S5754 When the Party Ends: Methamphetamine Induced Acute Liver Failure in a Healthy Young Man

Introduction: Methamphetamine abuse is a growing public health concern with well-documented neuropsychiatric and cardiovascular effects. However, acute liver failure induced by methamphetamine is rare, underreported, and not widely recognized among clinicians. Presenting this case highlights the potential severity of methamphetamine toxicity and aims to increase awareness of its hepatic complications in young, otherwise healthy patients. Case Description/Methods: A 22-year-old previously healthy male was brought to the emergency department unresponsive after suspected methamphetamine use. EMS found him apneic; bag-valve ventilation was initiated en route. On arrival, his Glasgow Coma Scale was 3, prompting immediate intubation and intensive care unit admission. Initial exam revealed intermittent posturing, sluggish pupils, and scattered skin lesions suggestive of intravenous drug use. Urine drug screen was positive for amphetamines and cannabinoids. Laboratory work showed rapidly rising liver enzymes: aspartate aminotransferase peaked at 2,825 U/L and alanine aminotransferase at 3,589 U/L, with international normalized ratio (INR) increasing to 1.6 and bilirubin peaking at 4.5 mg/dL. MELD score rose from 16 to 26 before improving. Acetaminophen levels were within normal limits; hepatitis panel was negative; and imaging was unremarkable. No hypotensive episodes occurred. The patient was diagnosed with methamphetamine-induced acute liver failure after excluding other causes. He also developed rhabdomyolysis and acute kidney injury, requiring 5 sessions of hemodialysis. With supportive care, liver and renal function progressively improved. At discharge, liver enzymes, INR, bilirubin, and renal function normalized, and dialysis was discontinued. He was referred for rehabilitation. Follow-up labs confirmed complete hepatic recovery, and he remained sober at follow-up. confirmed complete recovery of liver function. The patient remained sober at follow-up. Discussion: This case highlights methamphetamine as a rare but potentially life-threatening cause of acute liver failure. Hepatotoxicity may result from direct cellular injury or ischemia due to methamphetamine-induced vasoconstriction and hyperthermia. While liver transplantation is the mainstay for irreversible acute liver failure, this case demonstrates that full recovery is possible in select patients with drug-induced liver injury, particularly when other etiologies are excluded and complications are promptly managed. Early recognition and aggressive supportive care may prevent the need for transplant in otherwise healthy individuals.

Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001150476.08412.b6
Primary Topic
Forensic Toxicology and Drug Analysis
Type
article
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0.00
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article

S5754 When the Party Ends: Methamphetamine Induced Acute Liver Failure in a Healthy Young Man

The American Journal of Gastroenterology
Forensic Toxicology and Drug Analysis
article

S5754 When the Party Ends: Methamphetamine Induced Acute Liver Failure in a Healthy Young Man

article en

Abstract

Introduction: Methamphetamine abuse is a growing public health concern with well-documented neuropsychiatric and cardiovascular effects. However, acute liver failure induced by methamphetamine is rare, underreported, and not widely recognized among clinicians. Presenting this case highlights the potential severity of methamphetamine toxicity and aims to increase awareness of its hepatic complications in young, otherwise healthy patients. Case Description/Methods: A 22-year-old previously healthy male was brought to the emergency department unresponsive after suspected methamphetamine use. EMS found him apneic; bag-valve ventilation was initiated en route. On arrival, his Glasgow Coma Scale was 3, prompting immediate intubation and intensive care unit admission. Initial exam revealed intermittent posturing, sluggish pupils, and scattered skin lesions suggestive of intravenous drug use. Urine drug screen was positive for amphetamines and cannabinoids. Laboratory work showed rapidly rising liver enzymes: aspartate aminotransferase peaked at 2,825 U/L and alanine aminotransferase at 3,589 U/L, with international normalized ratio (INR) increasing to 1.6 and bilirubin peaking at 4.5 mg/dL. MELD score rose from 16 to 26 before improving. Acetaminophen levels were within normal limits; hepatitis panel was negative; and imaging was unremarkable. No hypotensive episodes occurred. The patient was diagnosed with methamphetamine-induced acute liver failure after excluding other causes. He also developed rhabdomyolysis and acute kidney injury, requiring 5 sessions of hemodialysis. With supportive care, liver and renal function progressively improved. At discharge, liver enzymes, INR, bilirubin, and renal function normalized, and dialysis was discontinued. He was referred for rehabilitation. Follow-up labs confirmed complete hepatic recovery, and he remained sober at follow-up. confirmed complete recovery of liver function. The patient remained sober at follow-up. Discussion: This case highlights methamphetamine as a rare but potentially life-threatening cause of acute liver failure. Hepatotoxicity may result from direct cellular injury or ischemia due to methamphetamine-induced vasoconstriction and hyperthermia. While liver transplantation is the mainstay for irreversible acute liver failure, this case demonstrates that full recovery is possible in select patients with drug-induced liver injury, particularly when other etiologies are excluded and complications are promptly managed. Early recognition and aggressive supportive care may prevent the need for transplant in otherwise healthy individuals.

The American Journal of GastroenterologyVol. 120(10S2)
Good health and well-being
Openalex Percentile: Top 37%
Forensic Toxicology and Drug Analysis
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