Introduction: As the 2019 coronavirus (COVID-19) pandemic reached the United States, there remained a paucity of literature on gastrointestinal (GI) manifestations. Severe acute respiratory syndrome coronavirus (SARS-CoV) 2 uses the angiotensin-converting enzyme 2 receptor (ACE2-R) to gain cellular entry into the lower respiratory tract, which is also highly expressed in GI epithelial cells. GI manifestations such as abdominal pain, nausea and diarrhea have now been well established. However, pancreatic injury due to COVID-19 has been scarcely reported.
Methods: A 72 year-old male with past history of diabetes mellitus and hypertension presented with 3 days of fever and dry cough. He was found to have COVID-19 pneumonia and was treated with IV antibiotics and hydroxychloroquine. He subsequently developed acute hypoxic respiratory failure, requiring intubation. Multiorgan failure ensued with mixed septic and cardiogenic shock, and acute renal failure. Strikingly, the patient required increasing amounts of insulin to maintain blood glucose between 140-180 mg/dL. His diabetes was well-controlled with a baseline hemoglobin A1c of 6.6% on admission. Therefore, it was unexpected that he required 70 units of insulin detemir BID (table 1) in addition to a sliding scale to maintain goal blood glucose. Pancreatic insufficiency was suspected and lipase was trended from normal to a peak of 2,538 unit/L (table 2). His lipase level and insulin requirement trended down to 7 units daily as he initially improved. Unfortunately, the patient expired due to fulminant viral illness and multiorgan failure. Discussion: In a recent retrospective study from Zhongnan Hospital of Wuhan University in China, 17% of 52 patients with COVID-19 pneumonia had pancreatic injury defined by amylase or lipase abnormality. Only 11% of these patients had abnormal blood sugar levels. Theoretically, COVID-19 infection could cause islet damage due to the high ACE2-R expression in pancreatic islet cells, resulting in pancreatic insufficiency. This was established during the SARS-CoV of 2003 as a mechanism of pancreatic injury. Pancreatic injury in COVID-19 could be secondary to this direct cytopathic effect or due to indirect systemic inflammatory and immune-mediated cellular response to severe SARS-COV-2 infection. We urge clinicians to be aware of a potential subset of patients that may have clinical pancreatic insufficiency as a presenting or concomitant disease entity in COVID-19 infection.