Using validated double-marker techniques to quantitate tryptic secretion we found that the mean 10-min output of trypsin in duodenal juice after a test meal was very similar to the peak 10-min output of trypsin after pancreozymin (2 Crick-Harper-Raper units/kg, Boots) both in controls as well as in non-diabetic patients with idiopathic chronic pancreatitis. These results show that the disproportionate reduction in mean tryptic activity after endogenous compared with exogenous stimulation in chronic pancreatitis is not due to impaired release of cholecystokinin-pancreozymin from the small intestine, nor to refractoriness of the pancreas to endogenously released hormone: instead, it is due to overdilution of secreted pancreatic enzymes because of accelerated gastric emptying, with or without gastric acid hypersecretion.

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