليل ــحمي الش البروتني من ــتوى مس ــكر، وأقل بداء الس بغير املصابني ل) مقارنة 1.7 ملي مول/ من (أكثر
.(p=0.0001) (1.15 ملي مول/ل (أقل من منخفضا عالي الكثافة ــحمى الش البروتني ــترول كوليس ــتوى مس كان فقط ــاء p=0.012) . وعند النس
العينة %49 من ب ــة 1.2 جرام/ل) مقارن من (أكثر ب - ــوع ن ميمٌ البروتيني الصَ ــن طبيعية م ــتويات غير مس ــكر الس بداء %57 من املصابني ــدى ل
 42% في منخفضا الكثافة عالي ــحمي البروتني الش ــتوى ومس ، ب عالية - البروتيني نوع ميمٌ والصَ ــريد الغليس ثُالَثِيُّ ــتويات مس كانت . الضابطة
(p=0.008) خلطورة احصائيا عالية مستويات السكر بداء املصابني (p=0.05) . لدى الضابطة العينة %26 من مقارنة ب السكر بداء املصابني من
ألكثر سنوات عشر مدى على االصابة خطر حرز مطابقني %34 من هؤالء ATP III  NCEP . ولكن مقياس- حسب الوعائية القلب بأمراض االصابة
االدوية باستعمال ATP III . نوصي تعليمات ــب حس الدم ــحوم ش في اضطراب ــكر الس بداء املصابني العمانيني من لدى الكثير اخلالصة: .10% من
حسب ــنوات س ــر مدى عش على اخلطورة مقياس ــتعمل عندما نس عليه املتعارف من أقل ــتويات مس في االخيرة تكون عندما الدم ــحوم افضة لش

فرامنجهام.

الشحمي البروتني صميم الشحميات، عمان، ، السكري املفردات املفتاحية: مرض



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Diabetes Mellitus is a growing health problem in Oman. According to the national Omani survey carried out in 1991, the prevalence 
was 10% for type 2 diabetes and 13% for impaired 
glucose tolerance (IGT).1 This study also showed that
the prevalence of diabetes in Oman rose with age and 
may exceed 50% in the seventh and eighth decade 
of life, in females and males respectively. Recently, it 
was reported that the prevalence of diabetes in Oman 
had increased over the past decade reaching 16.1% of 
the population aged 30-64 years old.2 Furthermore, a 
cross-sectional random sample survey reported that 
approximately 20% of the population had high fasting 
plasma glucose.3 

Type 2 diabetes is associated with an increased risk 
for cardiovascular disease.4 This risk in part is due to
diabetic dyslipidaemia.4,5 The report from National
Cholesterol Educational Program Adult Treatment 
Panel III (NCEP ATP III) recognized the importance 
of early detection of diabetic dyslipidaemia. According 
to the ATP-III report, the presence of diabetes or of 
multiple risk factors with a 20% high 10-year risk for 
coronary artery disease (CAD) events are now con-
sidered to be CAD equivalents, requiring aggressive 
treatment as for established CAD and other types of 
atherosclerotic diseases.5 ATP III had further endorsed 
the importance of including high density lipoprotein 
cholesterol (HDL-C) as part of their guidelines for as-
sessing the risk of CAD and had re-categorized some 
of the cut-off values of atherogenic lipoproteins. Fur-
thermore, NCEP ATP III had recommended a scoring 
system based on the Framingham Risk equation using 
clinical and lipid data. Thus, it helps to calculate the
10-year absolute CAD risk i.e. the percentage prob-
ability of having a CAD event in 10 years and to iden-
tify certain subjects with multiple (2+) risk factors for 
intensive treatment Therefore, this study was aimed to
determine the impact of the NCEP ATP-III on Omani 
subjects with type 2 diabetes in comparison with non-
diabetic subjects 

R E S E A R C H  D E S I G N  A N D  M E T H O D S

 PATI E N T  SE L E C TI O N
The study recruited 221 patients (86 females and 135
males) with type 2 diabetes and compared them with 

BMI and age matched 156 (70 females and 86 males) 
non-diabetic patients from patients attending Diabetic 
and Lipid Clinics at the Sultan Qaboos University Hos-
pital, between 1999-2002. All the subjects diagnosed 
as type 2 diabetics fulfilled the World Health Organi-
zation criteria for diagnosis of type 2 diabetes melli-
tus either by an abnormal oral glucose tolerance test 
(OGTT), or  two abnormal fasting blood glucose tests 
(>7.0 mmol/L).  None of the diabetic subjects were on 
insulin or Thiazolidinediones (TZDs)  therapy. 40% of
the diabetic subjects were on dietary control and the 
rest on oral hypoglycaemic agents, as follows: Gliben-
clamide (39%), Glipizide (24%), Gliclazide (6%), bigua-
nides (13%, Metformin) and combined therapy (10%).

Patients were excluded from the study if they had 
a myocardial infarction in the three months prior to 
entry to the study, or uncontrolled thyroid disease 
(hypo or hyperthyroidism), macro-proteinuria (posi-
tive urine protein dip-stick x2), severe hepatic impair-
ment (known subject with chronic active liver disease 
or those individuals with obstructive liver pattern) or 
renal impairment (creatinine level >114 ųmol/L) and 
those on lipid modifying agents. This study was ap-
proved by the Medical Ethics and Research commit-
tee at College of Medicine and Health Sciences, Sultan 
Qaboos University and patients gave informed con-
sent prior to the study. 

C L I N I C A L  A N D  L A B O R ATO RY  A S SE S SME N T
All subjects underwent a clinical physical examination 
and any abnormality was documented. The subjects’
blood pressure was measured to the nearest even digit 
using a sphygmomanometer, with the subject in the 
sitting position after a 5-10 minutes rest.  Subjects 
were labeled hypertensive if blood pressure was equal 
or greater than 140/90 mmHg on two repeated occa-
sions or by 24 BP monitoring and those on anti-hy-
pertensive therapy. BMI was calculated as weight (kg) 
divided by height (m2) and used as an index of adipos-
ity. Subjects were labeled CAD if they had had a pre-
vious myocardial infarction or had a  stable angina 
pectoris with positive thallium stress test or coronary 
angiogram or Percutaneous Coronary Angioplasty 
(PTCA).

Following a 10-hour overnight fast, blood sam-
ples were taken for measurement of HbA1c, TC, TG, 

TG, triglycerides; apoB, apolipoprotien B; apoA-, apolipoprotein A-; CAD,  coronary artery  disease; OGTT; Oral Glucose Tolerance 
Test, NCEP; National Educational Cholesterol Program; ATP III, Adult Treatment Panel III; BMI, Body Mass Index. 



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21

HDL-C, apoA-1, and apoB. Cholesterol, TG and glu-
cose measurements were performed using timed end-
point enzymatic methods on the Synchron CX system 
(Beckman, Brea, USA). The within-run and between-
run precisions for cholesterol (4.3 mmol/L) were 3% 
and 4.5%, respectively; for TG (2.0 mmol/L) 3% and 
4%, respectively; for glucose (5.5 mmol/L) 2 and 3%, 
respectively.

HDL-C was determined using a timed-endpoint di-
rect homogenous assay on the same system, with-run 

of 2.5% and between-run of 3% precisions for HDL-
C of 1.2 mmol/L. apoA-1 and apoB were determined 
using rate nephelometric immunochemistry assay by 
the IMMAGE system (Beckman). The within-run and
between-run precision profiles for apoB (1.2 g/L) were
2.5% and 2.9%, respectively; for apoA-1 (1.05 g/L) 
they were 3.4% and 3.9%, respectively. Both the apoB 
and apoA-1 methods used have been standardized 
according to the International Federation of Clinical 
Chemistry.6 LDL-C was calculated using the Fried-

Table 1 :The clinical and metabolic characteristics of subjects with type 2 diabetes compared to non-
diabetic subjects 

                       Non-diabetic subjects                    Subjects with type 2 diabetes
p value 

Diabetic vs. 
non-diabetic

Women Men Both Women Men Both

Number 70 86 156 86 135 221

Age 48.3 (1.8) 45.7 (1.5) 46.6 (1.3) 47.8 (1.1) 49.5 (1.0) 47.9 (0.91) 0.30

BMI 31.2 (0.76) 31.3 (0.61) 31.2 (0.5) 30.2 (0.98) 30.9 (0.8) 30.2 (0.61) 0.45

TG (mmol/L)
1.29 

(1.03-1.6) 
1.41

 (1.23-1.61) 
1.36  

(1.21-1.57)
1.77 

(1.65-2.01) 

1.86
(1.75-2.09) 

1.82 
(1.69-1.98)

<0.0001

TC (mmol/L)
6.2 (0.21) 5.8 (0.15)

5.93 (0.11)
5.92 (0.18) 5.75 (0.14)

5.85 (0.11) 0.79

LDL-C (mmol/L)
4.10 (0.19) 4.2 (0.13)

4.2 (0.10)
3.8 (0.11) 3.6(0.12)

3.7 (0.09) 0.04

HDL-C (mmol/L)
1.47

 (1.27-1.58) 
1.19 

(1.05-1.24)
1.24 

(1.13-1.37)
1.17 

(1.15-1.26) 
1.10 

(1.05-1.14)
1.12 

(1.10-1.18)
0.10

Apo B (g/L) 1.33 (0.05) 1.29 (0.04) 1.30 (0.03)
1.31(0.04) 1.23 (0.03)

1.25 (0.02) 0.53

ApoA1 (g/L) 1.3 (0.04) 1.13 (0.02) 1.18 (0.02) 1.24 (0.04) 1.15 (0.02) 1.18 (0.02) 0.89

Hypertension (%) 35 36 35 61 60 60 <0.0001

CAD % 15 25 20 22 40.8 34 <0.0001

Fasting glucose 
(mmol/L)

5.4 (0.12) 5.2 (0.11) 5.3 (01) 5.8 (0.22) 6.0 (0.21) 5.9 (0.2) 0.006

HBA1c (%) 5.5 (0.05) 5.4 (0.06) 5.4  (0.05) 8.09 (0.3) 7.6 (0.22) 7.7 (0.16)
<0.0001

NCEP risk-score 9.8 (0.8) 8.1 (0.9) 8.7 (0.8) 11.2 (0.8) 10.8 (0.5) 10.98 (0.4) 0.008

Data are number, means +/- SEM, 95% CI for Log transformed variables and %.  TG and HDL-c



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wald formula and was not calculated when TG level 
was >4.0 mmol/L. The Department of Biochemistry at
the Sultan Qaboos University Hospital is engaged in 
an external quality control scheme of the Royal Col-
lege of Pathologists, Association of Clinical Biochem-
istry, Australia.

The NCEP ATP III (2001) guidelines were used
to classify lipoproteins concentration into CAD risk 
categories.5 The LDL-C levels were defined as low
(<3.4 mmol/L), borderline (3.4-4.19 mmol/L), border-
line-high (4.2-5.0 mmol/L), and high (>5.0 mmol/L) 
risk categories. The risk categories of HDL-C levels
were defined as high (<1.05mmol/L), borderline (1.05-
1.15 mmol/L), and low (>1.15 mmol/L). However, no 
gender cut-off value was used. As far triglycerides, the
cut-off value of >1.7 mmol/L was used as borderline-
high risk level. The borderline high risk categories for 
cut-off values were <1.2 g/L for apoA-1 and >1.2 g/L
for apoB. These cut-off values were selected from the
Framingham Offspring study and the International
Federation of Clinical Chemistry guidelines.7 The 10-
year-risk for CAD was determined using the Fram-
ingham risk scoring system as recommended by the 
NCEP ATP III

Descriptive analysis including the estimation of 

mean values and the SEM for continuous variables 
were documented. Prevalence and frequencies were 
expressed as percentages. Skewed parameters were 
logarithmically transformed when a parametric test 
was used. Categorical variables were compared by the 
χ2 statistic with the Yates correction or the exact Fisher 
test when appropriate. Binary regression analysis was 
carried out to study the influences of diabetes and gen-
der on the probability of having high-risk categories 
for CAD for the different lipid and lipoprotein param-
eters, after adjustment of the other observational vari-
ables. ANOVA was used to determine differences in
subject characteristics. ρ value (two-tailed) <0.05 was 
considered as statistically significant. All data was ana-
lyzed with the SPSS. 

R E S U L T S

A comparison of clinical parameters and the means of 
fasting lipid profile between diabetic and non-diabetic
subjects showed that diabetics had significantly higher 
mean levels of TG (p<0.0001) and lower of HDL-C (for 
female gender only, p<0.0001) and LDL-C (p=0.04) 
[Table 1].  Using NCEP-ATPII cut-off values for high 
borderline and high risk categories [Figure 1] indicat-
ed that 29% of diabetic subjects had significantly lower

Probability LDL -C> 4.2 mmol/L
p 

value
TG  >1.7 
mmol/L

p 
value

HDL-C <1.15  
mmol/L

p 
value

Apo B >1.2 
g/L

p 
value

Apo A-1 <1.2  
g/L

p 
value

Diabetic 
subjects 
vs. non-
diabetic 
subjects

0.572  
(0.357-0.918)

0.02
2.183 

(1.344 -3.548)
0.002

1.334 
(0.836 -2.181) 0.25

1.334 
(0.776 -2.205)

0.31
1.205 

(0.170 -2.023)
0.48

Diabetic 
women 
vs. non-
diabetic 
women

0.581  
(0.259 -1.256)

0.15
2.520

(1.129 -5.627)
0.024

3.724 
(1.458 -9.522) 0.006

1.529 
(0.662 -3.760)

0.35
1.846 

(0.752 -4.536)
0.18

Diabetic 
women vs. 
diabetic 
men

2.472  
(1.485 4.115)

<0.0001
0.660 

(0.357 -1.221)
0.18

1.052 
(0.589 -1.945) 0.87

1.508 
(0.780 -2.910)

0.22
0.718 

(0.379 -1.377)
0.30

Diabetic 
men vs. 
non-
diabetic 
men               

0.495  
(0.265-0.926)

0.03
2.021 

(1.096 -3.725)
0.024

0.860 
(0.466 -1.586) 0.63

1.200 
(0.631 -2.282)

0.57
0.978 

(0.509 -1.879)
0.95

Women vs. 
men     

2.320  
(1.440-3.745)

0.001
1.275 

(0.819 -1.984)
0.28

0.468 
(0.296 -0.742) 0.001

1.170 
(0.746 -1.834)

0.49
0.658 

(0.417- 0.989)
0.04

 Data are odd ratio (95% CI). Adjusted for age, HBA1c, and BMI 

Table 2: Logistic regression analysis examining the influence of diabetes and gender on the probability of
having LDL-C, HDL –C, TG, apo B, and apo A-1 outside the recommended target



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23

LDL-C level of (>4.2 mmol/L), compared to 43% of 
non-diabetic subjects ((p=0.012) ). On the other hand, 
57% of diabetic subjects had abnormal apoB of >1.2 
g/L compared to 49% non-diabetic subjects. A signifi-
cantly higher level (p=0.01) of TG (>1.7 mmol/L), was 
found in diabetic subjects (63%) compared to non-
diabetic subjects (43%), irrespective of gender. The
percentage of diabetic (56%) and non-diabetic (48%) 
subjects showed no significant difference on abnormal
level of <1.15 mmol/L HDL-C when the same cut-off
value was used for both genders as recommended by 
NCEP ATP III guidelines. However, despite a signifi-
cantly larger percentage of male subjects, compared 
to female subjects, who had an HDL-C levels of <1.15 
mmol/L, (p=0.001), there was a significantly higher
(p=0.05) percentage of female diabetic subjects with 
abnormally low HDL-C levels compared to nondia-

betic subjects. Borderline high-risk of apoA-1 1.0-1.2 
g/L and high-risk of apoA-1 <0.9 g/L were detected 
in 60% of males compared to 48% of females subjects; 
such a difference was statistically significant (p=0.01).

Logistic regression analysis of the influence of
type 2 diabetes and gender on the probability of hav-
ing serum lipids that were outside the recommended 
targets adjusted for age, BMI and HbA1c , showed that 
diabetic compared to non-diabetics subjects had a sig-
nificantly higher likelihood ratio of having TG of >1.7
mmol/L and a lower likelihood ratio of having an ab-
normal, LDL-C of >4.2 mmol/L, irrespective of gender 
[Table 2]. Female diabetics had a significantly higher
likelihood ratio of having an abnormal HDL-C level 
of <1.15 mmo/L compared to female non-diabetic 
subjects. Furthermore, female subjects had a signifi-
cantly higher likelihood ratio of having an LDL-C of 

Combined dyslipidaemia Non-diabetic(%) Diabetic (%)

 LDL-C (>3.4 mmol/L) and TG (>1.7 mmol/L)* 24 34

TG (>1.7 mmol/L) and HDL-C (<1.15 mmol/L)* 23*   37*

 LDL-C (>3.4 mmol/L) and HDL-C (<1.15 mmol/L) 30 30

All the three 15 19

TG (>1.7 mmol/L) and Apo B (>1.2 g/L) 27*   43*

TG (>1.7 mmol/L), Apo B (>1.2 g/L) and HDL-C (<1.15 mmol/L) 18 25

* Statistically significant, p value  = 0.04

Table 3 :Proportion of subjects having combined dyslipidemia, borderline-high risk categories for C AD, 
according to the NCEP ATP III and the Framingham Offspring study

Figure 1:  Percentage of diabetic subjects with abnormal lipids and lipoproteins levels compared to 
non-diabetic subjects



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24

>4.2 mmol/L and a lower likelihood ratio of having an 
HDL-C of <1.15mmol/L and apoA-1 of <1.2 g/L com-
pared to males.

Combined dyslipidaemia of two or more lipid ab-
normalities was observed in 89% of diabetic and 76% 
of non-diabetic subjects. Combined raised levels of TG 
and apoB and raised TG and low level of HDL-C was 
highly prevalent (p=0.05) among diabetic compared to 
non-diabetic subjects, [Table 3].

Omani subjects with type 2 diabetes had signifi-
cantly higher (p=0.008) NCEP risk-score compared 
to non-diabetics [Table 1]. The Framingham scoring
divides subjects with multiple risk factors into those 
with 10-year-risk for CAD of >20%, 10%-20%, and 
<10%. The percentage of diabetic subjects (34%) with
a 10-year risk for CAD of >10%-20% was significantly
higher (p=0.05), compared to non-diabetics (24 %,).  

D I S C U S S I O N 

Detection and treatment of dyslipidaemia are means 
of reducing the risk of CAD associated with type 2 
diabetes.4,8 When applying the recent guidelines re-
leased by NCEP ATP III and the Framingham Off-
spring Study to classify lipoprotein concentrations, a 
large proportion of studied Omani diabetic subjects 
turned out to be dyslipidaemic. Combined raised 
levels of apoB, triglycerides and low levels of HDL-C 
were highly prevalent among Omani diabetic subjects 
compared to non-diabetic subjects, despite the fact 
that the proportion of Omani diabetic subjects with 
borderline-high and high-risk categories of LDL-C for 
CAD was significantly lower compared to non-diabet-
ic subjects. The NCEP recommends an optimal goal
of LDL cholesterol to be <2.6 mmol/L for diabetics.4 
When using this clinical end point, a substantial per-
centage of the diabetics would require intervention 
and ongoing monitoring to ensure that the recom-
mended LDL-C goal is reached and maintained. 

Although the gender comparisons for HDL-C risk 
categories were statistically significant, female sub-
jects with type 2 diabetes had a six to seven-fold in-
creased likelihood of having high-risk category levels 
of HDL-C for CAD compared to non-diabetics. This
may explain why the protective effect of gender against
CAD is not evident in diabetic women. However, a 
similar proportion of males with borderline-high and 
high-risk categories was noticed in both diabetic and 
non-diabetic subjects. The latter finding could in part
explain the high risk of CAD among the males com-

pared to the females. Given the recent findings of the
beneficial effect of increasing HDL-C levels, these data
indicate that increasing this lipoprotein, along with 
lowering LDL-C levels, should be an important target 
for intervention among Omani subjects irrespective of 
the diabetic status.9, 10 The 10-year absolute risk-score
for CAD was calculated for all subjects studied using 
the Framingham risk-scoring equation. This study in-
dicated that Omani subjects with type 2 diabetes had 
significantly higher risk-score for CAD compared to
non-diabetics and were more significant among those
diabetic subjects with established CAD. However, only 
a small proportion of Omani diabetic subjects showed 
a risk-score for CAD of >20%. A similar finding was
reported by Durrington in 2001, who highlighted 
the above point and suggested an CAD risk score of 
>15% over 10-year as a threshold for starting statin 
therapy.11

Recognizing that diabetes confers a cardiovascular 
risk equivalent to that of established atherosclerotic 
disease, the ATP III set the same LDL-C target (<2.6 
mmol/L) for diabetic patients and, therefore, recom-
mended aggressive treatment with lipid lowering drugs 
to achieve this target.  Clinical trials have confirmed
the benefits of LDL-C lowering as an effective primary
prevention strategy for diabetic patients8,12  and recom-
mended the use of statin without a particular thresh-
old level of LDL-C as the sole arbiter of which patients 
with type 2 diabetes should receive statins. However, 
in many patients with diabetes and cardiovascular dis-
ease, it will be difficult to attain an LDL-C goal of <1.8
mmol/L since approximately 25% of patients will re-
quire more than two lipid-lowering drugs at maximal 
doses to attain this goal, assuming 100% tolerance of 
lipid-lowering medications.13 There remains an im-
portant opportunity to improve the quality of care for 
these high-risk patients if the management of dysli-
pidemia is set optimally to achieve guideline-recom-
mended lipid targets14 , which may be achieved by the 
combination of drugs15 and/or rosuvastatin.16  Indeed, 
an economic simulation model suggested that increas-
ing the use of rosuvastatin can result in cardiovascular 
event reduction and cost savings.17 This implies that
our diabetic patients who have high prevalence of dy-
slipidemia, but low calculated CAD risk, may benefit
substantially from earlier intervention and therefore 
be prevented from having cardiovascular events.



L I P I D S - R I S K  C AT E G O R I E S  I N  O M A N I  T Y P E - 2  D I A B E T I C S

25

A C K N OW L E D GE ME N T
We would like to thank Dr. Ali Al-Hinai, consultant 
cardiologist, for his support in patients recruitment 
and the finncial support by Sultan Qaboos University
grant; IG/MED/BIOC/00/0

R E F E R E N C E S

1. Asfour MG, Lambourne A, Soliman A, et al. High 
prevalence of diabetes mellitus and impaired glucose 
tolerance in the Sultanate of Oman: Results of the 1991 
national survey. Diabet Med 1995; 12:1122-1125.

2. Al-Lawati A, Riyami A, Mohammed A, Jousihati P. In-
creasing prevalence of diabetes mellitus in Oman. Dia-
bet Med 2002; 19:954-957

3. Al-Lawati JA, Mohammed AJ, Al-Hinai HQ, Jousilahti 
P. Prevalence of the metabolic syndrome among Omani 
adults. Diabetes Care 2003; 26:1781-1785 

4. American Diabetic Association. Standards of Medical 
care for Patients with Diabetes Mellitus. Diabetes Care 
2003; 26:S33-S50

5. Third Report of the Expert Panel on Detection, Evalua-
tion and Treatment of High Blood Cholesterol in Adults 
(Adult Treatment Panel III). JAMA 2001; 285:2486-
2497

6. Jungner I, Marcovina SM, Walldius G, Holme I, Kolar W, 
Steiner E l. Apolipoprotein B and A-1 values in 127,576 
Swedish males and females, standardized according to 
the World Organization–International Federation of 
Clinical Chemistry First International Reference Mate-
rials. Clin Chem 1998; 44:1641-1649

7. Contois JH, McNamara JR, Lammi-Keefe CJ, Wilson 
PW, Massov T, Schaefer EJ. Reference intervals for plas-
ma apolipoprotein B determined with a standardized 
commercial immunoturbidimetric assay: Results from 
the Framingham Offspring Study. Clin Chem 1996;
42:515-523.

8. Collins R, Armitage J, Parish S, Sleigh P, Peto R. Heart 
Protection Study Collaborative Group. MRC/BHF 
Heart Protection Study of cholesterol-lowering with 

simvastatin in 5963 people with diabetes: a randomised 
placebo-controlled trial. Lancet 2003; 361:2005-2016. .

9. Haim M, Benderly M, Brunner D, Behar S, Graff E, Re-
icher-Reiss H, et al.  Elevated serum triglyceride levels 
and long-term mortality in patients with coronary heart 
disease: the Bezafibrate Infarction Prevention (BIP)
Registry. Circulation 1999; 100:475-482. 

10. Rubins HB, Robins SJ, Collins D, Fye CL, Anderson JW, 
Elam MB  et al. Gemfibrozil for the secondary preven-
tion of coronary heart disease in men with low levels 
of High-Density Lipoprotein Cholesterol Interventional 
Trial Study Group. N Engl J Med 1999; 341:410-18.

11. Durrington P. Calculation of coronary risk in Type II 
diabetes. Clinical Science 2001; 101:681-682.

12.  Colhoun HM, Betteridge DJ, Durrington PN, et al. Pri-
mary prevention of cardiovascular disease with atorv-
astatin in type 2 diabetes in the Collaborative Atorvas-
tatin Diabetes Study (CARDS): multicentre randomised 
placebo-controlled trial. Lancet 2004; 364:685-696.

13. Kennedy AG, MacLean CD, Littenberg B, Ades PA, 
Pinckney RG. The challenge of achieving national cho-
lesterol goals in patients with diabetes. Diabetes Care 
2005; 28:1029-1034.

14.  Yan AT, Yan RT, Tan M, Hackam DG, Leblanc KL, Kert-
land H, et al. Vascular Protection (VP) and Guidelines 
Oriented Approach to Lipid Lowering (GOALL) Regis-
tries Investigators. Contemporary management of dys-
lipidemia in high-risk patients: targets still not met. Am 
J Med 2006; 119:676-683.

15. Carmena R. Type 2 diabetes, dyslipidemia, and vascular 
risk: rationale and evidence for correcting the lipid im-
balance. Am Heart J 2005; 150:859-870. 

16. Guthrie RM. Rising to the challenge of treating high-
risk patients. Am J Manag Care 2006; 12:S318-S324.

17. Huse DM, Song X, Ozminkowski RJ, et al. Impact of ro-
suvastatin use on costs and outcomes in patients at high 
risk for cardiovascular disease in US managed care and 
medicare populations: A data analysis. Clin Ther 2006;
28:1425-1442.