ObjectivesStatins are the most commonly prescribed medications for the treatment of atherosclerotic cardiovascular disease. Statin-associated adverse effects occur in ∼10% of patients and are associated with polymorphisms in several key genes coding for transporters and metabolizing enzymes that affect statin pharmacokinetics. In the present study, we examine the association between cytochrome P450 3A5*3 (CYP3A5*3) T>C (rs776746), COQ G>C (rs4693075), and SLCO1B1 T>C (rs4149056) genetic variants with the risk of myopathy in South Indian patients on statin therapy.MethodsA total of 202 patients on atorvastatin or rosuvastatin therapy for 12 years were recruited in the study. Genotyping of drug metabolic CYP3A5*3 gene variant and drug transporter genes COQ G>C (rs4693075) and SLCO1B1 T>C (rs4149056) was analyzed by Sanger's sequencing.ResultsIn our study subjects, the percentage of patients diagnosed to have statin-induced myopathy was 18%. The majority of the patients were on 10 mg/day dose of either atorvastatin or rosuvastatin. The homozygous nonexpressors genotype CYP3A5*3/3 frequency of the CYP3A5 polymorphism was higher in patients with myopathy. But we could not find association of CYP3A5, COQ, and SLCO1B1 gene polymorphisms with either rosuvastatin or atorvastatin.ConclusionOur results clearly demonstrate that the frequency of CYP3A5*3 splicing variant is higher in myopathy group than in the tolerant group. We did not find significant association of genetic polymorphisms in CYP3A5, COQ, and SLCO1B1 with atorvastatin- or rosuvastatin-induced myopathy.
OBJECTIVES: To study the relationship between serum uric acid level and Killip classification in pateints with acute myocardial infarction (MI), and the use of serum uric acid levels as a marker of short-term mortality. METHODS: The present study involved 50 patients with acute MI and 50 controls. Serum uric acid level was measured on days 0, 3 and 7 of MI, and compared with all clinical parameters and mortality in the enrolled subjects. RESulTS: There was a statistically significant higher serum uric acid concentration in patients with MI on the day of admission compared with controls. Patients with history of MI had higher serum uric acid levels. On all days, serum uric acid levels were higher in patients who were in a higher Killip class. Two patients who died after three days of hospital stay had a serum uric acid level >7.0 gm/dL and both were in Killip class IV. CONCluSIONS: Serum uric acid levels were higher in patients with acute MI compared with normal healthy individuals. In acute MI, patients with hyperuricemia had higher mortality. Serum uric acid levels correlated with Killip classification in patients with acute MI. Serum uric acid level can be used as a marker of short-term mortality in acute MI, and hyperuricemia may be an indicator of poor prognosis. Serum uric acid levels were elevated in acute MI patients with systemic hypertension and diabetes mellitus.
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