STUDY OF APOLIPOPROTEIN-E GENE POLYMORPHISM IN TYPE -2 DIABETIC PATIENTS WITH CORONARY HEART DISEASE
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Aim of work: The aim of this work is to euaLuate the preuatence of apolipoprotein- E (Apo E) gene polymorphisms in type-2 diabetes mellitus (n* with coronary heart disease (CHI)) and their influence on the severity of the disease, lipid profile and other risk factors (e_g. smoking, hypertension, body mass index and glycosylated hemoglobin Ale). Patients and metlietv One hundred and twenty cases with type-2 DM were selected from those admitted to Internal Medicine and Cardiology Departments of Henna University Hospitals. Their ages ranged from 43 to 65 years (with a mean rigit, of 52± 8.21. They were demented into 3 groups: group I included 30 diabetic cases with ischemic ECG changes. group .11 included 30 diabetic cases with myocardial infarction (Study groups) and group III included 60 diabetic crises without CUD (Control group) Diagnor sts of type 2 diabetes mellitus was made according to the criteria of American Diabetes Association. Diagnosis of CUD was determined front the history of rnangina pectoris, ischemic ECG changes. documented myocardial infarction, or major Q waves on a resting electrocardiogram Results: The Apo E4 patients showed the highest prevalence of CUD (71.496), followed ay Apo E3 patients (47.7%) and lastly Apo E2 patients (20%). On comparison, there was a statistical significant difference between Apo E2 and Apo E4 genotype patients (P<0.05); while the dnference between Apo E2 and Apo E3 and between Apo £3 and Apo E4 genotype didn't yield statistical significant difference (P>0.05 respectively). On the contrary Apo E2 patients showed the highest prevalence of non-CUD (80%), followed by Apo E3 (52.3%) and Lastly Apo E4 (28.69&). Regarding the distribution of Apo E genotypes among groups with CUD and those without CHD, them were no statistical significant differences between each Apo E genotypes (Apo E2. E3 & E4) in group I compared to group II (P'>0.05 respectively), while there was a statistical significant difference between Apo E2 and Apo E3 patients in group III compared to group I and group II (P< 0.05 respectively). Also, no statistical significant differences were found between different Apo E genotypes (Apo E2, E3 & E4) and other CHD risk factors (e.g. smoking, hypertension, HIV)! and HbA Ic; P>0.05 respectively). As regarding the relationship between lipid profile and Apo E genotype; the results were as follows: For serum cholesterol. there was a highly significant difference between Apo £2 and each of Apo E4 and Apo E3 patients (P<0.05 respectively), while the dyrerence between Apo E4 and Apo E3 patients (E4>E3) was not too big to give a statistical significance (P>0.05). For serum low density Lipoprotein cholesterol ( LDL-c), there was a highly significant difference between Apo E2 and Apo E4 patients (Pc0.00.1), and significant dffferences between Apo E3 and each of Apo E2 and Apo E4 patients (P<0.05 & P<0.01 respectively). For serum triglycertdes(Ms) and serum high density lipoprotein cholesterol IHDL-c), the results of our study showed that Apo .E2 and Apo E4 genotype patients had higher TGs and lower HDL-c levels in comparison to Apo E3 patients but the differences were statistically insignificant (P>0..05 respectively)... Conclusion: Apoiipoprotein E gene polymorphism is an important risk factor for the development of CHD in type 2 diabetic patients, 64 allele plays as a risk factor and 62 allele plays as a protective factor. The role of 84 in the development of CUD is partly mediated by its effect on serum total cholesterol and LDL cholesterol levels. Recommendation: Further studies on large number of patients with long term follow-up periods are needed to determine the relationship between 84 allele and severity of disease in CUD diabetic poilionts Also further studies are recommended to know i164 can act as a predicettar of mortality in these patients and to explain the exact role of 64 allele in the development of aila in type 2 diabetic patients; and the contribution of lipid profile and other CUD riskfactors.