S3532 Severe Transaminitis and Acute Renal Failure in a Teenage Patient

Abstract

INTRODUCTION: Alcoholic hepatitis is one of the many different causes of acute onset of symptomatic severe transaminitis. Though the exact amount of alcohol consumption that places an individual at risk is unknown, the majority of patients endorse heavy alcohol use for several decades. We present a rare case of alcoholic hepatitis in a teenager with a marked 250-fold increase in ALT and 137-fold increase in AST. CASE DESCRIPTION/METHODS: A 19-year-old female presented with nausea and multiple episodes of nonbilious, nonbloody vomiting. She reported drinking a large amount of hard liquor at a party three days before going to the hospital and since then, she developed nausea, vomiting, worsening right upper quadrant abdominal pain, weakness, and fatigue. Patient worked as a bartender and endorsed drinking significant amounts of hard liquor on a daily basis. Labs showed ALT 11,780 (4–47), AST 5492 (15–40), INR 2 (0.9–1.2). Patient was given IV Acetadote for several days until AST and ALT were below 1000. She was placed on folic acid, multivitamin, and thiamine for alcohol use disorder. Patient’s creatinine (Cr) on admission was 1.41 but peaked at 9.09 (0.3–1.2), causing concern for the need to initiate dialysis. UA showed hematuria and proteinuria. Abdominal US demonstrated no hydronephrosis. Tylenol and salicylate level were normal, and the hepatitis panel was nonreactive. Ultrasound of the abdomen with Doppler to evaluate for Budd-Chiari showed normal flow and hepatic vessels. Ceruloplasmin, ANA, anti-smooth muscle antibody, and antimitochondrial antibody were all negative. EBV antibody IgG was elevated 490 ((0–17.9 U/mL), EBV nuclear antibody was IgG 477 (0–17.9 U/mL), and EBV Ab IgM was non-reactive signifying past EBV infection. Mitochondrial Ab, RPR, CRP, C-ANCA, MPO Ab, PR-3 Abs, and P-ANCA were all non-reactive. The patient was discharged once LFTs, INR, and Cr all decreased to normal levels. DISCUSSION: There are many causes of acute hepatitis, including viruses, ischemia, and drug toxicity. Patients usually have elevated transaminases, AST/ALT ratio greater than 2, and elevated INR due to the inflamed liver’s decreased production of coagulation factors. Higher transaminase levels, such as those in the patient, raise the suspicion of concurrent viral or ischemic hepatitis or Tylenol use (which can be toxic in therapeutic doses in patients who abuse alcohol). It is crucial to counsel the patient on treatment for alcohol use disorder once the acute episode of hepatitis has resolved.