Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007570 (celiac disease)
 13,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma secretin concentrations and pH in the second portion of duodenum were measured in the fasting state and during duodenal infusion of HCl in five patients with untreated celiac sprue, five celiac sprue patients after gluten-free diets, and five normal subjects. Mean fasting plasma secretin concentrations were insignificantly lower in untreated sprue patients (4.1 +/- 1.4 pg/ml) than in normal subjects (5.7 +/- 0.59 pg/ml). During 30-min intraduodenal infusions of 0.1 N HCl at 0.20 mEqH+/min, mean plasma secretin concentrations were significantly lower in untreated sprue patients (5.8 +/- 1.8 pg/ml) than in normal subjects (25.4 +/- 1.60 pg/ml, P less than 0.01). The increases in mean secretin concentrations over fasting were 2.1 +/- 0.82 pg/ml in untreated sprue patients compared to 19.7 +/- 1.47 pg/ml in normal subjects (P less than 0.01), a ninefold difference. The results indicate that endogenous release of secretin in response to duodenal acidification is impaired in patients with celiac sprue.
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PMID:Impairment of secretin release in celiac sprue. 3 Feb 79

Patients with coeliac disease have a highly significant reduction in the release of secretin and gastric inhibitory polypeptide from the upper small intestine, but a greatly increased release of enteroglucagon, and also of neurotensin, from the lower part of the small intestine. The release of gastrin and pancreatic polypeptide, from the antrum and pancreas respectively, is, however, normal. Thus the pattern of hormone release reflects the location of the mucosal lesion. The gut-hormone profile may also help to characterise other gastrointestinal diseases.
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PMID:Gut-hormone profile in coeliac disease. 8 11

Using immunohistochemical techniques we studied duodenal biopsies from 18 patients with coeliac disease and 24 patients with normal duodenal morphology. We had access to antisera against the following gastrointestinal peptides: cholecystokinin (CCK), gastric inhibitory peptide (GIP), gastrin-17, glucagon-enteroglucagon, motilin, neurotensin, pancreatic peptide (PP), secretin, somatostatin, substance P and vasoactive intestinal peptide (VIP). The somatostatin, GIP, CCK, and glucagon cells were increased in number in coeliac disease. The number of motilin cells was slightly increased, while secretin cells were reduced. Cells storing gastrin-17, substance P, or neurotensin were rare in all patients regardless of diagnosis. No PP immunoreactive cells were found and VIP was localised to neurons only. In biopsies from patients having a mucosa with ridging of villi the number of the various endocrine cell types did not differ from that in the control group.
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PMID:Duodenal endocrine cells in adult coeliac disease. 38 55

A secretin-pancreozymin test was conducted with 43 gastroenterologically healthy children and 12 patients with subtotal atrophy of intestinal mucosa. While the pancreas enzymes were normal, the patients with coeliac disease reacted to the injection of the peptide hormones by producing a larger volume of secretion than did the control group. Despite the increased secretion there was at the same time a significantly higher concentration of bile acids in the duodenal juice. Analysis of the bile acid distribution indicated no deviation from the norm. There was, however, a striking discrepancy between the bile acid and the bilirubin excretion in the children with subtotal atrophy, whose bilirubin secretion, compared to that of the control group, was greatly reduced.
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PMID:[Investigation of the bile acid metabolism of children with subtotal atrophy of intestinal mucosa (author's transl)]. 56 15

Production of antibodies to secretin for radioimmunoassay is straightforward. Secretion is iodinated by weak oxydation with lactoperoxydase and subsequent purification by ionexchange chromatography (Sephadex C25). The specific activity of fresh label is between 650 and 900 mCi . mol-6. The label is highly purified and may be used in radioimmunoassay for several months. In order to eliminate plasma interference sepharose-beads with covalently coupled secretin antibodies are used to produce secretin-free standard plasma samples. Delay in the separation of plasma from fresh blood samples can lead to erronous results, even to falsely elevated secretin levels.--Duodental acidification only leads to physiological increases of secretin plasma levels. This may happen by intraduodenal instillation of acid, or by an acidic oral drink, or to a lesser extent after a meal. Secretin is distributed throughout the plasmavolume and has a short halflife of around 3 minutes. Impaired release of secretion is found in children with coeliac disease. The role of secretin in peptic ulcer however is not clear. Chronic pancreatitis and renal insufficiency are without effect on plasma secretin levels.
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PMID:[Secretion radioimmunoassay, physiology and pathophysiology in man]. 65 85

43 gastroenterologically healthy infants and children as well as 45 patients with different malabsorption and maldigestion syndromes were investigated during the basic secretion and after injection of secretin and pancreozymin in order to establish the total quantity and also the distribution of the secreted bile acids. The total concentration and quantity were determined enzymatically; column and thinlayer chromatography were utilized to separate the bile into 30 different bile acids. While the total quantity of bile acids was found to be independent of age, the compounding of bile changed during the first years of life. Patients with coeliac disease reacted to injection of peptide hormones by producing a larger volume of secretion than did the control group. Despite the increased secretion there was at the same time a significantly higher concentration of bile acids in the duodenal juice. In this group the analysis of the bile acid distribution indicated no abnormality but striking changes were found in patients with cystic fibrosis, biliary atresia, M. Wilson, and in children after subtotal resection of the small bowel.
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PMID:[Bile acids in the intestinal juice of infants and children with malabsorption and maldigestion syndromes]. 70 May 80

The purpose of the present study was to evaluate the effects of several gastrointestinal hormones on the gastric submucosal arterioles using an in vivo microscopy technique. Alteration in diameter of submucosal arterioles, 40 to 90 mu in diameter, in response to infusion of different agents into the celiac axis, was measured in the anesthetized cat. Pentagastrin, the octapeptide of cholecystokinin, natural secretin, and histamine produced arteriolar dilation. Only with histamine and the octapeptide of cholecystokinin did this occur with doses that might be considered physiological. Synthetic secretin had no vasodilator activity, suggesting the presence of a contaminating agent in natural secretin. Glucagon had no effect on the submucosal arterioles. In addition, the effect of glucagon on the smaller (10 to 30 mu) terminal and subterminal submucosal arterioles was studied in the rat by in vivo microscopy. Again no effect was observed with glucagon, but norepinephrine in small doses produced vasoconstriction.
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PMID:The effect of gastrointestinal hormones on the gastric microcirculation. 95 93

In four dogs with chronic pancreatic and gastric fistulas, dose-response studies of pancreatic bicarbonate and protein secretion were done with intravenous infusions of secretin, octapeptide of cholecystokinin (OP-CCK), and 2-deoxyglucose (2-DG). The pancreatic response to a meal and to duodenal perfusion of graded concentrations of HCl, sodium oleate, and tryptophan were also studied. These observations were repeated after division of both the hepatic and celiac vagal branches to produce extragastric vagotomy, and subsequently after transthoracic truncal vagotomy. The responses to secretin, OP-CCK, and to duodenal perfusion of HCl were either unaltered or only slightly decreased by either extragastric or truncal vagotomy. Basal pancreatic secretion and the responses to duodenal perfusion of oleate and tryptophan were markedly depressed by extragastric vagotomy. These findings indicate that tonic vagal activity contributes to basal pancreatic secretion but has little effect on the response of the pancreas to secretin or CCK or on the release of secretin from the intestine. The decreased pancreatic response to intestinally perfused oleate and tryptophan seen after extragastric vagotomy could be caused either by interruption of reflex paths between gut and pancreas or by interference with CCK release. Extragastric vagotomy reduced pancreatic responses to a meal and to 2-DG and subsequent truncal vagotomy caused still further reduction, possibly, at least in part, by depressing release of antral gastrin.
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PMID:Effect of extragastric and truncal vagotomy on pancreatic secretion in the dog. 113 May 17

Intrinsic factor is produced by the gastric parietal cell. Its secretion is stimulated via all pathways known to stimulate gastric acid secretion: histamine, gastrin, and acetylcholine. There is, however, a different mode of secretion for both substances: atropine, vagotomy, and H2 receptor antagonists inhibit both intrinsic factor and acid secretion, but secretin and the hydrogen-potassium ATPase antagonist omeprazole have no effect on intrinsic factor while substantially reducing acid secretion. Cobalamin in food is bound to animal protein. Cobalamin deficiency due to inadequate dietary intake is rarely seen in extreme vegetarians (vegans). In the stomach cobalamin is liberated from its protein binding by peptic digestion and bound to R-proteins. Hypochlorhydria or achlorhydria, whether medically induced or not, may impair cobalamin uptake. The cobalamin-R-protein complex is split by pancreatic enzymes in the duodenum, where cobalamin is bound to intrinsic factor. Pancreatic insufficiency may lead to cobalamin deficiency. Lack of intrinsic factor is the commonest cause of cobalamin deficiency; very rarely, aberrant forms of intrinsic factor are produced, but the clinical syndrome is similar. Gram-negative anaerobe bacteria bind the cobalamin-intrinsic factor complex, and bacterial overgrowth of the small intestine diminishes cobalamin resorption. Parasitic infections with fish tape-worm and Giardia lamblia are also associated with cobalamin malabsorption. The cobalamin-intrinsic factor complex binds to the ileal receptors in the terminal ileum. Cobalamin absorption may be impaired after resection or by diseases affecting more than 50 cm of the terminal ileum, such as Crohn's disease, coeliac disease, tuberculosis, lymphoma or radiation. There is clearly a wide diversity in the aetiology of cobalamin deficiency, which requires a versatile diagnostic approach.
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PMID:Intrinsic factor secretion and cobalamin absorption. Physiology and pathophysiology in the gastrointestinal tract. 177 33

This study was designed to determine the extent of pancreatic insufficiency in untreated coeliac disease and whether pancreatic secretion is impaired after a prolonged gluten free period. Three groups of patients were studied: group A comprised 44 patients, mean (SD) age 4.0 (3.1) years, with coeliac disease and total or subtotal atrophy of the intestinal mucosa; group B comprised 67 patients, mean age 4.4 (3.0) years, with coeliac disease but with normal morphology of the intestinal villi (after 12.9 months of a gluten free diet); group C comprised 49 control subjects, mean age 3.2 (3.0) years, with normal jejunal histology. In all subjects exocrine pancreatic function was determined by the secretin-caerulein test; bicarbonate concentration and lipase, phospholipase, and chymotrypsin activity were measured after an intravenous injection of secretin 1 clinical unit (CU) + caerulein 75 ng/kg body weight. Faecal chymotrypsin concentration was also assayed. No significant difference was found between values of the duodenal output of pancreatic enzymes and bicarbonate obtained in the three groups; however, 10 of 44 untreated coeliac patients showed tryptic or lipolytic activity, or both, below the normal limit for our laboratory. The mean value of the faecal chymotrypsin concentration was significantly lower in untreated than in treated coeliac patients (p less than 0.0001) or in control subjects (p less than 0.0001). It is concluded that untreated coeliac patients may have pancreatic deficiency independent of a decrease in enterohormone release. No primary or secondary pancreatic insufficiency was found in coeliac patients where the intestinal mucosa had returned to normal.
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PMID:Exocrine pancreatic function in children with coeliac disease before and after a gluten free diet. 185 88


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