How cholecystectomy and gastrectomy contribute to pancreatic cancer development: a review

Despite advances in diagnostic tools and management, the 5-year survival rate of pancreatic cancer ranges from 2% to 9%. Given the poor prognosis and low survival rates, a better understanding of modifiable risk factors is essential for the prevention of this disease. The low survival rate is attributed to the fact that only 20% of patients present at an early, surgically resectable stage.

A literature review was conducted to evaluate the role of cholecystectomy and gastrectomy in the development of pancreatic cancer. PubMed, Google Scholar, Web of Science, and Embase were searched from each database's inception through the final search date, and all eligible studies were included.

The concentrated bile released from the gallbladder exerts negative feedback on intestinal cholecystokinin (CCK) release. After cholecystectomy, there is a continuous flow of unconcentrated hepatic bile into the intestine, which disrupts this feedback inhibition, increasing CCK levels and causing sphincter of Oddi relaxation with subsequent bile reflux into the pancreatic duct, which may contribute to the development of pancreatic cancer. Similarly, gastrectomy may promote pancreatic carcinogenesis by increasing the formation of carcinogenic N-nitroso compounds, enhancing CCK release due to rapid gastric emptying, and impairing the absorption of vitamin D and magnesium, thereby creating a procarcinogenic environment.

Cholecystectomy and gastrectomy should be performed only when clinically indicated to maximize patient benefit and minimize unnecessary risks. Careful patient selection and adherence to established clinical guidelines are essential when determining the need for either procedure.