Case Presentation:
A 25 year‐old Yemini man presented with three months of progressively worsening jaundice. The patient had no past medical history and physical exam was negative for stigmata of chronic liver disease. Laboratories were significant for a transaminitis (1000 U/L, ratio 1:1) and a predominantly direct hyperbilirubinemia (total 30 mg/dL) with relative preservation of synthetic liver function (albumin 3.2; INR 1.2). Liver Doppler and MRCP revealed a nodular liver with patent hepatic vessel and no evidence of portal hypertension, biliary ductal dilatation, or hepatic mass. Viral serologies were negative. ANA was positive (titer 1:640) as was smooth muscle antibody; immunoglobulin levels were normal. Further serologic studies to investigate other etiologies of underlying cirrhosis were unrevealing. Urine toxicology was negative but the patient endorsed a seventeen‐year history of heavy khat use. Liver biopsy revealed broad bridging fibrotic septa indicative of cirrhosis as well as cholestasic hepatitis most consistent with drug‐induced liver injury (DILI). The patient was treated with high dose oral steroids with improvement in transaminase and bilirubin levels, which later worsened on discontinuation of the steroids. The patient had a MELD of 19 and underwent orthotopic liver transplant workup.
Discussion:
In the Western world, DILI is responsible for nearly half of all cases of jaundice. Hospitalists are adept at identifying common causal substances such as alcohol, but often do not consider less common drugs such as khat (Catha edullis). A plant native to the Arabian Peninsula and Africa, khat is used for its amphetamine‐like properties. In animal studies, khat has been associated with dose and duration‐dependent liver injury. Several small case series have reported similar hepatotoxic effects in humans who chew the leaf. There is insufficient data to suggest an effective treatment other than supportive care, khat discontinuation, and transplantation in cases that have progressed to liver failure. Two case series document immunosuppressive treatment but either did not comment on treatment response or reported no response in cases of autoantibody‐negative severe liver injury. Here, we report a case of autoantibody‐positive khat‐induced liver injury where liver function improved on initiation of high dose steroids and subsequently worsened upon discontinuation of treatment. This case supports the hypothesis that steroid therapy may benefit a subset of patients with khat‐induced liver injury who have positive antibody titers.
Conclusions:
Khat‐related liver injury may be underreported, and cases may continue to increase in parallel with khat use, distribution, and migration of its users around the globe. This case to our knowledge is the first reported in the United States. As hospitalists we commonly encounter acute jaundice in the setting of liver dysfunction, and identification of cases related to rare culprits such as khat remains imperative to elucidating disease course, clinical features, histology, and personalized treatment options.