The pancreas and COVID-19: a clinical conundrum

Abstract

With the progression of the COVID-19 pandemic, the classic manifestations of COVID-19 (e.g., persistent fever, dry cough, pneumonia, and acute respiratory distress syndrome in the severe disease) have expanded to include less common complications of the extrapulmonary organs. Recent evidence has shown that COVID-19 patients with concomitant presence of GI symptoms are at higher risk of developing severe disease and have poor clinical outcomes. Recently, multiple SARS-CoV-2-induced acute pancreatitis (AP) cases have been reported. This literature review aims to provide an insight into SARS-CoV-2-directed invasion of the pancreas. We will also review the currently available literature on the clinical effects of SARS-CoV-2, including AP and mild elevation of lipase levels in patients with COVID-19. In addition, we will discuss plausible mechanisms that underly SARS-CoV-2-induced pancreatitis.

Keywords: COVID-19; SARS-CoV-2; amylase; cytokines; lipase; pancreas; pancreatitis.

Figure 1

The mechanistic rationale of SARS-CoV-2 elicited acute pancreatitis. A. Differential expression patterns of SARS-CoV-2 receptors in pancreatic cells can allow viral entry and thereby initiate acute pancreatitis or exacerbate an existing one; B. SARS-CoV-2 elicited lipotoxicity can initiate a pro-inflammatory cytokine storm to further aggravate acute pancreatitis, triggering acute respiratory distress syndrome and multiorgan failure.

Figure 2

Mechanisms of SARS-CoV-2-elicited pro-inflammatory cytokines (Interleukin-6, interleukin-8, and interleukin-10) that can mediate the development of acute pancreatitis.