European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026
HBV/HCV coinfection and anti-tuberculosis drug-induced liver injury: from risk assessment and exploration of mechanisms to preventive considerations.
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Li Xiao-Jing, Zhang Na, Zhang Qiang, Chen Rui, Yu Guo
Аннотация
PURPOSE: Anti-tuberculosis drug-induced liver injury (AT-DILI) is a common and clinically significant adverse event during tuberculosis treatment. Previous studies have frequently reported an increased risk of AT-DILI among patients coinfected with hepatitis B virus (HBV) and/or hepatitis C virus (HCV). This review aims to explore potential mechanisms underlying this heightened susceptibility and to discuss prevention considerations for patients with tuberculosis and HBV/HCV coinfection.
METHODS: We conducted a comprehensive literature search across PubMed, Web of Science, and Google Scholar, supplemented by clinical guidelines and authoritative reports, to identify relevant studies published through August 2026. Relevant articles were screened and thematically organized to synthesize evidence on risk estimation, underlying mechanisms, and prevention considerations.
RESULTS: Available evidence indicates that HBV/HCV coinfection is associated with increased AT-DILI risk, with the magnitude varying by viral activity, baseline liver disease, and virological indicator selection. Higher viral loads appear more closely associated with AT-DILI risk. Potential mechanisms include immune-inflammatory changes, altered drug metabolism, reduced hepatic reserve, and virus-specific liver injury, including HBV reactivation. These observations inform preventive strategies targeting these risks and potential mechanisms, including baseline hepatic and virological assessment, dynamic monitoring, antiviral therapy, individualized anti-tuberculosis regimen optimization, and selective use of hepatoprotective agents.
CONCLUSION: HBV/HCV coinfection increases the risk of AT-DILI and warrants active clinical attention. Future efforts should focus on individualizing prevention based on virological and hepatic status, while validating emerging biomarkers and artificial intelligence-based predictive tools to refine risk identification.
METHODS: We conducted a comprehensive literature search across PubMed, Web of Science, and Google Scholar, supplemented by clinical guidelines and authoritative reports, to identify relevant studies published through August 2026. Relevant articles were screened and thematically organized to synthesize evidence on risk estimation, underlying mechanisms, and prevention considerations.
RESULTS: Available evidence indicates that HBV/HCV coinfection is associated with increased AT-DILI risk, with the magnitude varying by viral activity, baseline liver disease, and virological indicator selection. Higher viral loads appear more closely associated with AT-DILI risk. Potential mechanisms include immune-inflammatory changes, altered drug metabolism, reduced hepatic reserve, and virus-specific liver injury, including HBV reactivation. These observations inform preventive strategies targeting these risks and potential mechanisms, including baseline hepatic and virological assessment, dynamic monitoring, antiviral therapy, individualized anti-tuberculosis regimen optimization, and selective use of hepatoprotective agents.
CONCLUSION: HBV/HCV coinfection increases the risk of AT-DILI and warrants active clinical attention. Future efforts should focus on individualizing prevention based on virological and hepatic status, while validating emerging biomarkers and artificial intelligence-based predictive tools to refine risk identification.