VOLUME 15 | ISSUE 3 | MAY 1995

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Hyperlipidemia among Saudi Diabetic Patients — Pattern and Clinical Characteristics

Abdul Rahman Al-Nuaim, mb,frcp(C),facp; Olufuncho Famuyiwa, MB,FACP; William Greer, PhD

From the Departments of Medicine (Dr. Al-Nuaim, Dr. Famuyiwa), King Khalid University Hospital, Riyadh and Biomedical Statistics and Scientific Computing (Dr. Greer), King Faisal Specialist Hospital and Research Centre, Riyadh.

How to cite this article:

AR Al-Nuaim, O Famuyiwa, W Greer, Hyperlipidemia among Saudi Diabetic Patients — Pattern and Clinical Characteristics. 1995; 15(3): 240-243

DOI: 10.5144/0256-4947.1995.240

Abstract

Premature development of atherosclerosis and increased rate of coronary artery and peripheral vascular diseases are characteristic features of patients with diabetes mellitus. Hyperlipidemia is an important precipitating factor for these diseases. Several patterns of lipid alteration among diabetics were described; the most common is hypertriglyceridemia. This study was constructed to look at the pattern of lipid alteration among Saudi diabetic patients. Forty-three percent of diabetic patients were dyslipidemic with an equal distribution of dyslipidemic patients with respect to type of dyslipidemia, i.e., combined hyperlipidemia, hypercholesterolemia and hypertriglyceridemia. There was a higher percentage of affected female patients with dyslipidemia compared with male patients. This predominance continued when risk factors such as obesity, poor glycemic control, duration and therapy of diabetes mellitus were considered. There is lack of awareness and treatment of dyslipidemic diabetic patients among practicing physicians in spite of the propagated knowledge on the decreased rate of coronary events and regression of atheroma in the vascular walls of the coronary arteries upon treatment of hypercholesterolemia. There is a need to periodically screen the diabetic population and implement vigorous therapy for dyslipidemic ones.

Ann Saudi Med 1995;15(3):240-243.

 

Coronary artery disease (CAD) is the leading cause of death among diabetic subjects. Dyslipidemia, which has a frequent occurrence among diabetics, has been shown to be the main contributor to the increased incidence of coronary events and deaths among diabetic subjects. The association of atherosclerosis, dyslipidemia and diabetes was recognized as early as 1927, when Joslin1 suggested that the cause of premature development of atherosclerosis among diabetic subjects was related to excess fat. Epidemiological studies2 since then have confirmed the association and have shown a several-fold increase in coronary deaths among diabetic subjects when compared with nondiabetic subjects.

 

Several lipoprotein abnormalities were described among diabetic subjects;3 among these, chylomicronemia syndrome with raised very low density lipoprotein (VLDL), chylomicron and lowered high density lipoprotein (HDL); endogenous hypertriglyceridemia with raised VLDL and low density lipoprotein (LDL) or hypercholesterolemia with raised LDL.

 

Insulin deficiency4 is the basic defect in lipid handling among insulin-dependent diabetic subjects (IDDM). Decreased elimination of VLDL and chylomicron due to insufficient activation of the insulin-dependent lipoprotein lipase system will result in an increase in triglyceride-rich lipoprotein. Insulin deficiency leads to decreased degradation of LDL cholesterol through decreased LDL receptor-binding which will result in increased LDL cholesterol concentration. This is augmented by the nonenzymatic glycolation which is a consequence of insulin deficiency.

 

The cause of the lipid alteration among noninsulin-dependent diabetic subjects (NIDDM) is differential insulin distribution,5 which leads to increase in VLDL and triglyceride production through hepatic hyperinsulinemia; this is combined with decreased catabolism of triglyceride-rich lipoprotein due to relative peripheral insulin deficiency. There is a decrease in the fractional catabolic rate of apoprotein B in LDL.6,7 In spite of this, the LDL concentration is not increased because of the alteration of lipid composition with increase in triglyceride-rich VLDL particles. The conversion to LDL, however, is decreased among NIDDM subjects.8,9

 

The reported prevalence of diabetic dyslipidemia has varied from 25% to 60%.10 This wide variation can be attributed to the studied population and the degree of glycemic control and to the variation of the definition of the "cut-off" for hypercholesterolemia and hypertriglyceridemia.

 

This study was conducted at King Khalid University Hospital, Riyadh, which is a general hospital with a wide catchment area and a large diabetes practice. The objective was to study the pattern of diabetic dyslipidemia among Saudi patients. In this study, serum cholesterol concentration >6.2 mmol/L, a level which was shown to correlate with significant increase in incidence of coronary artery disease, was interpreted as hypercholesterolemia (HC), while serum triglyceride concentration >2.3 mmol/L was interpreted as hypertriglyceridemia (HT).11

Methods

A total of 318 Saudi adult diabetic patients were studied. All had their lipid profile measured over a period of six months. Lipid analysis for triglyceride and cholesterol concentration were performed using enzymatic reactions (American Monitor Corp., Indianapolis, Indiana, U.S.A). Glycosylated hemoglobin (HbAic) was measured by Gel electrophoresis (Corning Diagnostic Corporation, Palo Alto, CA, U.S.A).

 

The following additional data were ascertained: sex, weight, height, body mass index (BMI), duration of diabetes mellitus and type of therapy for diabetes mellitus. Statistical analysis was performed using the SPSS/Windows programming. Quoted significance levels were obtained using the chi-square statistic with Yates continuity correction.

Results

There were 318 Saudi patients with Type II diabetes. Their ages ranged from 32 to 74 years with mean of 46 years; 163 (51%) were female and 155 (49%) were male patients who had their serum cholesterol and triglyceride measured. Based on the cited cutoff, patients were stratified into four groups. Table 1 shows the number of patients and the results of statistical comparison between male and female patients in each of the different groups.

 

One hundred and eighty-one (57%) patients were normolipidemic compared with 137 (43%) dyslipidemic patients. Among the dyslipidemic patients, combined hyperlipidemia, hypertriglyceridemia and hypercholesterolemia were found in 47 (15%), 46 (15%) and 44 (14%) patients respectively.

 

Figure 1 shows the dyslipidemia pattern among male and female diabetic patients.

 

There is a higher percentage of affected female patients with dyslipidemia compared with male patients except for the high cholesterol group, where there were an equal percentage of affected male and female patients.

 

Table 2 shows the relation between dyslipidemia in male and female diabetic patients and obesity (BMI >27), poor glycemic control (HbAic >10.5), duration and therapy of diabetes mellitus. Among obese diabetic patients, dyslipidemia was significantly more frequent among females (P<0.03). Among poorly controlled diabetic patients, dyslipidemia appeared to be more frequent among females but was not statistically significant.

 

The patients were divided into three groups based on duration of diabetes mellitus. Dyslipidemia was more frequent among females across the three groups; however, the only significant difference (P<0.04) in duration occurred between five and 15 years. The patients were also divided into three groups based on the therapy for diabetes mellitus. Dyslipidemia once again appeared to be more frequent among females within each group, but this did not reach statistical significance.

Discussion

Atherosclerosis accounts for approximately 80% of all diabetic mortality. About 75% of this mortality is the consequence of CAD; the remaining 25% results from accelerated cerebrovascular and peripheral vascular disease.

 

This study describes the magnitude and pattern of dyslipidemia among a group of Saudi diabetic patients; 43% of the patients in this group were dyslipidemic and the percentage would have been even higher if the cutoff used for serum cholesterol concentration had been >5.2 instead of >6.2 mmol/L.

 

The almost equal frequency of hypercholesterolemia and hypertriglyceridemia is not in agreement with most other studies which show normal cholesterol concentration.12 However, this can be partly explained by the poor glycemic control where increase in the nonenzymatic glycolation of LDL was postulated as an explanation for the hypercholesterolemia.13

 

Table 1. The number of diabetic patients and the result of statistical  comparison between male and female patients in different groups. 

Sex

No. (%)

Normolipid

No. (%)

Dyslipidemia

ch. ↑Tg

No. (%)

N.Tg ↑Ch.

No. (%)

N. Ch. ↑Tg

No. (%)

Male

155

(100)

99 (64)

17 (11)

22 (14)

17 (11)

Female

163

(100)

82 (50)

30 (18)

22 (13.5)

29 (18)

Total

318

(100)

181 (57)

47 (15)

44 (14)

46 (15)

P value*

 

< 0.03

< 0.03

NS

NS

*=comparing male and female patients.

 

Table 2. The relation between dyslipidemia and different variables among diabetic patients.

Variable

No.

Female

Male

value*

Normolipid

No. (%)

Dyslipid

No. (%)

Normolipid

No. (%)

Dyslipid

No. (%)

BMI > 27

123 (100%)

32 (36%)

53 (43%)

23 (19%)

15 (12%)

< 0.03

HBAIC > 10.5

127 (100%)

35 (28%)

39 (31%)

33 (26%)

20 (16%)

NS

Duration of diabetes mellitus

5years

96 (100%)

29 (30%)

16 (17%)

36 (38%)

15 (16%)

NS

5-15 years

159(100%)

40 (25%)

45 (28%)

48 (30%)

26 (16%)

< 0.04

> 15 years

47 (100%)

8 (17%)

16 (34%)

11 (23%)

12 (26%)

NS

Therapy of diabetes mellitus

Diet only

23 (100%)

9 (39%)

4 (17%)

10 (44%)

0 (0%)

NS

OHA

158 (100%)

37 (23%)

43 (27%)

45 (29%)

33 (21%)

NS

Insulin

133 (100%)

35 (26%)

33 (25%)

43 (32%)

22 (17%)

NS

NS=no significant difference; OHA=oral hypoglycemic agents.

 

Among dyslipidemic patients, there was a higher percentage of affected females compared with males, which is in keeping with other reports.14 This pattern was also evident within each of the subgroups except the hypercholesterolemic group.

 

The lipid pattern was then studied within the context of several other variables. There was a significantly higher percentage of obese diabetic females suffering from dyslipidemia compared with obese diabetic males, which has been shown to improve with fasting.15

 

The same observation can be made when diabetics with poor glycemic control were studied but this difference did not reach a significant level.

 

There was a higher percentage of dyslipidemic female patients compared with male patients in respect to the duration of diabetes mellitus, but it only reached significance for the duration of five to 15 years. This is likely related to the fact that most middle age diabetics fall into this group who tend to be obese.

 

As far as type of therapy is concerned, there was basically no significant difference between males and females. Females, however, continued to show a higher percentage of dyslipidemia.

 

It appears from this study that there was a higher percentage of dyslipidemic female patients when compared with males. This predominance continued when important risk factors were considered, such as obesity, poor glycemic control, and duration and therapy of diabetes mellitus. Such findings are likely to contribute to the increase in coronary events among diabetic females compared with diabetic males.

 

Several major studies have shown a decrease in coronary events and cardiac deaths as well as regression of atheromas upon control of hypercholesterolemia.16 Such findings have prompted practicing physicians to adopt a rather active attitude toward all hypercholesterolemic patients. It is more compelling for diabetic dyslipidemic patients, as they have more risk factors than the general population; in spite of this, there is severe lack of awareness among general physicians and specialists alike concerning the importance of periodic screening and vigorous therapy for dyslipidemia among diabetic patients. This was well illustrated in a study17 which showed that only 25% of a group of diabetics were aware of their hyperlipidemia and less than 10% were actually receiving treatment.

 

In this study, given the degree of dyslipidemia among our diabetic population, we are recommending periodic screening and early therapy for dyslipidemia among diabetic patients in Saudi Arabia.

 

Acknowledgment

The authors would like to thank Dr. Mohammed Hammami, Consultant Endocrinologist, for his critical review of the manuscript and Mr. Mohammed Ekram Ali for typing the manuscript.

References

1. Joslin EP. Arteriosclerosis and diabetes. Ann Chim Med 1927;5:1061-79.

2. Garcia MJ, McNamara PM, Gordon T, et al. Morbidity and mortality in the Framingham population. Diabetes 1974;23:105-11.

3. Howard BV, Savage PJ, Bennion LJ, et al. Lipoprotein composition in diabetes mellitus. Atherosclerosis 1978;30:153-62.

4. Howard BV. Lipoprotein metabolism in diabetes mellitus. J Lipid Res 1987;28:613-28.

5. Reaven GM. Noninsulin-dependent diabetes mellitus, abnormal lipoprotein metabolism and atherosclerosis. Metabolism 1987;36:1-8.

6. Briones ER, Maos JT, Palumbo PJ, et al. Analysis of plasma lipids and apolipoproteins in insulin-dependent and noninsulin-dependent diabetics. Metabolism 1984;33:42-9.

7. Reaven GM. Abnormal lipoprotein metabolism in noninsulin-dependent diabetes mellitus. Pathogenesis and treatment. Am J Med 1987;83(suppl 3A):31-40.

8. Goldberg RB. Lipid disorders in diabetes. Diabetes Care 1981;4:561-77.

9. Kosther, GM, Karadi J. Lipoprotein alterations in diabetes mellitus. Diabetologia 1988;31:717-22.

10. Barrett-Connor E, Grundy SM, Holdbrook MJ. Plasma lipids and diabetes mellitus in an adult community. Am J Epidem 1982; 115:657-63.

11. The Expert Panel. Report of the National Cholesterol Education Program. Expert panel on detection, evaluation, and treatment of high blood cholesterol in adults. Arch Intern Med 1988;148:36-69.

12. Briones ER, Mao SJT, Palumbo PJ, et al. Analysis of plasma lipid and apolipoproteins in insulin-dependent and noninsulin-dependent diabetics. Metabolism 1984;33:42-9.

13. Steinbrechner URSP, Witztum JL. Glucosylation of low density lipoprotein to an extent comparable to that seen in diabetes slows their metabolism. Diabetes 1984;33:130-4.

14. Walden CE, Knopp RH, Wahl PW, et al. Sex differences in the effect of diabetes mellitus on lipoprotein triglyceride and cholesterol concentration. N Engl J Med 1984;311:953-9.

15. Vessby B, Selinus I, Lithell H. Serum lipoprotein and lipoprotein lipase in overweight, Type II diabetics during and after supplemented fasting. Arteriosclerosis 1985;5:93-100.

16. National Institutes of Health Consensus Conference. Lowering blood cholesterol to prevent heart disease. JAMA 1985;253:2080-6.

17. Stern MP, Patterson JK, Haffner SM, et al. Lack of awareness and treatment of hyperlipidemia in type II diabetes in a community survey. JAMA 1989;262;360-4.

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