icon-    folder.gif   Conference Reports for NATAP  
  XIX International AIDS Conference
July 22-27, 2012
Washington, DC
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HCV/HIV Coinfection Higher Rates of Hepatic Decompnsation, Liver Cancer & Severe Liver Events
  Reported by Jules Levin
IAC Wash DC 2012 July 22-27

Increased risk of hepatic decompensation and hepatocellular carcinoma in HIV/HCV-co-infected patients compared to HCV-mono-infected patients despite combination antiretroviral therapy - slides attached

Isn't it obvious coinfected patients are at greater risk !!!! hello

Reported by Jules Levin
IAC 2012 Wash DC July 22-27

Presented by Vincent Lo Re (United States).

Rockstroh asked about the fact that avg baseline CD4 before HAART was <200 in 45% of patients in this study, so since patients today start HAART with higher CD4 wouldnt that mean this study finding that coinfected are at greater risk might not hold up when starting HAART at >350 CD$. The presenter said no, they did an analysis by stratifying baseline pre-HAART CD4 by <200, 201-350, and >351-500 and found no difference in higher risk for decompensation & cancer.

If you view this webcast you can hear my comments at the mic. This study suggests what I said years ago, that HAART, even successful HAART, does not necessarily slpw HCV disease progression, that it still can be much more accelerated in the coinfected patient. This study also finds coinfected having higher rates of decompensation & cancer compared to monoinfection. We should be treating all coinfected and I am sure tht will be the accepted approach as soon as we have multiple oral antiviral theray regimens capable of curing a very high percent of patients, very soon we will be capable of attaining 100% cure rates virologically, except of course for nonadherence & discontinuations due to toxicities.



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.