WEAB0102 - Oral Abstract
Increased risk of hepatic decompensation and hepatocellular carcinoma in HIV/HCV-co-infected patients compared to HCV-mono-infected patients despite combination antiretroviral therapy
Presented by Vincent Lo Re (United States).
V. Lo Re1,2, J. Tate3,4, M. Kallan1, J. Lim3,4, M. Goetz5, M. Klein6, D. Rimland7, M. Rodriguez-Barradas8, A. Butt9, C. Gibert10, S. Brown11, J. Kostman1, B. Strom1, R. Reddy1, A. Justice3,4, R. Localio1
1Perelman School of Medicine, University of Pennsylvania, Philadelphia, United States, 2Philadelphia VA Medical Center, Philadelphia, United States, 3VA Connecticut Healthcare System, West Haven, United States, 4Yale University School of Medicine, New Haven, United States, 5VA Greater Los Angeles Healthcare System, Los Angeles, United States, 6McGill University Health Centre, Montreal, Canada, 7Atlanta VA Medical Center, Atlanta, United States, 8Michael E. DeBakey VA Medical Center, Houston, United States, 9VA Pittsburgh Healthcare System, Pittsburgh, United States, 10Washington DC VA Medical Center, Washington, United States, 11James J. Peters VA Medical Center, New York, United States
Background: Few studies have examined the natural history of
chronic hepatitis C virus (HCV) infection among HIV-infected persons in the
era of combination antiretroviral therapy (cART). Our objectives were to: 1) compare
the incidence of hepatic decompensation between cART-treated HIV/HCV-coinfected
and HCV-monoinfected patients, and 2) evaluate determinants of decompensation among
coinfected patients on cART.
Methods: We performed a cohort study among 4,286 cART-treated
HIV/HCV-coinfected and 6,639 HCV-monoinfected patients in the Veterans Aging
Cohort Study Virtual Cohort (1997-2010). All patients had HCV viremia and were
HCV treatment-naïve. Coinfected patients received cART for at least one year
and had an HIV RNA result >500 copies/mL within 180 days prior to starting
cART (to identify new cART initiators). Hepatic decompensation events (defined
by diagnoses of ascites, spontaneous bacterial peritonitis, variceal
hemorrhage, or hepatocellular carcinoma) and death were evaluated. Cox
regression was used to determine the adjusted hazard ratio (aHR) of hepatic
decompensation associated with cART-treated coinfection and evaluated baseline
risk factors for decompensation (alcohol abuse, non-black race, diabetes
mellitus, FIB-4 >3.25, hemoglobin < 10 g/dL, and pre-cART CD4 count) in coinfected
patients on cART.
Results: Compared to HCV-monoinfected patients,
cART-treated HIV/HCV-coinfected had a higher cumulative incidence and risk of
hepatic decompensation (303/4,286 [7.1%] versus 370/6,639 [5.7%]; aHR=1.76
[1.50-2.06]) and hepatocellular carcinoma (50/4,286 [1.2%] versus
60/6,639 [0.9%]; aHR=1.69 [95% CI=1.14-2.49]). After decompensation, mortality was higher in
coinfected patients (228/303 [75.2%] vs. 210/370 [56.8%]; p< 0.001). Non-black
race (aHR=1.96 [1.53-2.49]), baseline FIB-4 >3.25 (aHR=7.18 [5.12-10.07]), and
baseline hemoglobin < 10 g/dL (aHR=2.86 [1.62-5.07]) were associated with
decompensation among coinfected patients.
Conclusions: Despite cART, HIV/HCV-coinfected patients had a
higher risk of hepatic decompensation and death compared to HCV-monoinfected
individuals. Risk of decompensation was higher for coinfected patients with advanced
liver fibrosis, severe anemia, and non-black race.
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