Meta-analysis reveals an association between acute pancreatitis and the risk of pancreatic cancer

Abstract

BACKGROUND Chronic pancreatitis is associated with pancreatic cancer (PC), although the relationship between acute pancreatitis (AP) and the risk of PC remains unclear due to inconsistent and contradictory results. AIM To conduct a meta-analysis of retrospective and prospective studies to explore the association between AP and PC risk. METHODS We first searched original articles on the association of AP with PC using PubMed, Web of Science, Cochrane, and EMBASE databases. Then we calculated the combined overall effect estimates (EEs) between AP and PC risk at a 95% confidence interval (CI) deploying a random-effects model, and assessed heterogeneity using the I2 test. The combined relative risk with 95%CI was performed to examine the relationship between AP and PC. Publication bias and subgroup analyses were also conducted. Furthermore, we performed sensitivity analysis to explain this heterogeneity. RESULTS Eleven studies were eligible for inclusion standards in this meta-analysis, resulting in pooled EEs of 2.07 (95%CI: 1.36-2.78) for AP and PC risk. Additionally, five prospective cohort studies reported 103961 patients in the AP group, relative to 1442158 subjects in the control group, with a pooled relative risk of 7.81 (95%CI: 5.00-12.19). We also performed subgroup analyses using different follow-up times and type of research methods (case-control or cohort). Results from analyses of different follow-up times revealed the following pooled effect values: 1-year lag period (EEs = 23.47, 95%CI: 3.26-43.68), 2-year lag period (EEs = 9.82, 95%CI: 3.01-16.64), 5-year lag period (EEs = 2.47, 95%CI: 1.93-3.02), 10-year lag period (EEs = 1.69, 95%CI: 1.26-2.11), and > 10-year lag period (EEs = 1.17, 95%CI: 0.78-1.57). With regards to the methods, the case-control studies recorded EEs = 3.03 (95%CI: -1.02 to 7.08), whereas cohort studies had EEs = 2.09 (95%CI: 1.22-2.97) pooled effect values. CONCLUSION Overall, our findings indicated an association between AP and PC risk. Based on subgroup analyses, AP is unlikely to be a causal factor for PC.