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
Contributions: (I) Conception and design: All authors; (II) Administrative support: MIBK Mohamad, MNAB Baharuddin; (III) Provision of study materials or patients: WHAABW Abdullah; (IV) Collection and assembly of data: WHAABW Abdullah; (V) Data analysis and interpretation: All authors; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.
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.
Keywords: Paracetamol toxicity (PCM toxicity); chronic alcoholism; lactic acidosis; diagnostic pitfall; case report
Received: 30 January 2025; Accepted: 01 August 2025; Published online: 25 September 2025.
doi: 10.21037/acr-25-31
Highlight box
Key findings
• A 53-year-old chronic alcoholic presented with acute respiratory distress and severe lactic acidosis, overshadowing signs of potential paracetamol (PCM) toxicity.
• Despite “therapeutic” PCM dosing, serum levels were significantly elevated, and the patient deteriorated rapidly with fulminant hepatic failure.
What is known and what is new?
• Chronic alcohol consumption can potentiate PCM toxicity through cytochrome P450 enzyme induction and decreased glutathione reserves. Guidelines and expert opinions differ on whether standard PCM dosing is safe in chronic alcoholics, reflecting an ongoing clinical controversy.
• This report emphasises an atypical presentation (dyspnea and lactic acidosis) that can delay the diagnosis of PCM-induced liver failure. It bridges two opposing clinical viewpoints—those who regard therapeutic PCM as unsafe in alcoholics and those who perceive it as safe—by illustrating that both stances have valid concerns.
What is the implication, and what should change now?
• Clinicians should maintain a high index of suspicion for PCM toxicity in chronic alcoholics, even when typical overdose histories are absent.
• Routine serum PCM-level checks in unexplained acute liver failure and early N-acetylcysteine therapy are crucial.
• Refinements to prescribing guidelines for alcoholics are warranted, balancing vigilance with practical analgesic use.
Introduction
Paracetamol (PCM), also known as acetaminophen, is a widely utilised analgesic and antipyretic medication which can be obtained by prescription and over-the-counter (1). Although classical pharmacological textbooks have theorised the potential notorious effect of PCM among alcoholics even with therapeutic doses, the notion was challenged and refuted, started by an in-depth article by Professor Laurie F. Prescott, a distinguished expert in pharmacology in the British Journal of Clinical Pharmacology in 2000 (2). He argued that there is minimal possibility of PCM toxicity in therapeutic doses, even among chronic alcoholics, and in fact, alluded to the protective effect of PCM if taken simultaneously with ethanol. The incidence of PCM toxicity at therapeutic dose among alcoholic patients reported in the previous years was attributed to inaccurate reporting and most likely due to the exceeding PCM dosage rather than because of alcohol itself. This was followed by many articles that were in line with the notion; among the recent ones was a systematic review by Caparrotta et al. in 2018 (3). This subsequently leads to some guidelines adopting indifference to PCM dosage among alcoholics.
That being said, there are anecdotal cases of liver failure among alcoholics who were prescribed therapeutic doses of PCM being reported occasionally (4). This is such a case in which, having the opportunity to manage the case, we could hypothesise the probable reasoning behind the incident. This case also illustrates an unusual presentation of PCM toxicity that clinicians should be cognizant of. We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-25-31/rc).
Case presentation
A 53-year-old male, a regular consumer of alcohol for 20 years with no known chronic liver disease, presented with sudden onset shortness of breath for around 6 hours. He had a history of toothache 3 days prior and was prescribed regular PCM doses, which he took as directed. He denied vomiting or abdominal pain prior.
On presentation, he was medium built, with an estimated body weight of 70 kg. He was alert but spoke in words. Vital signs showed normal temperature and blood pressure, but he was tachycardic with a heart rate of 140 bpm and tachypneic with a respiratory rate of 40 breaths per minute. The lung auscultation was clear, and there were no signs of chronic liver disease or bruises. Abdominal examination revealed a tender abdomen with hepatomegaly (4 finger breadths). Electrocardiogram revealed sinus tachycardia without ischemic changes. A bedside scan showed minimal free fluid over the hepatorenal region with normal liver echogenicity. Good heart contractility, hyperdynamic, and a collapsible inferior vena cava were noted via point of care cardiac ultrasound. The lung ultrasound showed an A-profile with a sliding sign present.
In view of his respiratory condition, he was initially started on a trial of non-invasive ventilation (NIV) and subsequently intubated shortly after as his condition deteriorated further. The initial point of care arterial blood gases revealed severe metabolic acidosis with hyperlactatemia (Table 1). Given the clinical features with high lactate, the initial impression was mesenteric ischemia with intra-abdominal sepsis. He was started on intravenous antibiotics and arranged for emergent computed tomography (CT) angiography of the abdomen, which was reported as normal with no evidence of mesenteric arterial or venous thrombosis.
Table 1
| Lab value | On admission | 12 h after admission |
|---|---|---|
| Total white blood cell (normal, 3.4–10 ×109/L) | 10.5 | 5.9 |
| Hemoglobin (normal, 11.6–15.1 g/dL) | 16 | 11.5 |
| MCV (normal, 83–101 fL) | – | 92.6 |
| MCHC (normal, 31–34 g/dL) | – | 31.7 |
| Platelets (normal, 150–410 ×109/L) | 14 | 7 |
| HCT (normal, 40–50%) | – | 36.3 |
| Renal profile | ||
| Urea (normal, 3.2–8.2 mmol/L) | 8.4 | 8.1 |
| Sodium (normal, 136–145 mmol/L) | 127 | 129 |
| Potassium (normal, 3.5–5.1 mmol/L) | 4.4 | 4.4 |
| Creatinine (normal, 62–115 μmol/L) | 138 | 171 |
| Liver function test | ||
| ALT (normal, 10–72 U/L) | 2,796 | 1,469 |
| AST (normal, 0–34 U/L) | 6,239 | 4,512 |
| ALP (normal, 46–116 U/L) | 124 | 101 |
| Bilirubin, total (normal, 10–72 μmol/L) | 189 | – |
| Bilirubin, direct (normal, 0–5 μmol/L) | 152 | – |
| Albumin (normal, 32–48 g/L) | 43 | 29 |
| LDH (normal, 120–246 U/L) | – | – |
| Creatine kinase (normal, 92–267 U/L) | 92 | 223 |
| Amylase (normal, 30–118 U/L) | 239 | 1,632 |
| Calcium (normal, 2.08–2.65 mmol/L) | 2.5 | 2.02 |
| Phosphate inorganic (normal, 0.78–1.65 mmol/L) | 2.56 | 3.07 |
| Magnesium (normal, 0.66–1.07 mmol/L) | 0.97 | 0.91 |
| Arterial blood gases | ||
| pH (normal, 7.35–7.45) | 6.81 | – |
| pCO2 (normal, 35–45 mmHg) | 9 | – |
| pO2 (normal, 80–100 mmHg) | 254 | – |
| HCO3− (normal, 22–28 mmol/L) | <3 | – |
| BE (normal, −3.2 to 1.8 mmol/L) | – | – |
| Lactate (normal, 0.4–0.8 mmol/L) | >15 | – |
| Coagulation profile | ||
| PT (normal, 11.7–15.3 s) | 77.8 | 72.4 |
| INR | 6.76 | 6.24 |
| aPTT (normal, 30.0–44.4 s) | 52.5 | 70.8 |
| Dengue IgM | Negative | – |
| Dengue IgG | Negative | – |
| BFMP | – | Negative |
| Leptospira IgM | – | Negative |
| HAV IgM | Non-reactive | – |
| HBs Ag | Non-reactive | – |
| HCV Ab | Non-reactive | – |
| ANA | Negative | – |
| HsTrop I (normal, <53.53 pg/mL) | 5.71 | 407 |
ALP, alkaline phosphatase; ALT, alanine aminotransferase; ANA, antinuclear antibody; aPTT, activated partial thromboplastin time; AST, aspartate aminotransferase; BE, base excess; BFMP, blood film for malarial parasite; HAV, hepatitis A virus; HBs Ag, hepatitis B surface antigen; HCO3−, bicarbonate; HCT, hematocrit; HCV Ab, hepatitis C virus antibody; HsTrop I, high-sensitivity troponin I; IgM/IgG, immunoglobulin M/G; LDH, lactate dehydrogenase; MCHC, mean corpuscular hemoglobin concentration; MCV, mean corpuscular volume; pCO2/pO2, partial pressure of carbon dioxide/oxygen; PT/INR, prothrombin time/international normalized ratio.
As the results of liver function were available, it was apparent that the patient was having acute liver failure (Table 1). He was promptly initiated on NAC infusion in accordance with the protocol for acute liver failure. About 6 hours after his presentation, the clinician, noticing the significantly abnormal liver function tests, decisively ordered a serum PCM level test. The results revealed that the level was double the normal range (Table 2). The NAC was then continued as per protocol for PCM toxicity. He was subsequently admitted to the intensive care unit (ICU). During admission, further investigations have ruled out other causes of liver failure, like autoimmune and viral hepatitis (Table 1). Unfortunately, his condition deteriorated further, and he succumbed on day 2 of admission. As the overall clinical features were consistent with PCM toxicity, no additional imaging or post-mortem examinations were conducted. Table 3 illustrates the full timeline of the event.
Table 2
| Lab value | On admission | 12 h after admission | Day 2 after admission |
|---|---|---|---|
| Paracetamol level (normal, 9.98–19.95), μg/mL | 46.6 | 29.9 | 24.5 |
Table 3
| Date/time | Event |
|---|---|
| Day −3 | Onset of toothache; prescribed regular PCM (therapeutic dose) |
| Day 0, ~−6 h | Sudden onset dyspnea; no vomiting or abdominal pain |
| Day 0, ED | Tachycardia, tachypnea, severe metabolic acidosis & hyperlactatemia |
| Day 0, ED | Initial Dx: mesenteric ischemia; IV antibiotics; CT angiography normal |
| Day 0, ~+6 h | LFTs markedly elevated; NAC infusion started for acute liver failure |
| Day 0, later | Serum PCM level double therapeutic; NAC continued per PCM toxicity protocol |
| Day 1 | ICU admission; further causes of liver failure excluded |
| Day 2 | Condition deteriorated to fulminant hepatic failure; death |
CT, computed tomography; Dx, Diagnosis; ED, emergency department; ICU, intensive care unit; IV, intravenous; LFT, liver function test; NAC, N-acetylcysteine; PCM, paracetamol.
All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient’s family member for the publication of this case report. A copy of the written consent is available for review by the editorial office of this journal.
Discussion
Without in-depth analysis, this case indicates the potential PCM toxicity taken at therapeutic levels among alcoholics. The previous description of many drug metabolisms being disrupted by alcohol, particularly PCM, was documented in the classical pharmacological textbook (5). Animal studies postulated the induction of cytochrome P450 enzyme system, particularly CYP2E1, which increases the conversion of PCM into its toxic metabolite, N-acetyl-p-benzoquinone imine (NAPQI). This was, however, challenged by Prof. Prescott, alluding to the insignificant effects of CYP2E1in causing liver toxicity among alcoholics (2). Notwithstanding, there are other studies that revealed the depletion of glutathione (GSH), an antioxidant that neutralises NAPQI in chronic alcoholics (6,7). A recent prospective data also reported that 20% of 311 patients with acute liver injury were secondary to therapeutic doses of PCM and concluded that excessive alcohol intake, period of fasting and several days of intake of PCM were predictors for liver injury (8). These arguments drive the ongoing debate on this issue.
We hypothesise that even if the pharmacological pathways might not be implicated entirely, the risk of being prescribed PCM at a therapeutic dose causing toxicity remains high among alcoholics. Two possible explanations for this: while the dose prescribed is standard, the behaviour of drug intake among this group of patients is less reliable, and the tendencies of repeated intake without complete realisation is indeed possible. Previous studies have confirmed the tendency of non-adherence to prescribed medications and one of the main reasons for the general deterioration of treatable health conditions among alcoholics (9). This also confirms a study that revealed the incidence of PCM toxicity due to staggered repeated doses of PCM is significantly higher among chronic alcoholics (10). It was also reported in a study that 31.9% of 128 alcoholics were found to use PCM at a supratherapeutic dose (7). Further, the pain itself was also reported to increase the risk of alcohol abuse (11).
The second reason is the probable undiagnosed underlying liver disease secondary to chronic alcohol intake, which had exacerbated the PCM toxicity even with the therapeutic dose. This is consistent with a recent meta-analysis that revealed the prevalence of liver cirrhosis of 1 in 8 among alcohol abusers, compared to 1 in 300 of the general population (12). Additionally, even though the therapeutic dose of PCM is argued as safe for chronic alcoholics, the tendency of hepatotoxicity due to overdose remains higher compared to non-alcoholics due to multifactorial reasons, among which the depletion of mitochondrial GSH level (13,14).
This case also illustrates the unusual way of patient presenting with PCM toxicity, which derailed the clinician in getting the timely correct diagnosis. Traditionally, the usual symptoms are nausea, vomiting, abdominal pain and symptoms directly related to liver failure like hepatic encephalopathy. These are related to the temporal effect of the toxin accumulation from exposure. In this case, the presentation was dyspnea, attributed to severe high-anion gap metabolic acidosis secondary to hyperlactatemia. This, in combination with generalised abdominal tenderness, has misled the managing clinicians towards the diagnosis of mesenteric ischaemia. Clinicians need to be cognizant of the occurrence of lactic acidosis in PCM toxicity, either as an association with liver failure (later phase) or in isolation (early phase), which were reported previously (15).
There are two valuable lessons from this case. First, the awareness of doctors on the potential danger of prescribing the usual PCM dose in alcoholic patients and the public awareness on the same issue, given that this drug can be easily obtained over the counter. Although the data are conflicting on the advisable PCM dose, the extra caution of the possible complications should be noted, and the advice for early presentation to the hospital should any symptoms appear should be given.
Second, the awareness of the clinician in the emergency department (ED) in having a high index of suspicion among alcoholic patients present with features of acute liver failure. The presentation of dyspnoea secondary to severe metabolic acidosis in a chronic alcoholic patient should have triggered the possibility of PCM toxicity from the beginning, even with the perceived therapeutic dose of PCM. Some authors have advocated N-acetylcysteine (NAC) in a patient suspected of PCM overdose with isolated lactic acidosis, as this could prevent into getting fulminant liver failure (15). The abnormal liver function test, particularly the extremely high level of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), which is highly indicative of PCM toxicity, also should have prompted the workup for PCM earlier (16). NAC remains the cornerstone of therapy, replenishing GSH reserves and directly scavenging NAPQI (17,18). Although, in this case, the NAC was started early due to acute liver failure, the practice of administrating NAC for this condition, not due to PCM poisoning, is not wide. As described in many guidelines, the effects of NAC will be less after 8 hours of exposure to PCM; hence, any delay could impact the prognosis dearly (19).
Be it as it may, this patient presented 3 days after the first intake of PCM with severe metabolic acidosis, hyperlactatemia, and fulminant liver failure. Fulfilling the King’s College Criteria, in addition to the hyperphosphatemia, the prognosis and the reversibility of the condition were very guarded, hence leading to mortality (20).
Conclusions
This case highlights the potential hepatotoxic effects of PCM at therapeutic doses in chronic alcoholics, challenging the traditional notion of its safety in this population. While mechanisms such as CYP2E1 induction and GSH depletion are well-documented contributors to PCM toxicity, emerging evidence points to multifactorial influences, including undiagnosed liver disease, staggered dosing, and behavioural factors unique to chronic alcoholics. These factors collectively increase the risk of hepatotoxicity, even when PCM is taken within recommended guidelines. The atypical presentation of PCM-induced acute liver failure in this case, characterised by dyspnoea and severe metabolic acidosis, highlights the diagnostic challenges that can delay timely recognition and management. It emphasises the importance of maintaining a high index of suspicion for PCM toxicity in chronic alcoholics, even in the absence of overt overdose history. Early diagnosis and prompt initiation of NAC remain critical cornerstones of therapy. This report reinforces the need for caution when prescribing PCM to chronic alcoholics, coupled with patient education on safe medication use and the importance of seeking medical attention promptly if symptoms arise. From a broader perspective, this case underscores the need for further research to refine PCM prescribing guidelines for chronic alcoholics and to investigate the interplay of contributing factors to hepatotoxicity in this vulnerable population. Clinicians should remain vigilant for the possibility of PCM toxicity in patients with chronic alcohol use and consider it as a differential diagnosis in unexplained cases of acute liver failure, ensuring timely management and improved outcomes.
Acknowledgments
The authors would like to appreciate and acknowledge the Ministry of Health Malaysia for allowing the publication of this case report.
Footnote
Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-25-31/rc
Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-25-31/prf
Funding: None.
Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-25-31/coif). The authors have no conflicts of interest to declare.
Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient’s family member for the publication of this case report. A copy of the written consent is available for review by the editorial office of this journal.
Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.
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Cite this article as: Abdullah WHAABW, Mohamad MIBK, Baharuddin MNAB. Beyond the dose: unmasking ‘therapeutic’ paracetamol toxicity in a chronic alcohol user with severe acidosis—a case report. AME Case Rep 2025;9:114.
