Pharmacological actions of calcitonin on the gastrointestinal tract and their therapeutical implications.

The role of calcitonin (CT) in the regulation of the calcium homeostasis in humans is doubtful, while the therapeutic use in various bone diseases gains increasing interest. Numerous investigations during the last eight years have indicated that CT affects a variety of gastrointestinal organs when CT is administered in pharmacological high doses: CT inhibits gastric acid and pepsin secretion, gastrin release, pancreatic enzyme secretion as well as the hormonally stimulated contraction of the lower esophageal sphincter and of the gallbladder. CT increases intestinal secretion. The therapeutic use of CT in gastric hypersecretory states appears to be inferior and less practicable compared to the histamine-H2-receptor antagonists. The benefit of CT in the clinical course of acute pancreatitis was observed in two controlled double blind studies but CT did not lower the mortality rate. CT does not influence increases in serum-amylase and -lipase occurring after ERCP.