sincalide and Celiac-Disease

The aim of this study was to evaluate the concept that pancreatic dysfunction in patients having gluten sensitivity (celiac disease [CD]) or cow's milk protein enteropathy (CMPE) may result from the lack of pancreatic enzyme stimulation in the absence or decrease of cholecystokinin (CCK) secretion caused by villous atrophy.. The following parameters were measured: plasma CCK in response to a fatty meal and human pancreatic fecal elastase in 24 patients with CD while on gluten-free diet and after gluten provocation and in 12 patients with CMPE at diagnosis and after a 6-month period of cow's milk-free diet. Intestinal mucosa morphology was examined by small bowel biopsy. Sixty-three controls having no organic gastrointestinal problems were investigated once at the time of diagnostic evaluation.. Fasting CCK, obtained at a time when patients with CD or CMPE had normal intestinal mucosa, was significantly different from postprandial and comparable to that of the control group. Fasting CCK obtained from patients with villous atrophy was also statistically different, but not significantly, from the postprandial. Fasting and postprandial plasma CCK and fecal pancreatic elastase values from patients having normal intestinal mucosa were significantly higher than those obtained from patients with villous atrophy. Significant correlation of intestinal mucosa morphology and CCK with fecal elastase concentration was documented.. Exocrine pancreatic dysfunction in individuals having villous atrophy may be the consequence of decreased CCK secretion. Cholecystokinin and pancreatic secretion is restored to normal, with intestinal mucosa regeneration.

Topics: Adolescent; Atrophy; Biopsy; Celiac Disease; Child; Child, Preschool; Cholecystokinin; Dietary Fats; Feces; Female; Humans; Infant; Intestinal Mucosa; Intestines; Male; Milk Hypersensitivity; Milk Proteins; Pancreas; Pancreatic Elastase; Sincalide

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.

Topics: Adolescent; Bile Acids and Salts; Celiac Disease; Child; Cholecystokinin; Cholic Acid; Cholic Acids; Digestion; Humans; Hypocalcemia; Hypoparathyroidism; Male; Pancreatin; Peptide Fragments; Sincalide

Topics: Adolescent; Adult; Celiac Disease; Cholecystokinin; Chronic Disease; Female; Humans; Lipase; Male; Middle Aged; Pancreas; Pancreatic Polypeptide; Pancreatitis; Pentagastrin; Peptide Fragments; Secretin; Sincalide; Trypsin