2443 Dealing With DILI: When the Diagnosis Is Not Always Clear Cut

Abstract

INTRODUCTION: Drug induced liver injury (DILI) is a rare, mostly reversible cause of liver failure (ALF); however, in rare cases DILI can unmask or trigger underlying chronic liver disease. We present a case of DILI with two novel findings: one, the patient consumed tea extract not yet cited on the LiverTox registry, and two, the patient's DILI likely triggered autoimmune hepatitis (AIH), an occurrence noted only a few times in the literature. CASE DESCRIPTION/METHODS: Patient is a 43-year-old female with no medical history who presented with acute onset jaundice and dark urine. She endorsed a “tea cleanse” which included dandelion roots, milk thistle and barks one month prior to admission. Her jaundice persisted despite cessation of the herbal tea intake. Liver function tests (LFTs) showed AST 2553, ALT 3022, alkaline phosphatase 135, total bilirubin 23.8, direct bilirubin 15.5, INR 1.8 and MELD 25. MRCP was consistent with acute hepatitis. ALF workup was negative except for elevated IgG1 and IgG4. Liver biopsy revealed panlobular mixed inflammatory cell infiltrate and necrosis but absent fibrosis, concerning for DILI, viral infection or AIH. Patient was managed supportively for DILI with downtrending LFTs. However, her LFTs worsened with total bilirubin 20 and INR 2.1. She developed ascites and lower extremity edema. The patient received corticosteroids for AIH despite negative ANA, anti-smooth muscle and anti-LKM antibodies with marked improvement in synthetic liver function. DISCUSSION: Although acetaminophen is the most common offending drug associated with DILI (40-50% of ALF cases annually), herbal or dietary supplements are not an uncommon cause, seen in 11-12% of cases per year. Accurate diagnosis of DILI can be made with clinical history, exclusion of other etiologies of ALF on laboratory evaluation, and with liver biopsy. The database LiverTox documents etiologies of DILI. “Be Well Teas,” consumed by our patient, yields no results but should be included to prevent future DILI cases. Further, despite biopsy consistent with DILI, rebound of total bilirubin and INR in our patient demanded further investigation. Likely the patient had pre-existent AIH triggered by DILI given her improvement with immunosuppression, cited previously in only in a few case reports. Concurrent, underlying AIH should be considered with relapse of liver dysfunction despite cessation of the inciting drug.