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)

Peptide YY (PYY) is exclusively localized in endocrine cells in the gut, and these cells are most numerous in the distal small intestine, colon, and rectum. We have earlier shown that PYY coexists with enteroglucagon in the gut endocrine cells. High basal and postprandial plasma enteroglucagon concentrations have earlier been found in patients with untreated coeliac disease. PYY circulates in human plasma and is detectable in most healthy adults. We have therefore studied the basal PYY levels in patients with coeliac disease. Marked elevated basal plasma PYY levels were found in patients with coeliac disease compared with an age- and sex-matched control group. The PYY levels were inversely correlated to the concentration of folate acid in serum. The PYY levels were studied in four patients with newly diagnosed disease and had normalized within 8 months on a gluten-free diet.
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PMID:Increased plasma levels of peptide YY in coeliac disease. 338 93

Antibodies to gliadin (AGA), detected in jejunal juice by immunofluorescence and enzyme-linked immunosorbent assay, have been found in 13 of 15 (87%) children with untreated coeliac disease. Jejunal AGA were also positive in 6 of the 9 (67%) coeliac children on gluten challenge, while they were consistently negative in coeliac children on a gluten-free diet and in controls. Jejunal AGA were always of immunoglobulin A (IgA) class, associated with IgM in some cases. Moreover, the presence of IgA AGA in jejunal juice was strictly related to the severity of intestinal damage. These data suggest that IgA AGA, detected in jejunal juice are synthesized from gut mucosa and are markers of its abnormal function. Like AGA, antibodies to milk and egg proteins were only found in jejunal juice of coeliac patients with flat intestinal mucosa, but their prevalence was significantly lower than that of AGA.
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PMID:Immunoglobulin A antigliadin antibodies in jejunal juice: markers of severe intestinal damage in coeliac children. 339 71

The segmental distribution of sympathetic preganglionic neurons (SPNs) and dorsal root ganglion cells (DRGs) was studied after Fluoro-gold injections into the major sympathetic ganglia and adrenal gland in rats. A quantitative assessment of the segmental and nuclear locations was made. Four general patterns of innervation were apparent: (1) a large number of SPNs (1000-2000/ganglion) innervate the sympathetic ganglia which control head or thoracic organs and a relatively small number of SPNs (100-400/ganglion) innervate the sympathetic ganglia controlling the gut, kidney, and pelvic organs; this difference in density of innervation probably relates to the level of fine control that can occur in these end organs by the SPNs; (2) the reverse pattern is seen in the DRG labeling where a large number of DRGs were labeled after Fluoro-gold injections into the preaortic ganglia (celiac, superior, and inferior mesenteric) and a small number were labeled after injections into the cervical sympathetic ganglia; (3) the intermediolateral cell column is the main source of SPNs except for the inferior mesenteric ganglion which is innervated predominantly by SPNs originating in the central autonomic nucleus (75%); the lateral funiculus is a source of SPNs mainly for the cervical sympathetic ganglia; and (4) each sympathetic ganglion and the adrenal gland receives a multisegmental SPN and DRG input with one segment being the predominant source of the innervation. The adrenal gland shows an intermediate position in terms of the density of SPN input (approximately 800 cells) and dorsal root input (approximately 300 cells); it has a widespread segmental input (T4-T12) with the T8 segment being the major source.
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PMID:Spinal origin of sympathetic preganglionic neurons in the rat. 341 86

The effect of intrapharyngeal infusion and subsequent passage of the lectin concanavalin A through the gastrointestinal tract of neonatal guinea pigs was examined. The lectin, administered at a concentration of 1 mg/ml, caused considerable mucosal damage in the stomach. Subsequent passage of the lectin through the small intestine caused little cellular damage to the mucosa, as judged by light and electron microscopy. Parallel morphometric analyses of the jejunum showed a decrease in mean villus height and an increase in mean crypt depth of 8% after 5 h of lectin administration. A 4.7-fold increase in jejunal crypt cell production rate was observed, accompanied by a statistically significant increase in the number of intraepithelial lymphocytes. These morphologic and kinetic changes were accompanied by a three-fold increase in the urinary lactulose:mannitol excretion ratio, indicative of a loss of mucosal integrity. No systemic antibody response to concanavalin A was demonstrated within 5 h of intragastric infusion of the lectin. Concanavalin A, conjugated with 10 nm colloidal gold particles, was also directly infused into the lumen of the jejunum in vivo. Within 60 min, both villous and crypt epithelial cells contained gold particles, demonstrating the rapid accessibility of crypt cells to the lectin. Intercellular spaces appeared within the villous epithelium, although both junctional complexes and spot desmosomes were retained. The brush border was abnormal with signs of incipient vesicularization. These findings have implications for our understanding of the pathogenesis of childhood coeliac disease and for the vulnerability of the neonatal gut to food proteins.
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PMID:Effect of the lectin concanavalin A on the neonatal guinea pig gastrointestinal mucosa in vivo. 343 Feb 51

Direct immunofluorescence (IF) studies of skin biopsies are of value in the diagnosis of most, but not all, cases of dermatitis herpetiformis (DH). Similarly, histologic studies are of help but may be questionable or completely nonspecific. Serologic studies for the presence of IgA-class anti-endomysial antibodies are very specific and are found in 70% of patients with DH and in all untreated patients with celiac disease. The titers of these antibodies are directly associated with the degree of gut disease in these patients. Thus, the presence of these antibodies even in the absence of classic direct IF and histologic findings are diagnostically important. We encountered three cases in which both direct IF and histologic studies were equivocal toward confirming the clinical diagnosis of DH. Serologic studies for the presence of IgA-class anti-endomysial antibodies provided evidence for the diagnosis of DH, and, in each case, results were confirmed by further direct IF studies. Since these antibodies are disease specific for DH and celiac disease and are found in most active cases of DH, they may be considered an adjunct to the direct IF and histologic studies of the skin.
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PMID:Anti-endomysial antibodies. A serologic marker of dermatitis herpetiformis. 351 13

The aim of this study was to assess the extent of collateral blood flow provided by the celiac and inferior mesenteric arteries to the intestines during total occlusion of the superior mesenteric artery (SMA). In anesthetized cats, blood flow to the pancreas, duodenum, jejunum, ileum, and colon was measured with radioactive micropheres (15 microns in diameter) before and during occlusion of the SMA. Superior mesenteric artery occlusion significantly decreased (by 63%) blood flow to the head of the pancreas. Flow to the neck and tail of the pancreas was not altered. Blood flow to the proximal and distal duodenum was significantly reduced by 35% and 61%, respectively. Along the entire jejunum and ileum, SMA occlusion markedly decreased blood flow by an average of 71%. In the proximal colon, blood flow decreased by 63%, whereas flow to the middle and distal colon was not affected by SMA occlusion. Reduction in total wall blood flow to the small and large intestines was largely due to a marked reduction in mucosa/submucosa blood flow; muscularis/serosa flow was not affected. The results of this study suggest that total occlusion of the SMA does not compromise blood flow to the neck and tail of the pancreas and middle and distal colon (tissues that are normally perfused with blood from either the celiac or inferior mesenteric arteries). Perfusion through collaterals maintains flow to the head of the pancreas and gut (from duodenum to proximal colon) to within 30%-65% of control (preocclusion) flow. An important new observation of this study is that collateral blood vessels are much more effective in preventing ischemia in the muscularis/serosa than in the mucosa/submucosa after SMA occlusion.
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PMID:Importance of collateral circulation in the vascularly occluded feline intestine. 355 16

IgA, IgE, IgG and IgM plasma cells in small bowel mucosal biopsies from 15 controls, 16 untreated and 14 treated coeliac patients and five patients with selective serum IgA deficiency (four of whom also had coeliac disease) were quantified using an indirect immunoperoxidase technique. The IgA, IgG and IgM plasma cell counts were significantly increased in the untreated coeliac patients. The cell counts were intermediate in the treated coeliac group. These changes were in parallel to production in vitro of IgA and sIgA, IgG, and IgM by cultured mucosal biopsies from the same patients. The IgA deficient patients had very few mucosal IgA cells but elevated IgG and IgM plasma cell numbers; again these changes were reflected in the production in vitro of immunoglobulins. IgE plasma cell counts were very low in all patients and there were no differences between patient groups. The changes in cell counts and mucosal immunoglobulin production were not reflected in serum IgA, IgM and IgG concentrations but serum secretory IgA was significantly elevated in the untreated coeliac patients compared with controls, with the treated coeliac patients being intermediate. The raised mucosal plasma cell counts reflect the local mucosal production of immunoglobulin but not the immunoglobulin concentrations of serum, emphasising the importance of studying the immune function of the gut itself in coeliac disease rather than immunological abnormalities in serum.
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PMID:Jejunal plasma cells and in vitro immunoglobulin production in adult coeliac disease. 365 27

The uptake of ovalbumin (OA) from egg and beta-lactoglobulin (BLG) from cow's milk into the blood was investigated for seven hours after a test meal in five children with coeliac disease on a gluten free diet and after gluten challenge, and in five children with normal jejunal mucosa. Ovalbumin was detectable by ELISA in three of five coeliac children (maximal concentrations 8-178 ng/ml serum) and in five of five controls (maximal 4-91 ng/ml serum). Beta-lactoglobulin was detected in three of five coeliac children (maximal 0.6-6 ng/ml serum) and in two of five controls (maximal 0.5 and 50 ng/ml serum). No clear relationship was seen between maximal antigen concentrations and titres of serum IgG or IgA antibodies determined by ELISA, or as percentage antigen binding in a Farr type radioimmunoassay. Ovalbumin and beta-lactoglobulin was seen in serum of all coeliac patients and controls by HPLC fractionation in combination with ELISA, either in high MW fractions, or at the Mr of native OA and BLG, respectively. In one control degradation products (about 17 kD) of BLG were detectable in serum. The serum concentrations of OA and BLG were increased on gluten challenge in four or five coeliac children, indicating increased macromolecular passage through the gut mucosa in untreated coeliac disease.
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PMID:Passage of dietary antigens into the blood of children with coeliac disease. Quantification and size distribution of absorbed antigens. 367 64

To evaluate the incidence of either evident anemia or a subclinical status of iron deficiency in celiac disease (CD), we studied 80 celiac children aged 6 months to 18 years. They were subdivided into various groups according to morphology of gut mucosa and diet. Only eight of 47 celiac children had an evident anemia at the time of the first peroral bowel biopsy. In addition, 51% of the patients with atrophic mucosa and 56% of the children on a gluten-containing diet had serum iron levels less than 50 micrograms/dl; 35% of patients of both groups had serum ferritin levels less than 12 micrograms/L. On the contrary, only a small number of children with normal mucosa on a gluten-free diet showed a laboratory, subclinical picture of iron deficiency. The results of our study can therefore be summarized in three major items: (a) Low levels of both serum iron and ferritin can frequently be found during active CD. (b) Regular determination of serum iron levels appears to be useful in controlling the state of iron stores in such patients, as well as in deciding whether and when to recommend temporary iron supplementation. (c) Serum ferritin tests did not offer more information than the easier and cheaper serum iron determinations.
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PMID:Iron deficiency in children with celiac disease. 369 63

Coeliac disease is a malabsorptive disorder caused by intolerance to gluten and is characterized by a remodelling of the intestinal mucosa including villus atrophy, crypt hyperplasia and net increase of mucosal volume. Changes of the number of mucosal mast cells (MMCs) in coeliac mucosa has recently been reported, suggesting that the mast cell activity could have a pathogenetic role in gluten enteropathy. MMCs located solely in the lamina propria are the main repository for small-gut mucosal histamine. A consecutive prospective study was designed to study the histamine content, MMC numbers, and the relative volume of lamina propria in intestinal biopsies from adult patients suffering from unexplained diarrhea and/or malnutrition. Histamine was measured by a HPLC-method, the number of MMC was counted after long toluidine-blue staining, and the relative volumes of lamina propria and epithelium were estimated morphometrically. The findings were correlated to the histopathological appearance of the mucosa. As compared to controls the histamine content increased by 80% and MMC numbers by about 60% in the coeliac mucosa. There was also a correlation between MMC numbers and histamine content for both normal and coeliac mucosae (r = 0.81). The morphometric estimation of the relative volumes of epithelium and lamina propria revealed that the lamina-propria compartment was increased by approximately 40% in coeliac mucosa. Taking the changes in compartmental volumes of the remodelled coeliac mucosa into account, our results suggest that the histamine content and MMC population were significantly increased. MMC and MMC-associated histamine may therefore be involved in the pathogenesis of gluten enteropathy.
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PMID:Histamine and mucosal mast cells in gluten enteropathy. 372 11


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