Human Immunodeficiency Virus (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

Abstract

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.

Retrospective-prospective study of safety and efficacy of sofosbuvir-based direct-acting antivirals in HIV/HCV-coinfected participants with decompensated liver disease pre– or post–liver transplant

“…As in HCV-monoinfected patients with SVR, HCC in HCV/HIV patients is decreased post-SVR but may still occur. 23 Overall, pre-LT participants received short-term benefits with good transplant free survival at 1y from SVR but not at 4y post-DAA (Figure 4). SVR was associated with improved indirect markers of fibrosis (APRI and FIB-4) but did not prevent progression of ESLD.…”

“…5 U/L (IQR 29.0-83.0) and at last follow-up was 21.0 U/L (IQR[16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34]. ALT improved significantly after DAA therapy (Figure1 A).…”

The treatment choices and outcome of hepatocellular carcinoma in hemophilic patients with human immunodeficiency virus/hepatitis C virus (HIV/HCV) coinfection due to contaminated blood products in Japan

“…Only 3 cases in this study had received DAA before the diagnosis of HCC, all of which could achieve SVR. The safety and efficacy of DAA in HIV/HCV coinfection has recently been confirmed, so that DAA might contribute to the improvement of both HCV/ HCC treatment in this population, as has already been shown in Western countries (13,14). As mentioned above, the reason of small number in HCV treatment with DAA in Japan might be the reluctant to adopt it because of the possible insufficient collaboration between the hepatologists and hematologists, and/or HIV physicians.…”

A Genome-Wide Association Study on Liver Stiffness Changes during Hepatitis C Virus Infection Cure

“…In spite of LS at SVR being a strong predictor of liver disease outcome in HCVinfected patients with pre-treatment advanced fibrosis [14,15], other factors have been independently associated with liver events' occurrence. For instance, HIV-infection and non-genotype 3-HCV-infection have been related to a lower risk of HCC [36], whereas the anti-HCV therapy used as well as the presence of diabetes have been associated with incremented risk of HCC [37]. Therefore, it will be necessary to explore if the genetic factors described herein have a role in the occurrence of these events as well as to determine their real effect, taking into account all those non-genetic factors.…”