ArticleClinical pharmacology and therapeutics2022
SLCO1B1*5 Allele Is Associated With Atorvastatin Discontinuation and Adverse Muscle Symptoms in the Context of Routine Care.
Article in Clinical pharmacology and therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
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- Atorvastatin Safety Reappraised: From Pharmacogenomic Mechanisms to Personalized Risk Management.Cardiovascular therapeutics · 2026Review
- CASTER-DTA: Equivariant Graph Neural Networks for Predicting Drug-Target Affinity.bioRxiv : the preprint server for biology · 2025Article
- CASTER-DTA: equivariant graph neural networks for predicting drug-target affinity.Briefings in bioinformatics · 2025Article
- A multi-centre observational cohort study on pharmacogenomic predictors of rosuvastatin discontinuation in a multiethnic population.Frontiers in pharmacology · 2025Article
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- An Introductory Tutorial on Cardiovascular Pharmacogenetics for Healthcare Providers.Clinical pharmacology and therapeutics · 2023Article
- Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The SLCO1B1 genotype is known to influence patient adherence to statin therapy, in part by increasing the risk for statin-associated musculoskeletal symptoms (SAMSs). The SLCO1B1*5 allele has previously been associated with simvastatin discontinuation and SAMSs. Prior analyses of the relationship between SLCO1B1*5 and atorvastatin muscle side effects have been inconclusive due to insufficient power. We now quantify the impact of SLCO1B1*5 on atorvastatin discontinuation and SAMSs in a large observational cohort using electronic medical record data from a single health care system. In our study cohort (n = 1,627 patients exposed to atorvastatin during the course of routine clinical care), 56% (n = 912 of 1,627 patients) discontinued atorvastatin and 18% (n = 303 of 1,627 patients) developed SAMSs. A univariate model revealed that SLCO1B1*5 increased the likelihood that patients would stop atorvastatin during routine care (odds ratio 1.2; 95% confidence interval (CI), 1.1-1.5; P = 0.04). A multivariate Cox proportional hazards model further demonstrated that this same variant was associated with time to atorvastatin discontinuation (hazard ratio 1.2; 95% CI, 1.1-1.4; P = 0.004). Additional time-to-event analyses also revealed that SCLO1B1*5 was associated with SAMSs (hazard ratio 1.4; 95% CI, 1.1-1.7; P = 0.02). Atorvastatin discontinuation was associated with SAMSs (odds ratio 1.67; P = 0.0001) in our cohort.
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