Prevalence of hepatotoxicity among HIV-infected patients in Ethiopia: a systematic review and meta-analysis

Abstract

Background Globally, the human immunodeficiency virus has been recognized as a major public health concern. The direct toxicity of antiretroviral medicines or their active metabolites causes liver cell destruction by different mechanisms, inducing immune-mediated inflammation, oxidative stress, and other mechanisms. On the other hand, the virus itself also produces hepatotoxicity. Therefore, this systematic review and meta-analysis aimed to assess the pooled prevalence of hepatotoxicity among HIV-infected patients in Ethiopia. Methods PubMed, Science Direct, Cochrane Library, Web of Science, and ResearchGate databases were used to find relevant articles. As well, various professional associations were searched to retrieve grey literature. The Newcastle–Ottawa Quality Assessment Scale was used to assess the quality of recruited studies. The data were extracted using Microsoft Excel, and the meta-analysis was carried out using STATA 14 software. I2 and Cochran’s Q test were employed to assess the presence of heterogeneity between studies. A random effect model was used. The funnel plot and Egger’s statistics were used to assess publication bias. Moreover, subgroup analysis and sensitivity analysis were also done. Results The pooled prevalence of hepatotoxicity among HIV patients in Ethiopia was 25.45% (95% CI = 20.06–30.84%). There was high heterogeneity, with an I2 value of 93.7%. Subgroup analysis by HAART status showed a higher pooled prevalence of hepatotoxicity among HIV patients taking HAART (23.63%) than among HAART naive patients (7.29%). In subgroup analysis, the pooled prevalence of hepatotoxicity among HIV/Tb co-infected and HIV mono-infected patients was 26.3% and 17.94%, respectively. Conclusion The current systematic review and meta-analysis showed a high prevalence of hepatotoxicity among HIV-infected patients. Therefore, regular monitoring of hepatotoxicity among HIV-infected patients is required in order to avoid liver damage and other complications. Systematic review registration PROSPERO (2022:CRD42022334704)

Clinical and Immunological Profiles of HIV/AIDS Patients With First-Line Antiretroviral Treatment Failure Attending a Tertiary Care Hospital

“…However, a systematic review of observational studies published between January 1998 and November 2013 revealed no sex difference in virologic or immunologic treatment outcomes [ 12 ]. The majority (77.8%) of ART failure patients had normal BMIs with a median BMI of 21.9, which agrees with other studies [ 6 , 13 , 14 ]. The biochemical investigations showed high mean serum transaminase levels among ART failure patients.…”

“…The biochemical investigations showed high mean serum transaminase levels among ART failure patients. Various studies have reported hepatotoxicity as a significant concern among patients on ART [ 14 , 15 ]. Opportunistic infections were present in 21.1% of ART failure patients.…”

Evaluating Hepatotoxicity: A Comparative Analysis of New Generation versus Historical Antiretroviral Agents

“…Antiretroviral (ARV) medications have the capacity to induce harm to hepatic cells, either through direct action or via the influence of their active metabolites [ 12 ]. Conversely, within the context of HIV viral pathogenesis and liver injury, a myriad of mechanisms come into play, encompassing immune-mediated injury, oxidative stress, mitochondrial impairment, lipotoxicity, cytotoxicity, the accumulation of toxic metabolites, gut microbial translocation, and systemic inflammation [ 13 ].…”

Hepatic Function and its Association with Clinical Outcomes in Non-Adherent HIV-1 Adults ‎‎

“…Emerging evidence shows that liver related derangements, common among PLHIV are among the leading determinants of non-HIV mortality [11]. Such derangements arise from liver damage caused by multiple stimuli, eventually translating into acute or chronic liver disease [12]. Among the HAART naive patients, high HIV viraemia and low CD4+ counts mediate liver damage by promoting fibrogenesis and hepatocyte apoptosis [13].…”