Main Article Content

Demonstration Of An Abnormality Of Apolipoprotein Ciii And Genetic Polymorphism In Gout Patients With Hypertriglyceridemia In Egypt


M Zahra
O M Hassanin

Abstract



Gout is the principal clinical manifestation of hyperuricaemia and leading cause of inflammatory arthritis in adult men. Lipids and apolipoproteins therefore plays an important role in the pathophysiology of the changes seen in hyperuricaemia. We conducted a study on the relationship between APOC3 SstI polymorphism and plasma triglyceride levels in persons with gout and determined whether these polymorphisms contribute to the pathophysiology of hyperuricaemia or to altered lipid levels in these individuals. The study was undertaken in 32 men with gout and 32 matched normal controls, none was receiving lipid lowering or urate lowering treatment. The plasma levels of lipoproteins, cholesterol, triglycerides and uric acid were studied. Both groups were genotyped for apolipoprotein CIII by means of an amplification technique followed by SstI digestion. The results showed that rare S2S2 genotype was highly prevalent in gout patients (21.58) as compared to the controls (6.25). S2 allele was almost two times more prevalent in the gout group as compared to control group. Multiple logistic regression revealed S1S2 individuals had odds ratio (OR) of 1.88 (95%CI: 0.82 – 5.60), with p< 0.05. While the OR for S2S2 to develop gout was found to be 4.23 (95% CI: 2.10 – 21.30, p < 0.001), which was highly significant. TG was significantly different among various genotypes (p < 0.001) in particular, the S2S2 individuals were associated with highest concentration of TG followed by S1S2 and then by S1S1. There is also significant differences were observed in TC, HDL at the same manner (p < 0.01). So it could be concluded that rare S2 allele of APOC3 gene may be represent a risk factor of developing coronary artery disease in Egyptians

Keywords: Apolipoprotein CIII, genetic polymorphism, gout, hypertriglyceridemia.

Egyptian Journal of Biochemistry and Molecular Biology Vol. 26 (1) 2008 pp. 55-66

Journal Identifiers


eISSN: 1687-1502