ArticleAntimicrobial agents and chemotherapy2025
Voriconazole-induced liver injury: incidence patterns and risk factors in a retrospective cohort.
Article in Antimicrobial agents and chemotherapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- TREM1-mediated macrophage activation drives voriconazole-induced hepatic steatosis: Diagnostic and therapeutic implications.Journal of pharmaceutical analysis · 2026Article
- Early-onset severe voriconazole-induced liver injury with progressive cholestasis in pulmonary aspergillosis: A case report.Respiratory medicine case reports · 2026Article
- Voriconazole-associated adverse drug reactions in Chinese patients: incidence, clinical features and the predictive value of ALBI score for hepatotoxicity.Frontiers in pharmacology · 2026Article
- Incorporating the metabolic ratio (C-Frontiers in pharmacology · 2026Article
- Case Report: Dual toxicity of voriconazole in a CYP2C19 poor metabolizer: a case analysis of life-threatening neutropenia and hepatocellular injury.Frontiers in pharmacology · 2026Article
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9 authors.
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Abstract
Voriconazole, a first-line therapy for invasive aspergillosis, carries hepatotoxicity risks lacking comprehensive epidemiological characterization. Current evidence is limited by heterogeneity in diagnostic criteria (e.g., varying thresholds for liver function abnormalities across studies), insufficient sample sizes, and inadequate adjustment for comorbidities, which compromises risk assessment accuracy. This study aims to systematically characterize the epidemiological profile of voriconazole-induced liver injury and identify modifiable independent risk factors. We analyzed 7,659 voriconazole-treated adults (2007-2020) from the First Affiliated Hospital of Zhejiang University to determine incidence and injury subtypes. Univariable and multivariable logistic regression identified risk factors, with model performance evaluated by ROC (receiver-operating characteristic) analysis; sensitivity analyses addressed potential confounders. In our results, voriconazole-induced liver injury occurred in 11.32% of patients, predominantly manifesting as hepatocellular (5.01%, 279/630), cholestatic (5.19%, 289/630), and mixed-pattern injuries (1.11%, 62/630). Key modifiable risk factors included intravenous administration (odds ratio [OR] = 1.88, 95% confidence interval [CI]: 1.43-2.46). Non-modifiable predictors comprised baseline elevated urea (OR = 1.47, 95% CI: 1.08-2.02), elevated triglycerides (TG) (cholestatic injury: OR = 1.47, 95% CI: 1.08-2.02), elevated C-reactive protein (CRP) (cholestatic injury: OR = 1.47, 95% CI: 1.08-2.02), pre-existing liver disease (liver cirrhosis, OR = 2.16, 95% CI: 1.58-2.96), diabetes (OR = 2.19, 95% CI: 1.70-2.80), and transplant status (hematopoietic stem cell transplantation, OR = 2.93, 95% CI: 1.85-4.65). Using this clinically substantial cohort (
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