4.2 Article

Association between Acute Pancreatitis and COVID-19: Could Pancreatitis Be the Missing Piece of the Puzzle about Increased Mortality Rates?

Journal

JOURNAL OF INVESTIGATIVE SURGERY
Volume 35, Issue 1, Pages 119-125

Publisher

TAYLOR & FRANCIS INC
DOI: 10.1080/08941939.2020.1833263

Keywords

SARS-CoV-2; acute pancreatitis; ACE II receptor

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This study evaluated the incidence and clinical manifestations of acute pancreatitis in COVID-19 patients. The results showed that COVID-19 patients with acute pancreatitis had higher hospitalization and mortality rates, and were associated with age, C-reactive protein, and ferritin levels.
Background: The COVID-19 pandemic caused by SARS-CoV-2 commenced in Wuhan China in 2019 and soon spread worldwide. SARS-CoV-2 enters the cell by binding to the ACE II receptor and begins viral replication. The effects and clinical findings of SARS-CoV-2 on the liver, kidney, heart, gastrointestinal (GI) system and especially lungs have been widely discussed. However, the effects on the pancreas-another organ that also expresses ACE II-have not been studied. Methods: This work prospectively evaluated data from 316 patients who were admitted with a diagnosis of COVID-19 pneumonia. The patients were categorized into three according to the severity of pneumonia (mild, severe, critical). Demographic data, rate of pancreatitis, biochemical parameters, and radiological images from each group were analyzed. The patients were divided into two groups and outcomes were compared: COVID-19 patients with acute pancreatitis (Group P) and without acute pancreatitis (Group C). Results: The median age was 54 (18-87), and the median age for patients with acute pancreatitis was 55 (26-84). As an expected finding, we found a positive correlation between advanced age and mortality (p = 0.0003). 12.6% of the patients had acute pancreatitis. While pancreatitis was not seen in patients on mild status, the rate of pancreatitis was 32.5% in critical patients. Hospitalization and mortality rates were higher in patients with COVID-19 accompanied by acute pancreatitis (p = 0.0038 and p < 0.0001, respectively). C-Reactive Protein (CRP) and ferritin were significantly higher in those who had pancreatitis (p < 0.0001). D-Dimer and procalcitonin levels had only a small difference (p = 0.1127 and p = 0.3403, respectively) Conclusion: Acute pancreatitis alone is a clinical condition that can lead to mortality and may be one of the reasons for the exaggerated immune response developing in the progression of COVID-19. Our results point out that the presence of pancreatic damage triggered by SARS-CoV-2 can deteriorate the clinical condition of patients and the mortality rate may increase in these patients.

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