2471 UnDRESSing Elevated Liver Enzymes

Abstract

INTRODUCTION: The differential diagnosis for liver transaminases over 1000 units/liters typically includes liver ischemia, acute viral hepatitis, acetaminophen-induced liver toxicity, autoimmune hepatitis, Wilsonian crisis, or acute Budd-Chiari. Prompt evaluation and exclusion of these causes must be completed as many of these etiologies can ultimately lead to fulminant liver failure. We present a case of liver transaminases over 1000 units/liter from an atypical etiology. CASE DESCRIPTION/METHODS: A 52-year-old male with hypertension, CKD stage 5, gastroesophageal reflux disease, and gout presented with intermittent fevers of 39C. He was recently hospitalized for Clostridium difficile colitis and treated with oral vancomycin. During this hospitalization he was started on allopurinol for an acute gout flare. Soon after starting allopurinol, he developed a diffuse morbilliform rash. On initial exam, vitals were within normal limits and temperature was 39C. Laboratory data revealed white blood cell count within normal limits, hemoglobin 7.9 gm/dL, platelet count 71 K/mcl, INR 1.1, AST 878 unit/L, ALT 1,117 unit/L, AKI, and peripheral eosinophilia. Viral hepatitis serologies, autoimmunity studies, as well as viral markers for EBV, CMV, HSV, and varicella were negative. Ceruloplasmin, Alpha 1 antitrypsin, and acetaminophen levels were within normal limits. N-acetylcysteine was administered due to suspicion for drug-induced liver injury. Given that he had taken allopurinol two weeks before presentation, presented with fevers, rash, and renal impairment and now developed peripheral eosinophilia, DRESS syndrome secondary to allopurinol was diagnosed. DISCUSSION: Drug reaction with eosinophilia and systemic symptoms (DRESS) is a rare, potentially life-threatening, drug-induced hypersensitivity reaction. Diagnosis is suspected in a patient who received a drug treatment in the previous two to six weeks and subsequently presents with characteristic symptoms including skin rash, liver involvement, hypereosinophilia, and lymphadenopathy. Dress typically causes transaminase elevations, but usually not in the 1000s, as was seen in our patient. The pathogenesis is hypothesized to involve a genetically deficient detoxifying enzyme resulting in an accumulation of drug metabolites. Supportive therapy and prompt withdrawal of the offending agent is the primary treatment for drug hypersensitivity reactions. Additionally, N-acetylcysteine has been shown to significantly increase survival in cases of drug-induced liver failure.