Health Care

Supervisor And Principal Investigator

Dr. Maher Abdel-Latife Rashed, Ph.D.

Health Care Services

 Dr. Maher Rashed

Lipid Abnormalities of Diabetics

Attending Mahalla Cardiac Center

By Dr, Maher Rashed et al., 2002^#

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Rashed MA*, El-Shourbagy OA**

*Cardiology specialist, Mahalla cardiac center, ministry of health and population.

**Professor of medical childhood studies, institute of postgraduate childhood studies, Ain Shams university.

Abstract.-

Atherosclerosis is the most important cause of morbidity and mortality in long- standing diabetes mellitus. Lipoprotein disorders commonly accompany diabetic patients promote atherosclerosis process and represent cumulative risks for these patients. Serum total cholesterol, triglycerides, high-density lipoproteins, and low-density lipoproteins were measured in 500 persons (diabetics and non-diabetics) attending Mahalla Cardiac Center, outpatient clinic. The present study approved altered lipid profile in diabetic patients. So, control of lipid abnormalities has to be reviewed with management of diabetes mellitus.

Background.- Lipid abnormalities are known of the major risk factors for atherosclerosis and ischemic heart disease patients. Lipoprotein disorders commonly accompany diabetic patients promote atherosclerotic process and represent cumulative risks for these patients.

Objective. -To review Effects of diabetes mellitus on lipid profile -in our community-, which constitute two major risk factors for coronary heart disease.

Design. -A case control study.

Participants. -A total of 500 persons attending Mahalla Cardiac Center (outpatient clinic departments) were studied. Subjects with primary and/or secondary dyslipidemia -rather than diabetes mellitus- were excluded. Our studied subjects were classified into two groups diabetics (no.=243) and non-diabetics (no.=257) groups.

Methods. - Complete medical history and examination. Laboratory assessment of total cholesterol, triglycerides, LDL-C and HDL-C.

Results. - Our results showed significantly increased TC, TG and LDL-C but decreased HDL-C by 20.3%, 43%, 10% and 10.6% respectively in diabetics versus non-diabetics.

Conclusion. - Lipid profile is hazardously affected by diabetes mellitus to duplicate the risk factors for ischemic heart disease. Management of dyslipidemia should be in conjunction with control of diabetes mellitus as a standard strategy for regression and control of IHD epidemics.

Key words: Lipid abnormalities in diabetes mellitus - Lipoprotein disorders in diabetics - Lipid abnormalities - Dyslipidemia and diabetes mellitus.

Introduction:

Diabetes is a group of metabolic diseases with characteristic hyperglycemia associated with defects in insulin secretion, insulin action, or both (Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 1998). The effect of diabetes is not limited to carbohydrate metabolism. Lipid and protein metabolism play an important role in the progression of the disease (Uusitupa and others, 1993).

Diabetes mellitus affects approximately 16 million people in the United States and accounts for about one sixth of all expenditures for health care. It is estimated that over 8 million people in the United States alone are unaware that they have the disease (Diabetes statistics, 1995). Patients with undiagnosed diabetes mellitus are at serious risk for coronary heart disease, stroke and peripheral vascular disease, and have a greater likelihood of dyslipidemia, hypertension and obesity (Florence and Yearger, 1999). The mortality rate in patients with diabetes may be up to 11 times higher than in persons without the disease (Diabetes statistics, 1995).

Along with the conventional risk factors for cardiovascular disease such as age, hypertension gender smoking, elevated cholesterol, and left ventricular hypertrophy, diabetes is a major independent cardiovascular risk factor (Stamler et al., 1993). Diabetes Mellitus is a major risk factor for cardiovascular disease. Cardiovascular disease includes coronary artery disease, peripheral and cerebrovascular disease, congestive heart pump failure, as well as autonomic and peripheral nervous system dysfunction (Raman and Neste, 1996).

Numerous factors including elevated cholesterol, high blood pressure, blood coagulation factors, and platelet hyper-reactivity contribute to the acceleration of atherosclerotic build-up people with diabetes (Kannel, 1985). Lipoprotein disorders commonly accompany diabetic patients promote atherosclerotic process and represent cumulative risks for these patients (Somogyi, 1993). Reports on the relationship between glycemic control and lipid abnormalities in diabetic patients are scare (Paterson et. al., 1990).

However, elevated serum total cholesterol level has been suggested by Roberts, (1989) to be the only risk factor for coronary artery disease. He also suggested that of the other eight factors commonly viewed as predictive of atherosclerotic events, six (male sex, familial history of coronary events in persons > 55, smoking, systemic hypertension, diabetes and severe obesity) " are best viewed as cholesterol-dependent [variables] not in themselves atherogenic in the absence of a serum total cholesterol < 150 mg/dl". The remaining two factors (definite clinical evidence of CAD and history of cerebrovascular or peripheral vascular disease) indicate that atherosclerosis is already present; it is inappropriate to include atherosclerotic event as an atherosclerotic risk factor "all of the other cholesterol-dependent factors" take effect when the serum total cholesterol level is < 150 mg/dl. Recently, Vogel (1998) has commented that certain risk factors such as hypercholesterolemia are thought to be directly causative for the development of coronary heart disease; other factors, such as obesity, are indirectly related.

Research now shows that people with diabetes can live longer and healthier lives with relatively small decreases in blood glucose, blood pressure and cholesterol (National Institute of Diabetes and Digestive and Kidney Diseases, 2001).

Lipoprotein abnormalities were reported by Diabetes Atherosclerosis Intervention Study Investigators (2001) to be a greater predictor of ischemic heart disease in type 2 diabetics than hyperglycemia. Coronary artery disease is the major cause of death in diabetics therefore any preventive measures will be important.

Aim of the study.:

In considering altered lipid profile may be associated with diabetic state, it is very stressful to evaluate these hazardous effects -in our community- in an attempt to determine whether these parameters might be a useful adjunct in routine management of diabetic patients.

Patients.:

This study included 500 subjects attending outpatient’s clinic, Mahalla Cardiac Center between June and December 2001.

Criteria of inclusion:

Our subjects were attended to Mahalla Cardiac center outpatient clinic either for routine medical chick-up or for medical examination. There was no age and/or sex limited.

Criteria of exclusion:

Known primary as well as secondary dyslipidemias were excluded -except for that may be precipitated by diabetes mellitus-. Secondary dyslipidemias were pointed out by Gilbert (1993) as follows: nephrotic syndrome, hypothyroidism, diabetes mellitus, chronic renal failure, and usage of thiazide diuretics, beta-adrenergic blocking drugs and alcohol-induced. Subjects were classified into diabetic and non-diabetic groups. Also, cases receiving lipid-lowering drugs were excluded.

Methods.:

All cases were instructed to fast for 14 hours, and 3 ml venous blood sample were obtained by venipuncture. Sera were separated and immediately used for biochemical determinations. Enzymatic colorimetric determination of total cholesterol was done according to Stein (1987). Triglycerides were measured by enzymatic colorimetric determination with lipid clearing factor (McGrown et al., 1983). High-density lipoproteins were measured according to Warnick et al., (1979). Low-density lipoproteins were calculated from the Friedwald formula (1972).

Statistical analysis was performed by SPSS (Soft Art. Inc., 1998) on IBM computer. Subjects were studied according to diabetic versus non-diabetic state. Also, subjects will be studied according to sex (male and female).

Results:

Table (1): Age Criteria According To Gender And Diabetes.

% Diff.: Mean percentage difference.                             S.D.: Standard Deviation.

--: Non significant.                                                               ***: Significant at 0.001.

 Table (1) shows age criteria (age, mean and standard deviation) in total studied subjects. It also shows age criteria of differentiated sex groups and also in diabetics versus non-diabetics with t-test and mean percentage differences.

Figure 1: Sex Grouping In Studied Subjects.

Figure (1) shows sex grouping differentiation (total number of cases, number of females, number of males and percentage of frequency of each).

Table 2: Lipid Profile according to sex.

% Diff.: Mean percentage difference.                                             S.D.: Standard Deviation.

--: Non significant.                                                                               *: Significant at 0.05.

**: Significant at 0.01.                                                                         ***: Significant at 0.001.

Table (2) shows criteria of lipid profile (range, mean, standard deviation, t-test and mean percentage difference) in total studied subjects and also in male and female groups.

Figure 2: Sex Grouping In Diabetics Versus Non-diabetics.

Figure (2) shows sex differentiation and grouping in female and male groups in both of diabetics and non-diabetics groups (total number of cases, number of females, number of males and percentage of frequency of each).

Table 3: Correlation Coefficient of TC And TG with Lipids and Age with Lipids

--: Non significant.                                                                               *: Significant at 0.05.

**: Significant at 0.01.                                        

Table (3) shows correlation coefficient and between lipids each other and between age and lipids.

Table 4: Lipid Profile In Diabetics Versus Non Diabetics.

% Diff.: Mean percentage difference.                                             S.D.: Standard Deviation.

--: Non significant.                                                                               *: Significant at 0.05.

**: Significant at 0.01.                                                                         ***: Significant at 0.001.

Discussion:

Most adult cardiovascular diseases, including coronary heart disease, are both highly prevalent and preventable. Despite recent declines in age-adjusted mortality, cardiovascular disease accounts for 42% of all deaths. Specifically, the most prevalent form of cardiovascular disease, coronary heart disease, results in 500,000 deaths, 1.25 million myocardial infarctions, and an economic burden of $46 billion each year (Miller and Vogel, 1996).

Evidence supporting the relation between blood cho­lesterol concentration and CHD risk has been strengthened by numerous animal studies showing progression and regression of atherosclerotic lesions as cholesterol concentrations rise and fall and by natural history studies of genetic hypercholesterolemias (such as familial hypercholesterolemia) (Marmot and Elliottl, 1992; Schaefer and others, 1994). Numerous single-population studies such as the Framingham Heart Study and international studies such as the Seven Countries Study have demonstrated close relationships between coronary heart disease mortality rates and total and low-density lipoprotein cholesterol (Vogel, 1998). Steiner (1985) has reported that atherosclerosis-related mortality in diabetes mellitus has steadily increased since the beginning of the insulin era, to the point where atherosclerosis now accounts for more than 70% of total mortality in all forms of diabetes.

Hyperlipidemia plays a crucial role in the etiology of atherosclerosis and coronary heart disease and its prognostic sequelae (Kwiterovich, 1990). Atherosclerosis is the most important cause of morbidity and mortality in long-standing diabetes mellitus (West, 1978). There is considerable evidence from intervention trials in non-diabetic populations that lowering serum cholesterol reduces the risk of coronary heart disease. Dunn, (1982) has also pointed out that changes in lipoprotein levels are major factor in the accelerated atherosclerosis, which is so prevalent in patients with diabetes in developed world. One percent declines in mean serum cholesterol result in a 1% to 1.5% decrease in subsequent cardiovascular events, respectively (Vogel, 1998).

In complementary, an increasing body of evidence supports aggressive treatment of elevated lipid levels in the patient with established coronary artery disease (NCEP, 1993 and Furberg, 1994).

The present study is designated to evaluate effect of diabetes mellitus on lipid profile (TC, TG, LDL-C, and HDL-C) in our community in Mahalla Cardiac Center.

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Mean lipoprotein concentrations for US adults were reported by Johnson (1993) as 206 mg% and 128 mg% for TC and TG levels. Cholesterol and Recurrent Events Trial has reported TC averaged 209 mg% and LDL-C averaged 139 mg% at baseline population (Sacks, 1996). Data in Middle East Communities in Jordan collected by Batieha and Hashem (1997), have recorded mean cholesterol and triglyceride levels 5.36+1.06 mmol/l and 1.92+ 1.21 mmol/l respectively.

HDL-C in ARIC study was reported to be substantially higher in black men than in white men (50 vs. 43 mg%). HDL-C was reported in ARIC study as in NHANES III to be virtually the same between black and white women but was substantially higher in black men than in white men (50 vs. 43 mg%) (Stamler, 1986).

Mean lipoproteins measurements in the World Health Organization Clofibrate Trial were -to some extent- different from that previously mentioned records were recorded. Its median baseline total cholesterol equals 247 mg%.  This trial was subjected for men aged 30-59 years who did not have manifested CHD (WHO Principal investigators, 1980, 1984). Mean baseline LDL-C was 188 mg% for asymptomatic men aged 44-55 years who were enrolled in Helsinki Heart Study. They had non HDL-C of at least 200 mg% and (Frick, 1987). HDL-C was reported by the third National and Health Examination survey (NHANES III promoted in 1988 and 1994) to equal 36 mg% in men and 40 mg% in women, which equals to 16th and 25th NHANES III percentiles (Downs, 1998).

In agreement with the last mentioned reports, our study has revealed similar results with mean TC, TG, LDL-C and HDL-C levels as 243, 233, 168 and 44 respectively (Table 2).

However, wide variations of human plasma lipoproteins measurements were encountered due to several factors. Racial differences were recorded by Stamler (1986). Gotto and Pownall (1999) have also reported nutritional status and genetically determined inter-individual differences.

Differences between rural and urban areas were reported by Singh (1998). The average serum cholesterol concentrations were 4.91 mmol/l in urban and 4.22 mmol/l in rural subjects without any sex differences.

Also, seasonal differences were also reported by Gordon et al., (1987). Serum lipid concentration levels for the December-January period exceed by about 2.5 percent those measured in the June-July period for total cholesterol and LDL-C levels. A non-significant change of 0.3 percent was calculated for HDL-C level. No detectable seasonal difference in the highly variable triglyceride serum levels.

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TC was reported by Miller and Najee (1992) to rise in both men and women through middle age. Ferara et al., (1997) has reported that TC and LDL-C begin to fall at about age 65 years in men and 75 years in women. HDL-C is relatively constant across age groups (Mathews et al., 1989; Johnson, 1993), with perhaps some decline in women after menopause (Mathews et al., 1989). Fasting TG rises gradually in both men and women, although at a slower rate in women; in middle age, it may decrease in men and continue to rise in women (The Lipid Research Clinics Program Epidemiology Committee, 1979).

Data in Middle East Communities in Jordan was recorded by Batieha and Hashem (1997). They have recorded mean cholesterol by age 25-39 years; 5.07+1.09 mmol/l and by age > 40 years 5.56+1.05 mmol/l respectively. So, Subjects less than 40 years of age have a lower pattern of hypercholesterolemia (15.5%) compared to older subjects (27.8%). Also, recorded mean triglyceride levels by age 25-39 years; 1.71+1.1 mmol/l and by age>40 years 2.06+1.25 mmol/l respectively. So, in the same side, hypertriglycedemia prevalence pattern was also reported to be lower in subjects less than 40 years of age (18.8%) compared to older subjects (27.1%).

In considering aging process, these results document our results as mean age in our subjects equals 47 years (Table 1). Age has been approved to statistically correlate positively and significantly with TC (r=0.106, p<0.05) and LDL-C (r=0.258, p<0.01). Also, age correlates positively but statistically non-significant with TG (r=0.008, p<0.05). Age –in our study- correlates significantly but negatively with HDL-C (r=0.122, p<0.01) (Table 3).

These data may explain some roles of the aging process in IHD. Age has been approved be significantly and independently associated with the presence of any coronary disease and obstructive coronary disease (95% confidence) (Guerci, 1998). Also, incidence of major manifestation of clinical coronary artery disease is doubled with each decade of life after age 45 (Kannel and colleagues, 1990).

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In adolescence, males show a significant drop in the level of HDL-C and an increase in the level of TG and VLDL-C, while females show insignificant changes in HDL-C, TG, VLDL-C and also total cholesterol and LDL-C accordingly (Kwiterovich, 1990). HDL-C values are generally higher in women than men (Mathews et al., 1989; Johnson, 1993), with perhaps some decline in women after menopause (Mathews et al., 1989).

An Arabian study of Saudi Arabian population revealed the mean levels of plasma total cholesterol were 184 mg% for normal males and 177 mg% for the normal females. Mean levels of plasma triglycerides were 136 mg% for normal males and 125 mg% for the normal females (Khoja et al., 1993). Another data in Middle East Communities in Jordan, promoted by Batieha and Hashem (1997) has recorded mean cholesterol level by gender in men 5.23+1.06 mmol/l and in women 5.44+1.1 mmol/l respectively. So, the pattern of hypercholesterolemia is higher in women (24.8%) than men (19.8%). Mean triglyceride levels by gender in men 2.11+1.41 mmol/l and in women 1.82+1.07 mmol/l respectively. So, the pattern of hypertriglyceridemia is higher in among men (27.6%) than women (22.5%).

HDL-C was reported as 36 mg% in men and 40 mg% in women (aged 65-73 years) in Air Force/Texas Coronary Atherosclerosis Prevention Study; which equals to 16th and 25th NHANES III percentiles (Downs, 1998).

Our study agree with the previously mentioned studies as mean levels of TC, TG, LDL-C and HDL-C were 241, 183, 115 and 43 mg% in males and 245, 200, 108 and 46 mg% consecutively in the female group; with mean percentage differences of 1.6% (t=0.9, p<0.05), 5.8% (t=2.86, p<0.01), 6% (t=2.59, p < 0.01) and 6.5% (t=3.7, p<0.001) (Table 2).

Difference of plasma lipoproteins in females in proportion to males may be explained by oestrogen usage as elevated HDL-C and decreased LDL-C levels are observed in estrogen users (Bradley et al., 1978).

From the other point of view, male gender was reported by Guerci et al.,  (1998) to be significantly associated with any coronary disease and obstructive coronary disease. Also, Price and Fowkes (1997) have evaluated the incidence of coronary artery disease -in industrialized countries- to be three to four times higher in men than in women. These data may be explained by means of effects of lipoproteins whether by diet control and/or smoking.

From the other point of view, the advanced lesions of atherosclerosis develop about 10 to 20 years earlier in young men than in young women. In males, this is thought to be caused by a greater severity and longer exposure to coronary risk factors, particularly dyslipidemia and smoking. At puberty, low-density cholesterol levels rise and high-density lipoprotein-cholesterol levels fall. In females, estrogens have beneficial effects on both endothelium and serum lipoproteins. Those benefits are lost after menopause (Vogel, 1998).

These slight differences in considering TG and HDL-C levels may be due to concomitant diabetic state and increased averaged male subjects in our study 51.4% (No.=257) of total subjects as compared to females 48.6% (No.=243) (Figure 1). Also, in spite of nearly equal mean age between male and female groups (47.6 and 47 years), lower mean age of diabetics (45.8 years) was shown as compared to non-diabetics (Table 1). Such age criteria was shown to be represented by higher percentage of males 68.5% (No.=176) than females 31.5% (No.=81) in non diabetics (No.=257) as compared to lower percentage of males 33.3% (No.=81) than females 66.7% (No.=162) in diabetics (No.=243) (Figure 2). This inverted male to female ratio in diabetics versus non-diabetics may explain the recorded difference about non-significant TG and significant HDL-C with aging.

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Diabetes has been shown in several studies to be the risk factor most strongly associated with cardiovascular risk, yet there is no conclusive evidence that improving diabetes control will lower risk. In the Diabetes Control and Complications Trial (1993) intensive glucose control prevented the microvascular complications of diabetes.

A new emphasis on treating diabetes comprehensively - that is, managing not only blood glucose, but also blood pressure, and cholesterol - could save lives. Marking November as National Diabetes Month, HHS and its partners are joining forces to inform the public that good diabetes management is more than lowering blood glucose. Control of blood pressure and cholesterol is crucial to help prevent heart disease and stroke, the leading killers of people with diabetes  (The U.S. Department of Health and Human Services, 2001).

A highly significant increase in total cholesterol (p<0.001) and low-density lipoproteins were indicated in diabetic children (controlled and uncontrolled) as compared to the normalize; while the mean high-density lipoprotein values apparently decreased in uncontrolled diabetics than normalize (Khoja et al., 1993).

Tan and Bettridge (1991) have also concluded that LDL-C is generally raised in poorly controlled diabetic patients. In vitro and in vivo experiments have shown that insulin increases LDL receptor activity. A further factor which may alter LDL receptor binding is glycosylation of the residues of LDL apoprotein B.

Mean high-density lipoprotein values apparently decreased in uncontrolled diabetics than normal controls (p<0.001) and also, in controlled than the normal control subjects (p<0.01) (Khoja et al., 1993).

Hypertriglyceridemia may be due to increased production and decreased clearance of triglycerides, in association with lipoprotein lipase deficiency in insulin lack and resistance (Anaja et al., 1995). Also, hypertriglyceridemia may be due to insulin deficiency, which causes excessive mobilization of free fatty acids and underutilization of chylomicrons and VLDL (Khoja et al., 1993). Diabetic patients with hypertriglyceridemia show decreased level of high-density lipoproteins necessary for transport of cholesterol from tissues (Zilva and Pannal, 1984).

Llyod and Reckless (1993) have also described that both HDL and HDL₂ in diabetes mellitus tend to decrease regardless of the duration of diabetes while HDL₃ may be increased. Apparently normal levels of HDL can mask a combination of low HDL₂ and high HDL₃ with its attendant increased risk of atherosclerosis. HDL metabolism is influenced by the enzyme hepatic lipase and lipoprotein lipase, both of which are sensitive to insulin. Other possibilities were also reported by Tan and Betteridge (1991); enrichment of TG, depletion of apo A and increased ratio of cholesterol to proteins.

In general, the most common lipid abnormalities in diabetes mellitus have been recorded by ADA “American Diabetes Association” (1993). They are increase serum triglycerides and decreased HDL-C; increased LDL-C may also be present. Also, many type 2 diabetics have increased triglycerides (TG) and decreased HDL-cholesterol (HDL-C) (Diabetes Atherosclerosis Intervention Study Investigators 2001).

Betteridge (1997) has described the lipid profile of people with diabetes to be characterized in typical way. Serum levels of total cholesterol (or low-density-lipoprotein (LDL)- cholesterol) and prevalence of hypercholesterolaemia are generally not different in diabetic and non-diabetic people. In contrast, serum concentrations of triglycerides and frequency of hypertriglyceridaemia are substantially higher in diabetes. More ever, the serum levels of high-density-lipoprotein (HDL)- cholesterol, a lipid fraction that is closely influenced by triglyceride contents, are more often lower in diabetic than non-diabetic people.

Our study agree with the previously mentioned studies as mean levels of TC, TG, LDL-C and HDL-C were 216, 140, 106 and 47 mg% in non-diabetics and 271, 246, 118 and 30 mg% consecutively in diabetics group; with mean percentage differences of 20.3% (t=15, p<0.001), 43% (t=28.6, p<0.001), 10% (t=4.5, p<0.001) and 10.6% (t=6.4, p<0.001) (Table 4).

A significant relation of either triglycerides or total cholesterol in uncontrolled diabetic children was found with all other plasma lipoproteins (Khoja et al., 1993). These data agree with our results as TC was found to correlate positively and significantly with TG (r=0.791, p<0.01); LDL-C (r=0.877, p<0.01) and HDL-C (r=0.438, p<0.01). Also, TG was found to correlate positively and significantly with LDL-C (r=0.476, p<0.01) and HDL-C (r=0.533, p<0.01) (Table 3).

On the other hand, the chronic hyperglycemia associated with diabetes mellitus modifies protein function and structure through the glycosylation of amino acid residues. Glycated proteins and local growth factors such as insulin stimulate the proliferation of smooth muscle cells. In diabetic individuals, plasminogen activator inhibitor-1 is increased, triglycerides and low-density lipoprotein are commonly elevated, and high-density lipoprotein cholesterol is reduced. When glycated, low-density lipoprotein is more readily oxidized. Postprandial chylomicrons and chylomicron remnants are also thought to be strongly atherogenic (Vogel, 1998).

Pathogenesis of dyslipidemia in type 2 diabetes was explained by Taskinen (2001). The recognition that hypertriglyceridemia is associated with multiple alterations of other lipoproteins that are potentially atherogenic has expanded the picture of diabetic dyslipidemia. Elevation of large VLDL1 particles initiates a sequence of events that results in generation of atherogenic lipoproteins including remnants and small dense LDL. This abnormality is also associated with the lowering of HDL cholesterol. The clinical implication is that the concentration of plasma triglycerides should be maintained as low as possible to avoid these deleterious consequences of hypertriglyceridemia.

Conclusion:

The risk of stroke in patients with diabetes is double that of non-diabetic patients, and the risk of peripheral vascular disease is 4-fold higher in diabetic patients than in non-diabetic patients. Subtle differences in the pathophysiology of atherosclerosis in patients with diabetes result in both earlier development and a more malignant course. Patients with diabetes therefore must have their measurable lipid abnormalities treated aggressively to lessen their risk of developing serious atherosclerosis (Scott and Anne, 2001).

So, circulating glucose levels have long been used as a measure of diabetes control; however, they are not reflective of the person's metabolic state. These data should compel us to consider the treatment of diabetes in terms of normalization of metabolism instead of normalization of glucose levels. Lipid abnormalities in diabetic patients are major associated metabolic abnormality; and may lead to acceleration of atherosclerosis. So, the control of diabetes and its associated altered lipid profile is mandatory for controlling atherosclerosis and coronary heart disease.

Recommendations:

* Treatment of diabetes is to provide optimal day -to- day care, while preventing microvascular and macrovascular complications in the future.

* On the other hand, public recognition of the adverse effects of high-fat and high-cholesterol diets has to be increased in our community.

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^{# Childhood Studies, Vol V, issue 14, Jan 2002.}

إختلالات الدهون فى مرضى السكر

المترددين على مركز القلب بالمحلة الكبرى^#

------------------------------

"الملخص العربى"

دكتور/ ماهر راشد* ، دكتور/ عمر الشوربجى**

* أخصائى القلب بمركز القلب بالمحلة الكبرى , وزارة الصحة والسكان.

** أستاذ الدراسات الطبية للطفولة , معهد الطفولة , جامعة عين شمس.

يعتبر تصلب الشرايين من أهم أسباب الإعاقة والوفيات لمرضى السكر. وتعمل أختلالات الدهون التى تصاحب مرضى السكر كمحث لعملية تصلب الشرايين والتى تمثل عوامل خطورة تراكمية لهذه الفئة من المرضى. ومن المعروف أن تصلب الشرايين هو أحد العوامل الرئيسية التى تؤدى على الإصابة بأمراض الشرايين التاجية للقلب. تم تصميم هذا البحث لدراسة مدى تأثير مرض السكر على معدل دهون الدم فى المرضى المصابين بالسكر المترددين على مركز القلب بالمحلة الكبرى. اشتملت الدراسة على 500 حالة سواء من مرضى السكر (243) أو من غير مرضى السكر (257). تم قياس الكوليسترول والدهون الثلاثية والدهون عالية الكثافة والدهون منخفضة الكثافة. بينت نتائج هذه الدراسة ارتفاع معدل الكوليسترول الكلى (20.3%) والدهون الثلاثية (43%) والدهون منخفضة الكثافة (10%) بخلاف انخفاض الدهون عالية الكثافة (10.6%). وبذلك أثبتت الدراسة بمركز القلب بالمحلة الكبرى اختلاف معدل دهون الدهون فى المرضى المصابين بمرض السكر غير غيرهم. ويتضح لنا من هذه الدراسة أن مرض السكر يؤدى إلى مخاطر الإصابة بإختلالات دهون الدم مما يضاعف من تعرض المريض لعوامل الخطورة والإصابة بأمراض الشرايين الناجية للقلب. وبهذا يتأكد أهمية إدراج علاج خلل الدهون ضمن عملية متابعة وتنظيم السكر للمرضى المصابين بالسكر وذلك من اجل منع مضاعفات مرض السكر وكذلك تقليل احتمالات الإصابة بأمراض الشرايين التاجية والقلب.

^# مجلة دراسات الطفولة , المجلد الخامس العدد 14 , يناير 2002.