ArticleLe infezioni in medicina2022
A case of ceftriaxone-induced liver injury and literature review.
Article in Le infezioni in medicina, 2022. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Ceftriaxone's Multifaceted Neuroprotection in Parkinson's Disease: Preclinical Evidence and Implications for Drug Repurposing.Drug design, development and therapy · 2026Review
- Article
- Clinical and biochemical characteristics, and outcome in 33 patients with ceftriaxone-induced liver injury.European journal of clinical pharmacology · 2024Article
- Ceftriaxone-induced hemolytic anemia managed successfully in a 54-year-old woman: a case report and literature review.Frontiers in pharmacology · 2024Article
- Ceftriaxone-induced cholestatic hepatitis in a child: A case report and a review of the literature.Frontiers in pediatrics · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Liver injury evoked by drugs spans various clinical manifestations ranging from mild biochemical abnormalities to acute liver failure. Ceftriaxone is a third-generation cephalosporin often used in clinical practice for its long half-life, high tissue penetration rate, wide spectrum and good safety profile. Ceftriaxone, as other cephalosporins have little hepatotoxicity; however, few cases of toxic hepatitis induced by this antibiotic have been reported. Case Presentation: We describe a case of acute, drug-induced liver injury ('hepatitis') in a 77 years-old female patient treated with ceftriaxone for pneumonia. After 48 hours from antibiotic administration, clinical condition worsened with a clinical and laboratory profile compatible with an acute non cholestatic liver injury. Ceftriaxone administration was immediately stopped and the patient was treated with hydro-electrolyte replacement, high-flow oxygen, vitamin K infusion, steroids and proton-pump inhibitors with a progressive clinical improvement. Conclusions: Even if rare, a ceftriaxone-induced hepatotoxicity (confirmed by RUCAM score), should be considered when all other possible causes have been excluded.
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