Abstract
Background: Atorvastatin (ATO) is a fundamental treatment for dyslipidemia, and pharmacogenetic factors can contribute to variation in clinical outcomes.
Objective: This study intended to evaluate the effect of the CYP3A4 rs2242480 variation on ATO therapeutic responses in Iraqi patients.
Methods: This cross-sectional, observational study was conducted from October 2025 to April 2026 and enrolled 200 Iraqi adults with dyslipidemia managed by 40 mg/day of ATO as monotherapy for at least 3 months. Genotyping was made using allele-specific polymerase chain reaction. Fasting lipid profiles (total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C)) Castelli risk indexes I (CRI-I), and atherogenic coefficient (AC) were investigated and serum creatine kinase (CK) levels was measured. Data were analyzed using IBM SPSS Statistics version 26 software, Shapiro–Wilk, Kruskal–Wallis, Dunn's post hoc test with Bonferroni adjustment, and chi-square test, with the predefined level of statistical significance set at P < 0.05).
Results and Conclusion: The distribution of CYP3A4 rs2242480 variation was 59.5% for wild CC type, 30% for heterozygous TC type, and 10.5% for homozygous TT type. The serum levels of TC, TG, LDL-C, CRI-I, and AC were significantly lower, while HDL-C was higher in patients carrying one or two mutant T alleles compared with the wild CC type (P < 0.001). The cholesterol-lowering effect was clearly evident in the TT group (P < 0.001). Conversely, T-allele carriers had significantly higher serum CK levels in both genders (P < 0.001). The CYP3A4 rs2242480 polymorphism is prevalent among Iraqi patients with dyslipidemia. and significantly associated with more favorable lipid profiles, lower cardiovascular risk indices, and higher CK levels.
| Has the manuscript been published | not published |
|---|---|
| Intend to be published in the IJPS ? | Yes |
