S5582 From Pacific Isles to Liver Trials: Unraveling the Toxic Tale of Kava

Introduction: Kava, a drink consumed across several South Pacific islands, has grown in popularity for its sedative, hypnotic, and muscle relaxant effects. As its use increases, understanding its toxicological profile becomes crucial. A pilot health survey has shown that heavy kava use has been linked to hematological conditions, liver damage, and rashes. Here we present a case of a 20-year-old woman patient, with no significant past medical history, admitted with elevated liver enzymes and a diffuse rash in the setting of kava use. Case Description/Methods: The patient presented with a 5-day history of facial edema and a worsening pruritic, vesiculopustular rash involving her abdomen, extremities, face, and scalp. She had associated symptoms of fevers, chills, and nausea. Prior to presentation, significant changes to her medication history included recent kava tea consumption. On admission, she was febrile to 100.4°F, but otherwise hemodynamically stable. Labs were significant for mild leukocytosis, and anemia, platelets at 194 10³/µL, hepatocellular pattern of liver injury (aspartate aminotransferase 117 U/L alanine aminotransferase 195 U/L alkaline phosphatase 128 U/L), and total bilirubin 0.4. ESR and C-reactive protein elevated. She did not demonstrate evidence of encephalopathy or synthetic dysfunction. Hepatitis panel, HIV, tick-borne panel, and autoimmune panel were all negative. Ultrasound of the right upper quadrant was only significant for mild hepatomegaly. The patient ultimately underwent a skin biopsy which revealed pathology suspicious for drug-induced/supplement-induced hypersensitivity reactions. She was started on a steroid taper resulting in an improvement in her rash, symptoms and liver enzymes. The timing of symptom onset relative to kava consumption and the exclusion of other causes of acute liver injury, support a diagnosis of drug-induced liver injury (DILI) from Kava. Discussion: Kava-induced hepatotoxicity results from oxidative stress in hepatocytes. Oftentimes kava results in a hepatocellular pattern of injury that can progress to fulminant liver injury. There have been 30 reported incidences of hepatotoxicity in Europe and 4 have required transplants. The hepatotoxic potential of kava necessitates caution. This case underscores the warnings issued by health authorities and adds to the growing body of evidence on kava toxicity. Furthermore, this case emphasizes the importance of considering herbal supplements as part of a comprehensive medication history, when evaluating patients with unexplained elevated liver enzymes.