Extended-release naltrexone for people with alcohol use disorder on therapeutic anticoagulation: A case series.

WHAT IS KNOWN AND OBJECTIVE: Individuals with medication adherence challenges or a preference for long-acting medications may benefit from extended-release naltrexone (XR-NTX) for treatment of alcohol use disorder (AUD). Individuals on therapeutic anticoagulation were excluded from XR-NTX studies and its safety in this population has not been reported. CASE SUMMARY: We conducted structured retrospective chart review of six individuals who received XR-NTX for AUD while on therapeutic anticoagulation between November 2019 and Deccember 2020. We found no documented complications among six individuals who received up to 11 doses of XR-NTX while on therapeutic anticoagulation. WHAT IS NEW AND CONCLUSION: XR-NTX may be safely tolerated by patients on therapeutic anticoagulation. We need larger studies evaluating XR-NTX administration in patients on therapeutic anticoagulation and those with coagulopathies, including individuals with alcohol-related liver disease, to better quantify risks and benefits for shared decision-making.

Effect of SLCO1B1 T521C on Statin-Related Myotoxicity With Use of Lovastatin and Atorvastatin.

The association between the c.521T>C variant allele in SLCO1B1 (reference single nucleotide polymorphism (rs)4149056) and simvastatin-induced myotoxicity was discovered over a decade ago; however, whether this relationship represents a class effect is still not fully known. The aim of this study was to investigate the relationship between rs4149056 genotype and statin-induced myotoxicity in patients taking atorvastatin and lovastatin. Study participants were from the Genetic Epidemiology Research on Adult Health and Aging (GERA) cohort. A total of 233 statin-induced myopathy + rhabdomyolysis cases met the criteria for inclusion and were matched to 2,342 controls. To validate the drug response phenotype, we replicated the previously established association between rs4149056 genotype and simvastatin-induced myotoxicity. In particular, compared with homozygous T allele carriers, there was a significantly increased risk of simvastatin-induced myopathy + rhabdomyolysis in homozygous carriers of the C allele (CC vs. TT, odds ratio [OR] 4.62, 95% confidence interval [CI] 1.58-11.90, P = 0.003). For lovastatin users, homozygous carriers of the C allele were also at increased risk of statin-induced myopathy + rhabdomyolysis (CC vs. TT, OR 4.49, 95% CI 1.68-10.80, P = 0.001). In atorvastatin users, homozygous carriers of the C allele were twice as likely to experience statin-induced myopathy, though this association did not achieve statistical significance (CC vs. TT, OR 2.00, 95% CI 0.44-6.59, P = 0.30). In summary, our findings suggest that the association of rs4149056 with simvastatin-related myotoxicity may also extend to lovastatin. More data is needed to determine the extent of the association in atorvastatin users. Altogether, these data expand the evidence base for informing guidelines of pharmacogenetic-based statin prescribing practices.