Chronic pancreatitis patients have an increased risk of developing
pancreatic cancer. The cause of this increase has yet to be fully explained but smoking and
inflammation may play an important role. To these, we must now add a new potential risk factor, namely duodenal acidity. Patients with
chronic pancreatitis very often present pancreatic exocrine insufficiency combined with a persistently low duodenal pH in the postprandial period. The duodenal mucosa in chronic pancreas patients with
pancreatic insufficiency has a normal concentration of s-cells and, therefore, the production of
secretin is preserved. Pancreatic ductal cells are largely responsible for the amount of
bicarbonate and water secretion in response to
secretin stimulation. When gastric acid in the duodenum is not well-balanced by alkaline pancreatic secretions, it may induce a prolonged
secretin stimulus which interacts with the pancreatic ductal cells resulting in an increased rate of ductular cell activity and turnover. N-
Nitroso compounds from tobacco, identified in human pancreatic juice and known to be important
carcinogens, may then act on these active cells, thereby increasing the risk of
cancer. Duodenal acidity is probably of particular concern in patients who have undergone a duodenum-preserving pancreatic head resection, since, in this anatomic situation, pancreatic juice transits directly via the jejunal loop, bypassing the duodenum. Patients undergoing a Whipple procedure or side-to-side
pancreaticojejunostomy are probably less critically affected because secretions transit, at least in part, via the papilla. If the duodenal acidity hypothesis proves correct, then, in addition to stopping smoking, reduction of duodenal
acid load in patients with
pancreatic insufficiency may help decrease the risk of
pancreatic cancer.