Evidence map›Paper›PMID 41210458›Full record

ArticleAME case reports2025

Beyond the dose: unmasking 'therapeutic' paracetamol toxicity in a chronic alcohol user with severe acidosis-a case report.

W Hamdi Addini Alia Bin W Abdullah, Mohamad Iqhbal Bin Kunji Mohamad, Muhammad Nur Azmi Bin Baharuddin

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Article in AME case reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

W Hamdi Addini Alia Bin W AbdullahDepartment of Emergency Medicine, Faculty of Medicine, Universiti Teknologi MARA, UiTM Sungai Buloh Campus, Jalan Hospital, Sungai Buloh, Selangor, Malaysia.
Mohamad Iqhbal Bin Kunji MohamadDepartment of Emergency Medicine, Faculty of Medicine, Universiti Teknologi MARA, UiTM Sungai Buloh Campus, Jalan Hospital, Sungai Buloh, Selangor, Malaysia.ORCID https://orcid.org/0000-0002-1080-6580
Muhammad Nur Azmi Bin BaharuddinDepartment of Emergency Medicine, Faculty of Medicine, Universiti Teknologi MARA, UiTM Sungai Buloh Campus, Jalan Hospital, Sungai Buloh, Selangor, Malaysia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Paracetamol (PCM), widely used for its analgesic and antipyretic properties, is generally considered safe at recommended doses. However, its metabolism can be significantly altered in chronic alcohol users due to enzyme induction and glutathione (GSH) depletion. While some clinicians maintain that "therapeutic" doses remain harmless in alcoholics, others argue there is no safe threshold. This case report bridges these opposing views by highlighting an atypical presentation of PCM-induced toxicity in a chronic alcoholic. It adds to existing literature by illustrating how severe lactic acidosis may overshadow more typical hepatic symptoms, thereby delaying diagnosis and treatment. Case Description: A 53-year-old male with a 20-year history of alcohol use presented to the emergency department (ED) with sudden-onset dyspnea and profound metabolic acidosis. Initially misdiagnosed as mesenteric ischemia, subsequent investigations revealed strikingly elevated aminotransferases, coagulopathy, and a PCM level above the normal therapeutic range-despite the patient's claim of following standard dosing. Intravenous N-acetylcysteine (NAC) was started, but the patient deteriorated rapidly and succumbed on day 2. Autopsy or long-term follow-up data were unavailable due to the acute course and lack of liver transplantation options. Although previous guidelines have debated whether PCM dosing must be reduced in chronic alcoholics, this case underscores the potential dangers, even within seemingly acceptable intake levels. Conclusions: Clinicians must maintain a high index of suspicion for PCM toxicity in chronic alcoholics, recognising that atypical presentations-such as isolated lactic acidosis and respiratory distress-can conceal the true aetiology. This case reinforces the need for routine PCM-level checks in unexplained acute liver failure, prompt NAC administration, and a balanced perspective regarding "therapeutic" dosing in alcoholics. The findings underscore the call for more nuanced guidelines and further research to determine appropriate dose thresholds and monitoring strategies for alcohol-dependent individuals. By harmonising these divergent clinical stances, patient safety can be enhanced through tailored, vigilant practice.

Indexed as

case reportchronic alcoholismdiagnostic pitfalllactic acidosisParacetamol toxicity (PCM toxicity)

Identifiers

PMID41210458
PMCPMC12593094

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