S1425 An Atypical Presentation of COVID-19 as Acute Pancreatitis

Abstract

INTRODUCTION: While gastrointestinal manifestations of the novel coronavirus infection (COVID-19) viral infection is reported, the extent of organ involvement is unknown. Effect of the virus on the pancreas is unclear. We report a rare case of viral acute pancreatitis (AP) likely secondary to COVID-19 infection. CASE DESCRIPTION/METHODS: 34 year-old healthy hispanic male presented with epigastric pain, bilious vomiting and nausea for 5 days. He endorsed shortness of breath, cough, fever, chills and recent exposure to a known COVID-19 positive patient. He denied previous surgeries, medication or alcohol use. Vital signs were BP 156/90, HR 112, T103 F, R20 with 98% saturation on room air. Exam was pertinent for epigastric tenderness to palpation. As seen in Table 1, labs showed elevated lipase, transaminitis and acute kidney injury on admission. He was admitted to medicine for presumed COVID viral infection and started on ceftriaxone, azithromycin, hydroxychloroquine and IV fluids. Subsequent nasal swab was positive for SARS-COV-2 viral infection. On day 3, the patient complained of worsening abdominal pain, fever of 103.6 and elevation of lipase to 211, greater than 3 times ULN ( >200 U/L). Liver function enzymes, lipase and inflammatory peaked on day 5 with subsequent clinical improvement. Further investigations were negative for causes of AP including hypertriglyceridemia, hypocalcemia, gallstones, autoimmune pancreatitis, leading to diagnosis of exclusion of acute pancreatitis secondary to COVID-19 viral infection. Patient improved clinically with complete resolution of fever and abdominal pain on day 9, and was discharged with outpatient follow up. DISCUSSION: Although AP due to has been known to be caused by a few viruses (CMV, Mumps, and Influenza), the effect of COVID-19 on the pancreas is unclear. There are only four reports of AP attributed to COVID-19. While Wang et al. reported pancreatic injury in COVID-19 patients, the elevations in pancreatic enzymes were mild, and there were no signs of clinical AP. Our case features a patient with COVID-19 infection presenting with predominantly gastrointestinal symptoms that resolved on symptomatic management as the viral inflammatory response subsided. Possible mechanisms include virus affinity to ACE-2 receptors, expressed in pancreatic islet cells and cytotoxic injury from inflammatory response. By outlining this rare gastrointestinal manifestation of COVID-19, we hope to improve current clinical understanding.Table 1.: Laboratory values through hospital stay showing rising lipase, liver function tests and inflammatory markers