Persistent Hepatocellular Secretory Failure Secondary to Flucloxacillin-Induced Liver Injury: A Case With Successful Response to Rifampicin

We report the case of an 80-year-old male who developed severe cholestatic jaundice following two courses of flucloxacillin prescribed for a soft-tissue infection. Despite discontinuation of the antibiotic, serum bilirubin remained markedly elevated eight weeks later, accompanied by persistent pruritus. Comprehensive evaluation for acute liver injury, including viral, autoimmune, and metabolic studies as well as abdominal imaging, was unremarkable. A liver biopsy demonstrated preserved hepatic architecture with prominent hepatocellular cholestasis, consistent with hepatocellular secretory failure. After consulting with a specialist hepatology centre, the patient was initiated on rifampicin monotherapy, resulting in gradual symptomatic improvement and a progressive decline in bilirubin levels over subsequent weeks. This case highlights the importance of maintaining a high index of suspicion for hepatocellular secretory failure in patients with persistent hyperbilirubinemia following withdrawal of a potential hepatotoxic agent. Targeted therapy with rifampicin can result in both symptomatic and biochemical improvement in hepatic function.

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Publication Details

Journal
Cureus
Published
2025-10-24
DOI
https://doi.org/10.7759/cureus.95348
Primary Topic
Drug-Induced Hepatotoxicity and Protection
Type
article
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article

Persistent Hepatocellular Secretory Failure Secondary to Flucloxacillin-Induced Liver Injury: A Case With Successful Response to Rifampicin

S. M. Qasim Hussaini, Zainab Mustapha, Mohammad Adjmal Rummun, Vijeta Rummun
Cureus
Drug-Induced Hepatotoxicity and Protection
article

Persistent Hepatocellular Secretory Failure Secondary to Flucloxacillin-Induced Liver Injury: A Case With Successful Response to Rifampicin

S. M. Qasim Hussaini, Zainab Mustapha, Mohammad Adjmal Rummun, Vijeta Rummun
article en

Abstract

We report the case of an 80-year-old male who developed severe cholestatic jaundice following two courses of flucloxacillin prescribed for a soft-tissue infection. Despite discontinuation of the antibiotic, serum bilirubin remained markedly elevated eight weeks later, accompanied by persistent pruritus. Comprehensive evaluation for acute liver injury, including viral, autoimmune, and metabolic studies as well as abdominal imaging, was unremarkable. A liver biopsy demonstrated preserved hepatic architecture with prominent hepatocellular cholestasis, consistent with hepatocellular secretory failure. After consulting with a specialist hepatology centre, the patient was initiated on rifampicin monotherapy, resulting in gradual symptomatic improvement and a progressive decline in bilirubin levels over subsequent weeks. This case highlights the importance of maintaining a high index of suspicion for hepatocellular secretory failure in patients with persistent hyperbilirubinemia following withdrawal of a potential hepatotoxic agent. Targeted therapy with rifampicin can result in both symptomatic and biochemical improvement in hepatic function.

CureusVol. 17(10)
University of Liverpool (GB), Blackpool Victoria Hospital (GB), East Lancashire Hospitals NHS Trust (GB)
Openalex Percentile: Top 60%
Drug-Induced Hepatotoxicity and Protection
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