Risk of acute liver injury after statin initiation by human immunodeficiency virus and chronic hepatitis c virus infection status

Background. Patients with human immunodeficiency virus (HIV) and/or chronic hepatitis C virus (HCV) infection May be prescribed statins as treatment for metabolic/cardiovascular disease, but it remains unclear if the risk of acute liver injury (ALI) is increased for statin initiators compared to nonusers in groups classified by HIV/HCV status. Methods. We conducted a cohort study to compare rates of ALI in statin initiators vs nonusers among 7686 HIV/HCV-coinfected, 8155 HCV-monoinfected, 17 739 HIV-monoinfected, and 36 604 uninfected persons in the Veterans Aging Cohort Study (2000–2012). We determined development of (1) liver aminotransferases >200 U/L, (2) severe ALI (coagulopathy with hyperbiliru-binemia), and (3) death, all within 18 months. Cox regression was used to determine propensity score–adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) of outcomes in statin initiators compared to nonusers across the groups. Results. Among HIV/HCV-coinfected patients, statin initiators had lower risks of aminotransferase levels >200 U/L (HR, 0.66 [95% CI, .53–.83]), severe ALI (HR, 0.23 [95% CI, .12–.46]), and death (HR, 0.36 [95% CI, .28–.46]) compared with statin nonusers. In the setting of chronic HCV alone, statin initiators had reduced risks of aminotransferase elevations (HR, 0.57 [95% CI, .45–.72]), severe ALI (HR, 0.15 [95% CI, .06–.37]), and death (HR, 0.42 [95% CI, .32–.54]) than nonusers. Among HIV-monoinfected patients, statin initiators had lower risks of aminotransferase increases (HR, 0.52 [95% CI, .40–.66]), severe ALI (HR, 0.26 [95% CI, .13–.55]), and death (HR, 0.19 [95% CI, .16–.23]) compared with nonusers. Results were similar among uninfected persons. Conclusions. Regardless of HIV and/or chronic HCV status, statin initiators had a lower risk of ALI and death within 18 months compared with statin nonusers.