Abstract
Statins treat dyslipidemia associated with metabolic syndrome. Genetic factors contribute to variable response. Sterol regulatory element-binding factors cleavage-activating protein (SCAP) pathway regulates lipid homeostasis, so effect of SNP in SCAP gene on rosuvastatin response was studied.
Metabolic syndrome patients with low-density lipoprotein-cholesterol ≥130 mg/dl, were prescribed rosuvastatin 5 mg for 3 months. Lipids were measured initially and finally, and genotyping done.
Sixty-three patients completed the study. Twenty-three were homozygous for AA while 40 were heterozygous. Significant association was found between post-treatment lipid values and SCAP genotypes but not with baseline values. Cholesterol (p = 0.002) and low-density lipoprotein-cholesterol (p = 0.008) were significantly reduced in patients carrying G allele as compared with AA. There was a significant effect of G allele on cholesterol reduction (p = 0.043). Out of total responders (achieving >23.58% total cholesterol reduction), 80.5% were 2386G carriers (GG+GA) and only 19.5% were homozygous for A allele (p = 0.0048). SCAP 2386A>G gene polymorphism is a significant predictor of hypolipidemic response.