Analysis of HCV antiviral therapy outcomes in HIV-infected patients with liver cirrhosis

Objective. To analyze the features of the course of chronic hepatitis С virus (HCV) and effectiveness of its treatment in patients with HIV infection. Patients and methods. The study was conducted on the basis of the State Budgetary Health Institution “Samara Regional Clinical Center for AIDS Prevention and Control”. Twenty-two HIV-infected patients with HCV genotype 2 and 3 and HCV-related liver cirrhosis were observed. All patients had compensated cirrhosis (class A according to the Child-Pugh classification). Patients were aged between 33 and 65 years, with an average age of 46.5 years. There were 17 (77.3%) male and 5 (22.7%) female patients. Results. The effectiveness of antiviral therapy (AT) for HCV with progression to liver cirrhosis and the dynamics of clinical and laboratory parameters in 22 HIV-infected patients were assessed. HCV genotypes were distributed as follows: genotype 3 was detected in 20 patients (91%), genotype 2 – in 2 patients (9%). According to the results of elastometry, the stages of fibrosis were distributed as follows: F0–F2 – in 0 (0.0%) patients, F3 – in 3 (13.6%) patients, F4 – in 19 (86.4%) patients. Serum levels of HCV RNA prior to treatment averaged 310,335 copies/mL (1,020 to 795,000 copies/mL). After 8 and 12 weeks of antiviral therapy for HCV, all 22 patients had no HCV RNA in the blood. However, in one patient HCV RNA levels reached 53,856 copies/mL 24 weeks after the end of antiviral therapy (reinfection due to the injection of psychoactive substances). Conclusion. Thus, all 22 treated patients with HIV infection and HCV with progression to liver cirrhosis achieved sustained virologic response 12 (SVR12) after an 8-week course of antiviral therapy for HCV (glecaprevir/pibrentasvir). Hepatitis C virus eradication is likely to reduce the risk of fibrosis progression, decompensated cirrhosis, and hepatocellular carcinoma formation. In turn, laboratory manifestations in the form of hepatocyte cytolysis syndrome (AST/ALT) and intrahepatic cholestasis (GGT) ceased by the end of treatment. Against the background of antiviral therapy for HCV, CD4 cell count tended to increase in patients, which would subsequently reduce the risk of severe opportunistic infections and complications. There were no adverse events during treatment with glecaprevir/pibrentasvir (neither clinical symptoms nor change in clinical and biochemical blood tests), which confirms the safety of the chosen treatment regimen. The only problem remains the adherence to treatment of such a complex group of patients as HCV/HIV co-infected, as well as the possibility of HCV reinfection through sexual contact with HCV patients and/or through injecting psychoactive substances. Key words: antiretroviral therapy, HIV infection, direct-acting antivirals, chronic hepatitis C, liver cirrhosis