title: Hypocalcemia and steatorrhea--clues to etiology.
abstract: Two boys with idiopathic hypoparathyroidism had extensive studies of gastrointestinal function during hypocalcemia accompanied by steatorrhea. No evidence of generalized gastrointestinal moniliasis or abnormal mucosal structure or function was observed. Studies of pancreatic function and bile salt metabolism during hypocalcemia demonstrated deficient meal-stimulated intraluminal pancreatic enzyme concentrations in both subjects and reduced bile salt concentrations in one subject. However, following stimulation with exogenous octapeptide of cholecystokinin, intraluminal pancreatic enzyme and bile salt concentrations were normal in both. Cholic acid pool sizes were markedly increased in both subjects during hypocalcemia (9 and 12 times larger than during normocalcemia) and cholic acid turnover was reduced during hypocalcemia in one subject. Our findings suggest that during hypocalcemia, insufficient endogenous cholecystokinin is released by the duodenal mucosa during a meal stimulus to stimulate normal gallbladder contraction and pancreatic enzyme secretion.
mesh_terms: D000293:Adolescent; D001647:Bile Acids and Salts / Q000378:metabolism; D002446:Celiac Disease / Q000209:etiology* / Q000378:metabolism; D002648:Child; D002766:Cholecystokinin / Q000378:metabolism; D019826:Cholic Acid; D002793:Cholic Acids / Q000378:metabolism; D004063:Digestion; D006801:Humans; D006996:Hypocalcemia / Q000209:etiology* / Q000378:metabolism; D007011:Hypoparathyroidism / Q000150:complications*; D008297:Male; D010194:Pancreatin / Q000378:metabolism; D010446:Peptide Fragments; D012844:Sincalide
chemical_list: D001647:Bile Acids and Salts; D002793:Cholic Acids; D010446:Peptide Fragments; D010194:Pancreatin; D002766:Cholecystokinin; D019826:Cholic Acid; D012844:Sincalide