Abstract

Chronic pancreatitis is a disease with varying etiologic factors. It is relatively easy to diagnose in its later stages, but notoriously difficult early in its course. Treatment is often unsatisfactory. The clinical features of chronic pancreatitis are abdominal pain and the consequences of destruction of the exocrine and endocrine pancreas--steatorrhea and diabetes mellitus. Pain is less common in patients with chronic calcific pancreatitis than in chronic noncalcific pancreatitis. It may be absent even in patients continuing to abuse alcohol (1). Recently, a report appeared indicating that treatment with oral pancreatic extracts can relieve the pain of some patients with chronic pancreatitis (2). This has been attributed to a negative feedback mechanism in which trypsin in the duodenum inhibits the secretion of chymotrypsin by decreasing the release of cholecystokinin (3). The steatorrhea of chronic pancreatitis can usually be controlled by adequate replacement treatment with pancreatic extracts (4). However, fecal fat excretion is rarely reduced to normal levels. Inactivation of lipase by acid in the duodenum in the face of reduced duodenal bicarbonate secretion may account for failure of substitution therapy in some patients (5). In this issue of the journal Begley and RobertsThomas report three patients with chronic pancreatitis confirmed by ductal changes seen on ERCP who appear to have experienced a spontaneous reduction in the fecal excretion of fat; from 60 to 6 and 11 g/day in two patients and from 9 g while on substitution therapy to 3 g/day off treatment in the third. The duodenal bicarbonate concentration after secretin increased slightly as the steatorrhea decreased in one patient. The period of observation extended over 3, 22, and 27 years in the three patients. Diabetes was present in two patients, and the glucose tolerance test was mildly abnormal in

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