S5928 Liver Transplantation Due to Khat Ingestion

Introduction: Khat is a plant cultivated and consumed primarily in the Arabian and East African countries. Chewing khat has been a longstanding social tradition in these regions since the 13th century. In the US, Khat is classified as a controlled substance, making its possession or use illegal. As a result, patients may be reluctant to disclose their khat use to their physicians. Case Description/Methods: A 25-year-old man patient, who immigrated recently from Yemen, with a past medical history of hepatitis and possible cirrhosis, presented with worsening jaundice and dark urine. Physical examination showed normal vital signs but there were scleral icterus and jaundiced skin without any abdominal tenderness. Initial labs showed aspartate aminotransferase 368, alanine aminotransferase 438, Alkaline Phosphatase 351, total bilirubin 21.8, direct bilirubin 19, gamma-glutamyl transferase 331, ammonia 123, PT 15.6, international normalized ratio 1.2, aPTT 28.8. The viral hepatitis panel was negative, except for a history of hepatitis A indicated by IgG. Alpha one antitrypsin and ceruloplasmin were normal. ANCA and anti mitochondrial antibodies were negative. MRCP showed liver cirrhosis without any hepatic mass or portal hypertension. Although ANA and anti-smooth muscle antibodies were positive, liver biopsy was consistent with drug-induced hepatotoxicity “marked cholestasis with feathery degeneration and patchy lobular necroinflammation, enlarged portal tract with mild lymphoplasmacytic inflammation mixed with eosinophils, bile duct damage and reaction”. Upon questioning the patient about any drug abuse, he reported using Khat frequently. Six years later the patient was presented with decompensated liver cirrhosis, ascites, and spontaneous bacterial peritonitis. MELD-Na score: 29 and MELD score: 26. EGD showed esophageal varices. MRCP showed liver cirrhosis with no HCC. The patient was listed for liver transplantation during this admission and underwent the LT on 11/2019. Discussion: The first documented case of acute hepatitis linked to khat use was reported in the UK in 2005. The exact mechanism behind khat-induced liver damage remains unclear. However, there is a theory suggests that liver toxicity is caused by khat alkaloids, which undergo extensive hepatic metabolism. Alternative theories propose that khat use can trigger autoimmune mechanisms, leading to liver injury in individuals with a genetic predisposition. Further research is needed to better understand the underlying mechanisms of khat-induced liver injury, with the goal of developing effective treatment options for this condition.

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Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001151172.02968.3b
Primary Topic
Forensic Toxicology and Drug Analysis
Type
article
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article

S5928 Liver Transplantation Due to Khat Ingestion

Ahmed Elhawary, Mohamed Eldesouki, Joseph A. Odin
The American Journal of Gastroenterology
Forensic Toxicology and Drug Analysis
article

S5928 Liver Transplantation Due to Khat Ingestion

Ahmed Elhawary, Mohamed Eldesouki, Joseph A. Odin
article en

Abstract

Introduction: Khat is a plant cultivated and consumed primarily in the Arabian and East African countries. Chewing khat has been a longstanding social tradition in these regions since the 13th century. In the US, Khat is classified as a controlled substance, making its possession or use illegal. As a result, patients may be reluctant to disclose their khat use to their physicians. Case Description/Methods: A 25-year-old man patient, who immigrated recently from Yemen, with a past medical history of hepatitis and possible cirrhosis, presented with worsening jaundice and dark urine. Physical examination showed normal vital signs but there were scleral icterus and jaundiced skin without any abdominal tenderness. Initial labs showed aspartate aminotransferase 368, alanine aminotransferase 438, Alkaline Phosphatase 351, total bilirubin 21.8, direct bilirubin 19, gamma-glutamyl transferase 331, ammonia 123, PT 15.6, international normalized ratio 1.2, aPTT 28.8. The viral hepatitis panel was negative, except for a history of hepatitis A indicated by IgG. Alpha one antitrypsin and ceruloplasmin were normal. ANCA and anti mitochondrial antibodies were negative. MRCP showed liver cirrhosis without any hepatic mass or portal hypertension. Although ANA and anti-smooth muscle antibodies were positive, liver biopsy was consistent with drug-induced hepatotoxicity “marked cholestasis with feathery degeneration and patchy lobular necroinflammation, enlarged portal tract with mild lymphoplasmacytic inflammation mixed with eosinophils, bile duct damage and reaction”. Upon questioning the patient about any drug abuse, he reported using Khat frequently. Six years later the patient was presented with decompensated liver cirrhosis, ascites, and spontaneous bacterial peritonitis. MELD-Na score: 29 and MELD score: 26. EGD showed esophageal varices. MRCP showed liver cirrhosis with no HCC. The patient was listed for liver transplantation during this admission and underwent the LT on 11/2019. Discussion: The first documented case of acute hepatitis linked to khat use was reported in the UK in 2005. The exact mechanism behind khat-induced liver damage remains unclear. However, there is a theory suggests that liver toxicity is caused by khat alkaloids, which undergo extensive hepatic metabolism. Alternative theories propose that khat use can trigger autoimmune mechanisms, leading to liver injury in individuals with a genetic predisposition. Further research is needed to better understand the underlying mechanisms of khat-induced liver injury, with the goal of developing effective treatment options for this condition.

The American Journal of GastroenterologyVol. 120(10S2)
Openalex Percentile: Top 59%
Forensic Toxicology and Drug Analysis
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