ArticleGE Portuguese journal of gastroenterology2019
Carvedilol-Induced Liver Injury, a Rare Cause of Mixed Hepatitis: A Clinical Case.
Article in GE Portuguese journal of gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 8 citations in OpenAlex.
- Metabolic Disturbances Associated with Beta-Blocker Therapy: New Insights from a Large-Scale Pharmacovigilance Study.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Metabolic activation and cytotoxicity of carvedilol mediated by cytochrome P450s in vitro and in vivo.Archives of toxicology · 2025Article
- Carvedilol impairs bile acid homeostasis in mice: implication for nonalcoholic steatohepatitis.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- β-Blocker-Induced Liver Injury: A Class Effect With Incidental Rechallenge.ACG case reports journal · 2019Article
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Authors and funding
7 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
introductionDrug-induced liver injury is an increasingly prevalent consequence of the diversification of available therapeutic weapons, mostly idiosyncratic and with several possible mechanisms and patterns of specific damage for each drug. Carvedilol, a widely used non-selective alpha and beta blocker leads, in very rare cases, to injury of the bile ducts by toxic metabolites, resulting in a mixed-pattern hepatitis with possible progression to chronic cholestatic syndrome and cirrhosis. The authors report the second known case of this important toxicity. CLINICAL CASE: An 83-year-old woman was admitted to the Internal Medicine ward for etiological clarification of a mixed-pattern hepatitis. Clinical history was unremarkable and structural, infectious, and autoimmune causes were excluded by blood tests and imaging exams, ultimately leading to the diagnosis of toxic hepatitis that was further confirmed by liver biopsy with morphologic findings of mixed-pattern liver injury. Carvedilol, started 6 months before, was deemed the causal agent since it was the only drug with a clinically, temporally, analytically, and histologically compatible pattern. The withdrawal of the drug resulted in slow reversal of the referred abnormalities.
conclusionIn very rare cases, carvedilol can cause important liver toxicity as a chronic cholestatic syndrome which can evolve to cirrhosis. It should be taken in consideration as causal agent in similar cases and stopped immediately upon suspicion, as the timely withdrawal results in reversion of the pathological findings.
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