433. The Risk of Acute Liver Injury with Statin Use in Chronic Hepatitis C Virus Infection
Session: Poster Abstract Session: Hepatitis C
Thursday, October 27, 2016
Room: Poster Hall
Posters
  • Byrne_MSCE_Poster_IDWeek_2016_final.pdf (230.1 kB)
  • Background: Patients with chronic hepatitis C virus (HCV) infection may be prescribed statins for metabolic/cardiovascular disease, but it remains unclear if the risk of acute liver injury (ALI) associated with statin use is higher for chronic HCV-infected persons.

    Methods: We conducted a cohort study among  3,768 chronic HCV-infected statin initiators, 23,535 HCV-uninfected statin initiators, 12,073 chronic HCV-infected statin non-users, and 30,808 HCV-uninfected statin non-users in the Veterans Aging Cohort Study from 2000-2012. We determined development of: 1) liver aminotransferases >200 U/L, 2) severe ALI (international normalized ratio ³1.5 and total bilirubin >2 times upper limit of normal (ULN)), 3) hospitalization with an ALI diagnosis, and 4) all-cause mortality. Cox regression was used to determine propensity score-adjusted hazard ratios (HRs) with 95% confidence intervals (CI).  

    Results: Chronic HCV-infected statin initiators had higher risks of liver aminotransferases >200U/L, severe ALI, hospitalization with ALI, and death, than HCV-uninfected statin initiators.   In contrast, HCV-infected statin initiators had lower risks of liver aminotransferases >200 U/L, severe ALI, hospitalization with severe ALI, and death compared those HCV-infected not using statins.  The risk of death was lower for HCV-infected statin initiators than HCV-uninfected statin non-users.

                                                                                

    Table 1:   Propensity score-adjusted relative hazards of specified outcomes

    Conclusion: Chronic HCV-infected statin initiators had a higher risk of ALI events and death than HCV-uninfected statin initiators but a lower risk of ALI outcomes and death than chronic HCV-infected statin non-users and lower risk of death than HCV-uninfected statin non-users.

    Dana Byrne, MD, MSCE, Cooper University Hospital, Camden, NJ, Janet P. Tate, ScD, VA Connecticut Healthcare System, West Haven, CT, Kimberly Forde, MD, MHS, Division of Gastroenterology, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, Jay R. Kostman, MD, Jonathan Lax Treatment Center, Philadelphia FIGHT, Philadelphia, PA, Jason Roy, PhD, Center for Clinical Epidemiology and Biostatistics, Department of Biostatistics and Epidemiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA and Vincent Lo Re III, MD, MSCE, Center for Pharmacoepidemiology Research and Training, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA

    Disclosures:

    D. Byrne, None

    J. P. Tate, None

    K. Forde, None

    J. R. Kostman, Gilead Sciences: Scientific Advisor , Consulting fee

    J. Roy, None

    V. Lo Re III, AstraZeneca: Grant Investigator , Research grant
    Gilead Sciences: Grant Investigator , Research grant

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