HIV infection is associated with lower risk of hepatocellular carcinoma after sustained virological response to direct-acting antivirals in hepatitis C infected-patients with advanced fibrosis

Background The aim of this study was to assess the impact of HIV infection on the risk of developing hepatocellular carcinoma (HCC) in HCV-infected patients who achieve sustained virological response (SVR) with direct-acting antiviral (DAA). Methods Multisite prospective cohort study, where HCV-monoinfected patients and HIV/HCV-coinfected individuals were included if they met: 1) SVR with DAA-based combination; 2) Liver stiffness (LS) ≥9.5 kPa previous to treatment; 3) LS measurement at the SVR time-point. The main endpoint was the occurrence of HCC. Propensity score (PS) was calculated to address potential confounders due to unbalanced distribution of baseline characteristics of HIV/HCV-coinfected and HCV-monoinfected patients. Results 1035 HCV-infected patients were included, 667 (64%) coinfected with HIV. After a median (Q1-Q3) follow-up time of 43 (31-49) months, 19 (1.8%) patients developed HCC [11 (3.0%) HCV-monoinfected, 8(1.2%) HIV/HCV-coinfected individuals; p=0.013]. In the multivariable analysis, HIV co-infection was associated with a lower adjusted risk of developing HCC [sHR=0.27, 95% IC (0.08-0.90); p=0.034]. Predictors of HCC emergence were: HCV genotype 3 [sHR=7.9 (2.5-24.9); p<0.001], MELD score at SVR>10 [sHR=1.37 (1.01-1.86); p=0.043] and LS value at SVR [sHR=1.03 (1.01-1.06) for 1 kPa increase; p=0.011]. Using inverse probability weighting method on the PS, HIV-infected patients had a lower risk of HCC [powered HR=0.33 (0.11-0.85)]. Conclusions Among HCV-infected patients with advanced fibrosis, who achieve SVR with DAA, HIV-coinfection seems to be associated with a lower risk of HCC occurrence. The underlying causes for this finding need to be investigated.