The study aimed to determine liver fibrosis in human immunodeficiency virus (HIV) positive individuals using transient elastography (FibroScan^®), Fibrosis-4 (FIB-4) score, and aspartate aminotransferase (AST) to Platelet Ratio Index (APRI) in the HIV Department from Infectious Diseases Hospital “Victor Babeș” Craiova, Romania. Of the analyzed HIV-positive subjects (n = 161), 93 (57.76%) had HIV mono-infection, and 68 (42.24%) had Hepatitis B Virus (HBV) co-infection. The prevalence of advanced liver fibrosis was higher (F2: 11.76% and F3: 13.24%, F4: 4.41%) in the HIV-HBV co-infected group compared to the HIV mono-infected group. The univariate and multivariate analysis identified HBV co-infection (OR = 5.73) male sex (OR = 5.34), serum aspartate amino-transferase levels (Pearson’s rho = 0.273), low platelet count (Pearson’s rho = −0.149) and erythrocyte sedimentation rate (OR = 1.030) as risk factors for the presence of liver fibrosis. Body mass index (OR = 1.08), serum lipid levels (OR = 0.96), viral load at diagnosis (OR = 1.00005), and low CD4+ cell count (OR = 0.977) were also correlated with liver fibrosis. The FIB-4 and APRI scores were strongly correlated with each other. In conclusion, HBV co-infection seems to be a determinant factor for liver fibrosis development in people living with HIV, together with other risk factors.

The advent of highly active antiretroviral therapy (HAART) in 1996 has markedly enhanced the life expectancy of people living with HIV (PLWH), largely due to the effectiveness of reverse transcriptase inhibitors (RTIs). These drugs target the reverse transcriptase enzyme, crucial for the HIV virus to convert its RNA into DNA within host cells, effectively disrupting the viral replication process. This action reduces the patient’s viral load, helping preserve immune function and prevent progression to AIDS. Consequently, the predominant causes of mortality among individuals living with HIV have transitioned from opportunistic infections and AIDS-related cancers to liver disease and cardiovascular complications. Liver damage in PLWH could arise from multiple sources including co-infections, chronic substance use, and notably, antiretroviral therapy itself, which can be hepatotoxic. This review highlights the risks of hepatic damage associated with nucleoside and non-nucleoside RTIs and underscores the variability in hepatotoxicity risks among different drugs. It emphasizes the necessity for regular monitoring of liver health in PLWH and adjusting antiretroviral regimens to minimize liver fibrosis risk. This risk is particularly pronounced in patients who associate the infection with hepatitis B or C virus, where the potential for hepatotoxicity significantly increases.