S2626 Alcoholic Hepatitis and COVID-19: The Question of Steroids

Abstract

INTRODUCTION: The SARS-CoV-2/Novel Coronavirus-19 (COVID-19) has created new challenges for managing acute alcoholic hepatitis (AH). The decision to initiate steroids in AH is now more difficult, as data suggests worsened outcomes in COVID-19 patients treated with steroids. How patients with AH respond to steroids while also COVID-19 infected is an open question. We present a case of severe AH in a COVID-19 infected patient who received steroids. CASE DESCRIPTION/METHODS: Fifty-seven-year-old man with chronic alcohol abuse and alcoholic cirrhosis with portal hypertension presented with dry cough, fatigue, and melena. He had been drinking 1 pint of vodka daily for 1 week. He had normal hemodynamics and oxygen saturation was 98% on room air. Rectal exam was unremarkable. Laboratory data showed normal BUN/Cr, Hgb/Hct 6.4 g/dL/21.6%, PLT 54 K/mL, total bilirubin/direct bilirubin 10.3 mg/dL/ 6.0 mg/dL, Alk Phos 162 IU/L, AST 260 IU/L, ALT 53, and INR 1.9. Viral hepatitis panel was unremarkable. COVID-19 PCR was positive. Chest x-ray revealed bibasilar opacities. Right upper quadrant ultrasound with doppler revealed liver with cirrhotic morphology and no portal vein thrombosis. MDF was 59.1. MELD score was 22. He was started on an octreotide infusion, IV pantoprazole, and IV ceftriaxone. On hospital day 3, he became encephalopathic and was started on lactulose and rifaximin. He developed hepatorenal syndrome and was treated with albumin. He then had worsening coagulopathy and a rising total bilirubin. MDF increased to 37 and prednisolone 40mg daily was started. Seven days into therapy, total bilirubin down trended and kidney function improved. Lille score was 0.980. Although the Lille score suggested he may be a steroid non-responder, his improved mental status, total bilirubin and kidney function led to the decision to treat for 28 days. DISCUSSION: The COVID-19 pandemic creates a new challenge in treating AH. The recommendation is that steroids should be avoided in viral infections. The decision to initiate steroids in patients with AH is influenced by the MDF. However, steroid initiation based on MDF becomes problematic as hepatic injury is a known consequence of COVID-19. Thus, an elevated score may not solely be related to alcohol-induced inflammation. In our case, risk of mortality appeared to be driven by AH and thus steroids were initiated. Despite being a non-responder per the Lille score, the patient improved. This case reveals that it may be safe to use steroids in patients with severe AH and COVID-19 positivity.