Adv Clin Exp Med. 2026 Jan 5. doi: 10.17219/acem/203504. Online ahead of print.
ABSTRACT
BACKGROUND: Hyperlipidemia is a major risk factor for cardiovascular diseases and is associated with complications such as atherosclerosis and tendon injury. Though atorvastatin reduces cholesterol, genetic variants (CYP2D6-4, SULT1A1, CYP2C192) affect its response. These genetic variations influence atorvastatin metabolism, thereby affecting its therapeutic effectiveness.
OBJECTIVES: To advance personalized therapeutic drug monitoring and improve lipid profile management, this study aims to develop a robust and LC-MS/MS method for quantifying atorvastatin levels in human plasma. Additionally, to investigate the influence of genetic polymorphisms – particularly CYP2D6-4-on plasma concentrations of atorvastatin in patients with hyperlipidemia.
MATERIAL AND METHODS: Ethical approval for the study was obtained from the appropriate institutional review boards, and written informed consent was obtained from all participants. Atorvastatin was measured using LC-MS/MS. PCR-based methods were used for genotyping. Statistical analyses were performed to evaluate relationships between plasma atorvastatin levels and genetic variants.
RESULTS: The LC-MS/MS method demonstrated excellent linearity, accuracy, precision, and stability, for the quantification of atorvastatin in human plasma. Higher atorvastatin concentrations were tied to CYP2D6-4. Furthermore, the study validated the analytical method for consistent and reliable measurement of atorvastatin levels in clinical samples.
CONCLUSIONS: This study successfully developed and validated a straightforward and reliable LC-MS/MS method for quantifying atorvastatin levels in human plasma. Significant CYP2D64 – atorvastatin links highlight the value of pharmacogenetic dosing. Integrating pharmacogenetics – especially in the Jordanian population – may enhance the safety, efficacy, and individualization of atorvastatin therapy.
PMID:41489862 | DOI:10.17219/acem/203504
