Abstract
INTRODUCTION: The clinical presentation of pancreatitis in the course of novel coronavirus infection (COVID-19) is not well understood. The etiology may be a direct cytopathic effect mediated by local SARS-CoV-2 replication versus an injury caused by the cytokine release induced by the infection. We present 2 cases of COVID-19-associated pancreatitis. Both had severe multi-organ failure requiring ventilator and dialysis support. CASE DESCRIPTION/METHODS: Case 1: 57 year old man with diabetes mellitus type 2 and hypertension presented with a PCR-confirmed COVID-19 infection. Leukocytes were 14.6 K/uL and C-reactive protein was 89⋅7 g/L, AST was 98 IU/L, ALT was135 IU/L, and INR was 1⋅3. Serum amylase and lipase levels were 398 IU/L and 2726 IU/L, respectively. Triglyceride level was179 mg/dL. He had no alcohol use and viral hepatitis panel and urine drug scree were all negative. After extubation, he ate well with minimal symptoms despite lipase levels peaking at 3,369 IU/L on day 11 and declined only to peak again on day 20 to 4,620 IU/L. C-reactive protein remained under 10 g/L during the first peak and began to climb only with the second peak. He was discharged on day 23 with lipase declining to 2,856 IU/L while asymptomatic and off dialysis. Case 2: 70 year old man was admitted with PCR confirmed COVID19 systemic infection requiring mechanical ventilation. Two weeks after extubation, he developed mild abdominal pain and anorexia that promptly resolved but his lipase level was found to be 1,874 IU/L. This continued to fluctuate mildly down to 1,247 IU/L over 10 days despite lack of symptoms. DISCUSSION: Viral pancreatitis has been reported with Coxsackie virus, CMV, HIV, HSV, mumps, VZV, among others. We describe pancreatitis associated with COVID-19 that may be related to direct viral invasion. Both persons had conspicuously absent symptoms despite substantial elevations of lipase levels. In both, the amylase paralleled the lipase levels trending while but there was no correlation between these enzyme levels and those of C-reactive protein making cytokine release less probable as an etiology.
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