Effect of an SNP in SCAP gene on lipid-lowering response to rosuvastatin in Indian patients with metabolic syndrome.

PMID 27885915 | DOI 10.2217/pgs.16.30 · Pharmacogenomics · 2016 · View on PubMed ↗

AIM: 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. MATERIALS & METHODS: 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. RESULTS & CONCLUSION: 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.