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)

Sixty children with chronic diarrhoea, age ranging from 9 months to 3 years and 15 normal healthy children of same age group, all belonging to the low socio-economic families formed the basis of this study. Fifty-six out of these 60 children were undernourished and were marasmic. Stool examination showed enteropathogenic E. coli in 24 (40 per cent), Ascaria lumbricoides in 12 (20 per cent) and Giardia lamblia in 6 (10 per cent). Coeliac disease was detected in 2 (3 per cent) and combined IgA-IgG deficiencies were found in one case (2 per cent). No cause could be found in 15 (25 per cent) cases. Multiple aetiological factors were found in 7 (12 per cent) cases. Stool IgA levels were significantly elevated in the patients than in the controls and more so in the patients with giardiasis and also in patients with coeliac disease. Serum IgA levels were remarkably raised in the patients with diarrhoea due to enteropathogenic E. coli, indicating probable spilling of gut-associated IgA into the circulation. No IgA was detected in the stool of a dysgammaglobulimic patient, who had both serum IgA and IgG deficiencies.
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PMID:Raised stool and serum IgA levels in undernourished infants with chronic diarrhoea and associated parasitic infestations. 235 7

Over the past 15 years the basic details of the mucosal immune response have been described. The challenge of the next decade is to expand these details and to relate this basic information to pathologic processes in the gastrointestinal tract. It is now clear that secretory IgA is the main immunoglobulin produced by the mucosa. Further, we know that oral rather than parenteral priming preferentially stimulates a secretory IgA response. IgA protects mainly by binding to an intraluminal microorganism or toxin and thereby interfering with its absorption across the gut epithelium. The cellular basis for the IgA response has also been elucidated to some degree. It is clear that the response is highly T cell dependent and requires both helper T cells and switch T cells. With the use of monoclonal antibodies, we have begun to learn about cell-mediated functions in the gut. Suppressor/cytotoxic lymphocytes are largely sequestered in the epithelium whereas helper/inducer lymphocytes mainly reside in the lamina propria. In diseases such as celiac disease and inflammatory bowel disease, several alterations in the gastrointestinal immune system have been described. Some, such as the finding of antibody to gliaden, may be causally related to the disease. Others, such as antibodies to luminal bacteria, likely are secondary events. The challenge of the next decade is to expand these details and to relate this basic information to pathologic processes along the gastrointestinal tract.
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PMID:Gastrointestinal immune system and its disorders. 240 76

Celiac disease, a common chronic gastrointestinal disorder, is gluten induced and is controlled with a gluten-free diet. While the management of CD with a gluten-free diet is quite effective, the diagnosis is rather difficult. The ESPGAN criteria for the diagnosis of CD seems to be tedious and time-consuming. Serological tests for IgA class endomysial antibodies, as detected by indirect immunofluorescence, on human and primate smooth muscles are specific and sensitive markers of celiac disease. Of all the specimens examined, endomysial antibodies were present in patients with gluten-sensitive enteropathy. These antibodies occurred in all active cases of celiac disease, in 90 percent suspected celiac patients where all the ESPGAN criteria has not been fulfilled. This contrasts to the presence of endomysial antibodies in 46 percent of confirmed and 17 percent of suspected celiac patients maintained on a gluten-free diet for various time intervals. Endomysial antibodies also occurred in all cases with chronic diarrhea and gut histology consistent with CD and 8% of asymptomatic family members of CD patients. None of the patients with other gastrointestinal and liver diseases had endomysial antibodies. These studies thus emphasize the specificity and sensitivity of endomysial antibodies for celiac disease.
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PMID:Endomysial antibodies in the diagnosis of celiac disease and the effect of gluten on antibody titers. 249 36

110 children suffering from malabsorption underwent several biopsies of the gut to confirm coeliac disease (CD) following the ESPGAN criteria. We studied the values for alkaline phosphatase (AP) in the intestinal mucosa after gluten challenge. In 42 patients the after challenge biopsy was normal, thus excluding coeliac disease. In 68 children the mucosa was severely damaged confirming CD. In all biopsy specimens lactase, invertase, maltase and alkaline phosphatase were measured. We found a good correlation between PA values and severity of mucosal damage, showing that measurement of PA in the mucosa is helpful in assessing the degree of mucosal atrophy in children suffering from malabsorption.
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PMID:[Alkaline phosphatase in the intestinal mucosa of children with the malabsorption syndrome]. 250 30

Immunohistochemistry has been used to investigate disulfide- and non-disulfide-linked forms of the T cell receptor gamma/delta heterodimer (TcR gamma/delta) in blood and intestinal epithelium of normal human small intestine, intestine of patients with untreated coeliac disease (in whom T cells expressing TcR gamma/delta are disproportionately raised), intestine of patients with tropical malabsorption, and in the human fetus. In blood from adult volunteers, 90% of T cells expressing TcR gamma/delta use the disulfide-linked form. In contrast in the epithelium in normal small intestine, coeliac disease and tropical malabsorption, most of the T cells expressing TcR gamma/delta use the non-disulfide-linked form. This is especially prominent in untreated coeliac disease where the increase in TcR gamma/delta T cells is mainly restricted to those using the non-disulfide-linked form. In human fetal small intestinal epithelium, however, only cells using the disulfide-linked form are present. These variations in expression of different forms of TcR gamma/delta in the gut epithelium in different conditions suggests that antigen, or some as yet undefined factor may determine the frequency of each subpopulation.
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PMID:Expression of disulfide-linked and non-disulfide-linked forms of the T cell receptor gamma/delta heterodimer in human intestinal intraepithelial lymphocytes. 252 59

Non-selective enkephalin analogs, such as [D-Ala2, Met5]enkephalinamide, have been found to increase jejunal absorption in the rat and dog after their intracerebroventricular administration. In the present investigation, experiments were designed to characterize the brain opiate receptor subtype mediating this action in the rat proximal jejunum in situ and to assess the involvement of extrinsic sympathetic nerves innervating this gut region in opioid-induced absorption. Changes in jejunal water transport were examined in rats pretreated with bolus i.c.v. doses (less than or equal to 1 microgram) of the respective mu-, delta-, or kappa-opiate agonists [D-Ala2, N-Me-Phe4, Gly5-ol]enkephalin (DAGO), [D-Pen2, D-Pen5]enkephalin or U-50488 and infused intravenously with the secretagogue prostaglandin E1 (PGE1, 5 micrograms/kg-min). In saline-pretreated rats, PGE1 produced large, time-dependent decreases in jejunal fluid absorption. Of the opiate agonists examined, only DAGO in submicrogram doses significantly inhibited PGE1 actions 60 to 90 min after its administration. Extirpation of the celiac and superior mesenteric ganglia, major sources of sympathetic neurons innervating the upper gut, significantly attenuated both the antiabsorptive actions of PGE1 and the proabsorptive actions of DAGO (0.3 micrograms, i.cv.). These results suggest that CNS mu-opiate receptors modulate jejunal absorption in the rat, an action mediated through extrinsic sympathetic nerves innervating the upper small intestine.
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PMID:Jejunal proabsorptive actions of selective opiate agonists administered via the cerebral ventricles. 255 Aug 43

The activity of tyrosine hydroxylase (TOH), the rate-limiting enzyme in norepinephrine biosynthesis, was measured in selected sympathetic ganglia to develop a quantitative measure of sympathetic autonomic neuropathy in streptozocin-induced diabetic rats. Surprisingly, TOH activity was elevated twofold in diabetic prevertebral ganglia innervating the alimentary tract (i.e., superior mesenteric, celiac, and inferior mesenteric), which has terminal processes that develop neuroaxonal dystrophy in this model system. TOH activity of paravertebral ganglia (i.e., superior cervical and stellate) with nonalimentary targets was not increased in the same animals. Increased TOH activity in the prevertebral ganglia 1) developed within the 1st wk of diabetes and persisted for 10 mo, 2) did not represent a change in TOH affinity for d-1,6-methyl-5,6,7,8- tetrahydropterine cofactor, 3) was prevented by both nicotinamide pretreatment and early institution of insulin therapy, and 4) did not develop as a result of classical transsynaptic induction. Pair-feeding experiments confirmed that the most likely cause of increased TOH activity in this system was the marked hypertrophy and hyperplasia of the diabetic bowel resulting from compensatory hyperphagia. We conclude that TOH activity does not represent a suitable marker for sympathetic autonomic neuropathy in this experimental system. Rather, the increase appears to be an example of a selective increase in the synthesis of neurotransmitter enzymes, possibly in response to increased trophic support provided by the expanded target, i.e., the hypertrophic gut. The additional synthetic stress imposed on prevertebral neurons by the expansion of the innervation of the alimentary target coupled with the complex diabetic metabolic milieu may contribute to the development and selective distribution of dystrophic axonopathy to the innervation of the alimentary tract.
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PMID:Tyrosine hydroxylase activity in sympathetic nervous system of rats with streptozocin-induced diabetes. 256 57

It has been shown that GGT activity in the duodenal biopsy homogenates of the children with coeliac disease (n-10) in remission (1 to 3 years of gluten-free diet) is lower than in those with other gastrointestinal tract diseases (n-6). In children with coeliac disease after gluten challenge (1 g of gluten) kg BW for 3 to 6 months) the GGT activity decreased fourfold (n-10). After a few months of gluten challenge there was in coeliac children (n-5) a marked predominance of GGT without sialic acid (the asialic GGT). Similarly there was a prevalence of this form (n-5) in the gut tissue of 3 month old human fetus. In the homogenates of the duodenal bioptates of the children with other gastrointestinal tract diseases (n-6) there was a predominance of the sialic form of the GGT. In the gut tissue of children older than 3 years (n-6) and adults who died of reasons other than gastrointestinal a marked predominance of the sialic form of GGT was found. It has been suggested that presence of asialic form of GGT in coeliac disease is connected with the lectin-like activity of gluten. The process of sialization or desialization takes place within or outside enterocytes. It changes the gut permeability and causes a secondary reaction to the penetrating allergens.
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PMID:[Activity and molecular form of intestinal gamma-glutamyltransferase (GGT) EC 2.3.2.2. in celiac disease]. 257 27

The possibility that dietary antigens contribute to the pathogenesis of rheumatoid arthritis (RA) has been proposed. Moreover, occasional patients have been described in whom coeliac disease and RA coincide. Furthermore, most RA patients are treated with non-steroidal anti-inflammatory drugs (NSAIDs), which are known to increase gut permeability. For these reasons antibodies against gliadin were measured in a group of 43 patients with rheumatoid arthritis (RA) and a group of 43 age- and sex-matched controls. The median IgA antigliadin ELISA index was 7.1 (range 2.1-22.4) for the RA group and 3.1 (range 0.3-34.9) for the controls (p = 0.0001). The median IgG and IgM antigliadin indexes for the RA group didn't differ significantly from those of the controls. In the RA group, the level of antigliadin antibodies did not correlate with the daily dose of NSAIDs. The elevated IgA antigliadin titre in the RA group might be ascribed to the use of NSAIDs, which are harmful to the gut, but the immunological trigger effect of gluten cannot be ruled out.
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PMID:Elevated level of IgA gliadin antibodies in patients with rheumatoid arthritis. 261 82

Using the horseradish peroxidase (HP) retrograde method for ascertaining connections of the celiac plexus of the white rat with various afferent centers, HP-marked neurocytes have been revealed in caudal nodes of the vagus nerves and in spinal nodes at the Th4-L2 level. Negative results have been obtained at investigation of the cervical spinal nodes and intramural nodes in the cat ileocecal part. Similar data are obtained, when connections of the celiac plexus with the same area of the cat gut are investigated. Therefore, the problem on interrelations of the celiac plexus with the proper afferent centers of the diaphragmatic+ nerve and the second type cells of Dogel in the cat intramural ganglia is still disputable.
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PMID:[Projection of the celiac plexus to the afferent centers demonstrated by the horseradish peroxidase retrograde transport method]. 268 99


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