S5639 Kratom-Induced Acute Liver Failure in a Healthy Adult

Introduction: Kratom is a popular, unregulated herbal supplement used for its psychotropic and opioid-like effects. Despite its widespread perception as safe, Kratom has been increasingly implicated in drug-induced liver injury (DILI), with rare reports of acute liver failure (ALF). We present a case of ALF in a previously healthy individual following Kratom use. Case Description/Methods: A 43-year-old woman with a past medical history of plaque psoriasis presented to the emergency room with confusion, nausea, and jaundice for the past week. She reported drinking multiple bottles of Kratom daily for chronic back pain for the past 5 months. She denied any prior liver disease, alcohol, or illicit substance use. She started drinking Kratom 5 months prior for her chronic back pain. Liver function tests (LFTs) were notable for a bilirubin of 23 mg/dL, alkaline phosphatase 1,436 U/L, aspartate aminotransferase 644 U/L, alanine aminotransferase 115 U/L, and international normalized ratio 1.18. Physical exam was notable for jaundice with no asterixis. Ultrasound showed a non-specific finding of coarsened hepatic echotexture. MRI MRCP showed no evidence of biliary tree pathology. Liver biopsy showed severe portal and lobular hepatitis with small bile duct injury and a predominantly lymphocytic infiltrate containing plasma cells, neutrophils, and eosinophils. Liver serological workup was unremarkable for alternative etiologies of elevated liver enzymes. She was started on empiric N-acetylcysteine for 3 days and Budesonide 9 mg daily for one week, with improvement in LFTs. Strict stoppage of Kratom was advised. At the 2-month follow-up, LFTs showed continued improvement, with bilirubin levels down to 3.9 mg/dL. Discussion: Acute liver failure from Kratom is a rare but serious side effect. As there are over 40 metabolites in Kratom, the exact mechanism of liver injury is unclear. Unlike most reported cases with a 1–8 week latency, our patient developed peak bilirubin levels after 5 months, suggesting that Kratom-induced injury may follow a prolonged or subclinical course. Biopsy findings were consistent with resolving drug-induced liver injury. Notably, the patient recovered without transplantation, highlighting the potential for reversibility with early recognition. Given Kratom’s wide availability and perceived safety, clinicians should maintain a high index of suspicion, especially in younger patients presenting with unexplained liver injury and no traditional risk factors.

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Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001150016.15318.9b
Primary Topic
Alkaloids: synthesis and pharmacology
Type
article
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article

S5639 Kratom-Induced Acute Liver Failure in a Healthy Adult

Matthew C. Cave, Sanjiv Patel
The American Journal of Gastroenterology
Alkaloids: synthesis and pharmacology
article

S5639 Kratom-Induced Acute Liver Failure in a Healthy Adult

Matthew C. Cave, Sanjiv Patel
article en

Abstract

Introduction: Kratom is a popular, unregulated herbal supplement used for its psychotropic and opioid-like effects. Despite its widespread perception as safe, Kratom has been increasingly implicated in drug-induced liver injury (DILI), with rare reports of acute liver failure (ALF). We present a case of ALF in a previously healthy individual following Kratom use. Case Description/Methods: A 43-year-old woman with a past medical history of plaque psoriasis presented to the emergency room with confusion, nausea, and jaundice for the past week. She reported drinking multiple bottles of Kratom daily for chronic back pain for the past 5 months. She denied any prior liver disease, alcohol, or illicit substance use. She started drinking Kratom 5 months prior for her chronic back pain. Liver function tests (LFTs) were notable for a bilirubin of 23 mg/dL, alkaline phosphatase 1,436 U/L, aspartate aminotransferase 644 U/L, alanine aminotransferase 115 U/L, and international normalized ratio 1.18. Physical exam was notable for jaundice with no asterixis. Ultrasound showed a non-specific finding of coarsened hepatic echotexture. MRI MRCP showed no evidence of biliary tree pathology. Liver biopsy showed severe portal and lobular hepatitis with small bile duct injury and a predominantly lymphocytic infiltrate containing plasma cells, neutrophils, and eosinophils. Liver serological workup was unremarkable for alternative etiologies of elevated liver enzymes. She was started on empiric N-acetylcysteine for 3 days and Budesonide 9 mg daily for one week, with improvement in LFTs. Strict stoppage of Kratom was advised. At the 2-month follow-up, LFTs showed continued improvement, with bilirubin levels down to 3.9 mg/dL. Discussion: Acute liver failure from Kratom is a rare but serious side effect. As there are over 40 metabolites in Kratom, the exact mechanism of liver injury is unclear. Unlike most reported cases with a 1–8 week latency, our patient developed peak bilirubin levels after 5 months, suggesting that Kratom-induced injury may follow a prolonged or subclinical course. Biopsy findings were consistent with resolving drug-induced liver injury. Notably, the patient recovered without transplantation, highlighting the potential for reversibility with early recognition. Given Kratom’s wide availability and perceived safety, clinicians should maintain a high index of suspicion, especially in younger patients presenting with unexplained liver injury and no traditional risk factors.

The American Journal of GastroenterologyVol. 120(10S2)
Openalex Percentile: Top 52%
Alkaloids: synthesis and pharmacology
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