Association of Scavenger Receptor Gene with Premature Coronary Artery Disease
Journal Title: The Egyptian Journal of Hospital Medicine - Year 2018, Vol 72, Issue 5
Abstract
<strong>Background: </strong>Coronary artery disease (CAD) is one of the greatest causes of morbidity and mortality worldwide. It is the principal threat to health in countries in Africa and the Middle East and one of the leading causes of disease burden in developing countries. Scavenger receptor class B type1 (SCARB1) is a multi-ligand cell surface receptor. This membrane protein facilitates the uptake of cholesterol esters from high-density lipoprotein cholesterol (HDL-C) and drives cholesterol from tissues to the liver in the various stages of reverse cholesterol transport pathway. <strong>Aim: </strong>The aim of this work is to study the association of rs5888 polymorphism of SCARB1 gene and premature coronary artery disease. <strong>Patients and Methods: </strong>PCAD group included 20 patients newly diagnosed angiographically with premature coronary artery disease, and non-PCAD group that included 20 age and sex matched non-CAD individuals who showed no luminal stenosis in coronary angiographic results. <strong>Results: </strong>The frequency of the wild type (CC) was higher in the control group (60%) than patients’ group (25%) and it can be considered as a negative risk factor for PCAD (OR: 0.71, 95% CI [0.60-0.82], p < 0.01). The homozygous and heterozygous mutations (TT & CT) were statistically more frequently distributed in PCAD patients compared to control subjects (30 % and 45 % respectively), however only the CT genotype was considered as positive risk factor for PCAD (OR: 4.02, 95% CI[1.96-10.54], p= 0.01). <strong>Conclusion: </strong>Allele frequencies of studied SCARB 1 SNP revealed a higher frequency of distribution of T alleles in patients' group when compared with control group; on the other hand it shows the higher frequency of distribution of C alleles in control group when compared to patients' group.
Authors and Affiliations
Eman Helal
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