Mitragyna Speciosa (Kratom)-Induced Cholestatic Hepatitis

Abstract

Purpose:Mitragyna speciosa Korth (vernacular name: kratom) is a tall, leafy tree in the family Rubiaceae. Kratom leaves have long been used as a narcotic and central nervous system stimulant. Herein, we report the first case of cholestatic hepatitis due to kratom use. Methods: A 34-year-old female with no significant past medical history was referred for evaluation of her extreme fatigue, pruritus, and jaundice. She was well until two weeks prior, when she started having back aches, for which she took a half-spoon of kratom for two consecutive days. Within a week, she started feeling fatigued, which subsequently worsened, and extreme pruritus ensued. The patient also noticed dark-colored urine and clay-colored stools. She denied any abdominal pain, fever, nausea, vomiting, chills, melena, rashes, confusion, excessive alcohol drinking, recent travel, intravenous drug abuse, or recent antibiotic use. She endorsed taking less than 2 grams of acetaminophen daily for the last three days. On examination, she was oriented to person, place, and time, with scleral icterus and multiple excoriation marks. No stigmata of chronic liver disease were noticed. Abdominal and neurological examinations were unremarkable. Upon presentation, liver biochemistries revealed alanine aminotransferase (ALT) 93 U/L [range: 12-78 U/L], aspartate aminotransferase (AST) 61 U/L [range: 15-37 U/L], alkaline phosphatase (ALP) 298 U/L [range: 50-136 U/L), and total bilirubin: 10.6 mg/dl [range: 0.2- 1.0 mg/dl]. No evidence of coagulopathy was noted. Serological tests for Hepatitis A, B, C, Epstein-Barr virus, cytomegalovirus, and auto immune hepatitis were negative. Her urine toxicology was negative, and alcohol level was normal. Wilson's disease, alpha 1 antitrypsin deficiency, primary biliary cirrhosis, and hemochromatosis were ruled out by appropriate testing. The patient was initially started on N-Acetylcysteine (NAC) protocol for potential acetaminophen toxicity. Abdominal ultrasound and hepatobiliary scan revealed no evidence of common bile duct obstruction. She was started on ursodiol 10 mg/kg/day and hydroxyzine for pruritus. Liver biopsy was preformed, which revealed cholestasis, lobular inflammation, and increased eosinophils within sinusoids, consistent with drug-induced liver injury. Given the absence of coagulopathy or encephalopathy, she was discharged home with follow-up. An appointment 40 days later revealed complete normalization of liver function tests and resolution of clinical symptoms. Conclusion: To our knowledge, this is the first reported case of kratom-induced cholestatic hepatitis. This case highlights the need for physicians to consider widely available substances, especially herbal supplements, when evaluating cholestatic liver injury.