Introduction: The COVIDPAN collaborative found that concurrent SARS-CoV-2 infection with acute pancreatitis significantly worsened 30-day patient outcomes. However, long-term data on acute pancreatitis in the pandemic era remains unknown. During the initial phase of the pandemic, nearly a quarter of patients presenting with acute pancreatitis also had an unknown aetiology, raising the question whether SARS-CoV-2 may be implicated as a novel aetiology for acute pancreatitis.
Purpose: We aimed to investigate the long-term diagnosis, management, and outcomes of patients presenting with acute pancreatitis and coexistent SARS-CoV-2 infection.
Materials and methods: A prospective international multicentre cohort study including consecutive patients admitted with acute pancreatitis during the COVID-19 pandemic was undertaken. Updated aetiology, diabetes mellitus, pancreatic exocrine insufficiency, and mortality data with 12-month follow-up are reported. Multilevel multivariable logistic regression was used to compare groups.
Results: Twelve-month follow-up data were collected on 1476 patients, of whom 118 were SARS-CoV-2 positive and 1358 were negative. After appropriate investigations over this 12-month period; patients with SARS-CoV-2 were more likely to have idiopathic acute pancreatitis (34.7% vs 13.9%, p<0.001), and after adjusting for confounders had an odds ratio (OR) of 5.34 (p<0.001) of having idiopathic acute pancreatitis. Rates of diabetes mellitus and pancreatic exocrine insufficiency were similar between SARS-CoV-2 positive and negative groups. 1-year mortality after discharge was 12.7% in the SARS-CoV-2 arm, compared to 5.4% in the negative group (log-rank p<0.0001). However, after adjusting for confounders, SARS-CoV-2 status was not however associated with 1-year mortality after discharge (hazard ratio 1.89; 95% CI: 0.93 - 3.85, p = 0.078), diabetes mellitus (OR 0.61; 95% CI: 0.13 - 2.96, p = 0.541) or pancreatic exocrine insufficiency (OR 1.11; 95% CI: 0.44 - 2.79, p = 0.828).
Conclusions: SARS-CoV-2 increases the risk of idiopathic acute pancreatitis, but not diabetes mellitus or pancreatic exocrine insufficiency. Further laboratory studies are required to demonstrate replication of SARS-Cov-2 virus in human pancreas cells with resultant cellular injury to establish an aetiological link.