Abstract

INTRODUCTION: COVID-19 is a global pandemic. However, the effects of underlying liver disease on COVID-19 in the United States is not well described. We investigated whether COVID-19 was associated with elevations in liver enzymes or hepatic decompensation in patients with underlying hepatic steatosis. METHODS: We retrospectively reviewed the charts of consecutive adults with RT-PCR positive for COVID-19 treated at Michigan Medicine between March 1 and April 30, 2020, who had ultrasound, computed tomography, or magnetic resonance imaging >30 days before COVID-19 diagnosis. Hepatic steatosis was defined based on imaging. Outcomes were: (1) peak ALT or bilirubin following COVID-19 diagnosis, (2) ALT >2 or 5 times upper limit of normal (ULN), defined as the higher of baseline ALT or 19 U/L in women and 30 U/L in men, (3) jaundice defined as bilirubin >2 or 4 mg/dl, and (4) new/worsening ascites or encephalopathy. We conducted regressions with the above outcomes as dependent variables and hepatic steatosis as the primary predictor, adjusting for age, sex, race, recent healthcare exposure, body mass index, hypertension, dyslipidemia, and diabetes. These regression models were logistic for outcomes of abnormal ALT or bilirubin, and linear for maximal ALT or bilirubin. RESULTS: Of patients with prior imaging, 80/159 (50.3%) had steatosis. Overall, 89% of patients were hospitalized, 51% were admitted to intensive care, and 16% died. 14% had chronic liver disease other than NAFLD, 5% had cirrhosis, and 2.7% had prior liver decompensation with ascites, variceal bleeding, or hepatic encephalopathy. Patients with steatosis were older, had higher body mass index, and were more often Black than those without steatosis (Table 1). Baseline ALT and total bilirubin were higher in the steatosis group (Table 1). Hepatic steatosis was associated with increased incidence of ALT >2x ULN (OR 2.93 [1.23–6.97]) or >5x ULN (OR 6.21 [1.45–26.62]), and with peak ALT (beta 39.7 [7.85–71.49]) (Table 2). Hepatic steatosis was not associated with increased bilirubin (Table 2). Rates of new/worsening ascites and encephalopathy were very low: 1.3% and 2.5%, respectively, with no difference based on NAFLD status (P > 0.4 for both). CONCLUSION: Hepatic steatosis is associated with acute hepatocellular injury with COVID-19 infection. Steatosis was not associated with jaundice. Rates of new/worsening ascites or hepatic encephalopathy were very low and unrelated to steatosis status.Table 1Table 2

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