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)

The study was aimed at determining relationship between thyroid function and the type and degree of malabsorption. Serum triiodothyronine (T3) and thyroxine (T4) levels were determined in children with celiac disease and the secondary malabsorption. Hundred fifty five children aged between 6 months and 7 years were followed up 3 years. Coeliac disease was diagnosed with classic Interlaken criteria. All children were divided into three groups: group I--57 children aged between 6 months and 3 years with suspected celiac disease; group II--55 children aged between 2.5 and 6 years after gluten-free diet therapy; group III--52 children aged between 3 and 7 years after gluten provocation test. Serum T3 and T4 levels for each group were compared with those in children with normal gut mucous membrane. Blood serum T3 and T4 were assayed with OPIDI kit (manufactured in Swierk). Serum T4 levels were significantly lower in children with mucous membrane atrophy in comparison with dystrophic children and normal gut mucous membrane. Both serum T3 and T4 were significantly lowered in the youngest children upto 12 months of life with mucous membranes atrophy. Serum T3 and T4 concentrations were below the normal values in 4 youngest children. Blood serum T3 and T4 levels did not depend on the morphology of the intestinal villi in children treated with gluten-free diet (some children did not observe the diet and had atrophic lesions to the mucous membrane of the small intestine). Blood serum T3 level was relatively increased in children of group II with mucous membrane regeneration; in comparison with the value determined in the period of active disease.
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PMID:[Serum triiodothyronine and thyroxine levels in children with celiac disease]. 143 93

Essentially all patients with dermatitis herpetiformis (DH) and dermal granular IgA deposits have a gluten-sensitive enteropathy as seen in coeliac disease. A gluten-free diet would normally restore mucosal morphology within months. The dapsone medication required to suppress the skin lesions could be gradually reduced and/or finally discontinued in most patients if they constantly adhere to the diet. The immunological reactions may also be reduced. The gluten-free diet could thus be successful both concerning manifestations from the skin and the gut. Although well known in dermatological literature, diet therapy in DH has attracted little interest in journals of nutrition. A survey of this causal diet therapy for the disease therefore seems appropriate.
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PMID:Dietary treatment of dermatitis herpetiformis. 160 Sep 29

In a longterm study, we have divided coeliac disease into two distinct entities (abortive and permanent) based on the occurrence of large granular lymphocytes and natural killer cells within the epithelium of the gut. The natural killer and large granular lymphocytes cells were characterised by either immunohistochemical or phase contrast microscopical procedures on the initial biopsies from 15 children with coeliac disease. They were compared with seven individuals with partial villus atrophy and eight with normal villous morphology. Although the histological findings were similar in the initial biopsies of all patients with coeliac disease, the patients with permanent coeliac disease had a significantly lower number (0.41(0.61)cells/mm2) of large granular lymphocytes and natural killer cells compared with those patients with abortive coeliac disease (11.93 (6.23) cells/mm2). Those in the permanent group developed a significantly more pronounced flat mucosa after gluten challenge or provocation compared with the abortive group and had to remain on a strict gluten free diet in contrast with those in the abortive group. Thus, the occurrence of intraepithelial large granular lymphocytes and natural killer cells characterises two distinctly different coeliac diseases. Based on our results neither the histological evaluation of the biopsy nor the utilisation of the revised European Society for Paediatric Gastroenterology and Nutrition (ESPGAN) Criteria are adequate in diagnosing the two types of coeliac disease.
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PMID:Occurrence of large granular lymphocytes and natural killer cells in the epithelium of the gut distinguishes two different coeliac diseases. 162 57

We have characterized the presence of the intercellular adhesion molecule-1 (ICAM-1) (CD54) on human intestinal adenocarcinoma cell lines as a nonreducible polypeptide of Mr 93 kDa, identified as a rhinovirus receptor. Expression of ICAM-1 was positively correlated with enterocytic maturation, in that the percentage of ICAM-1+ cells was highest in the most differentiated cell line Caco-2. ICAM-1 could be up-regulated only on the less differentiated cell lines HT29 and T84 by phorbol 12-myristate 13-acetate and by the cytokines interferon-gamma (IFN-gamma) and interleukin (IL) 1 beta. Enterocyte ICAM-1 was involved in adhesion to activated T cells through binding to the leukocyte function associated antigen-1 (LFA-1). These data provide evidence that colon adenocarcinoma cell lines express functional ICAM-1 sensitive to cytokine regulation. These findings support the hypothesis that lympho-epithelial interactions involving the ICAM-1/LFA-1 pathway may be implicated in immunosurveillance of colon adenocarcinomas, inflammatory bowel disease and celiac disease, where increased levels of proinflammatory cytokines are locally produced within the gut mucosa.
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PMID:Expression, function and regulation of the intercellular adhesion molecule-1 (ICAM-1) on human intestinal epithelial cell lines. 168 Jun 98

Lymphocyte migration into the lymphoid organs and sites of inflammation is controlled by lymphocyte-endothelial cell interaction at sites where lymphocytes exit from the blood. Expression of Hermes-defined CD44 class of lymphocyte homing receptor and HECA-452 antigen specific for high-endothelium-mediating physiologic lymphocyte extravasation was studied in dermatitis herpetiformis, celiac disease, psoriasis, mycosis fungoides, lymphocytosis cutis, atopic dermatitis, and allergic contact dermatitis. Also, duodenal biopsies of patients suffering from dermatitis herpetiformis or celiac disease were studied for existence of these antigens. Infiltrating lymphocytes in the skin and in the duodenal area expressed homing receptor molecules when studied with monoclonal antibodies, Hermes-1 and Hermes-3, that recognize the CD44 class of molecules involved in lymphocyte binding to high endothelial venules in peripheral lymph nodes, mucosa-associated lymphatic tissues, and inflamed synovium. However, the HECA-452 antigen was not detected on the venules, neither in the skin nor in the duodenum. Even the venules possessing high endothelium morphologically were HECA-452 negative. These findings suggest the CD44 class of lymphocyte homing receptor(s) is also involved in lymphocyte homing to inflamed skin and the duodenal area of the gut. However, on the basis of HECA-452 staining, high endothelial venules in inflamed skin and duodenum are not antigenically identical with high endothelial venules in organized lymphoid tissues. This finding indirectly supports the idea that molecules and/or mechanisms mediating lymphocyte extravasation might be distinct in these organs.
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PMID:Lymphocyte migration into the skin: the role of lymphocyte homing receptor (CD44) and endothelial cell antigen (HECA-452). 169 39

The subclass distribution of IgG-producing immunocytes was examined by two-colour immunohistochemistry in gastrointestinal mucosa of 14 patients with selective serum IgA deficiency providing the following biopsy material: gastric (n = 1); jejunal (n = 12); colonic (n = 1); and rectal (n = 2). All except two patients suffered from various infections, and coeliac disease was observed in six of them. Control reference data were based on biopsies from immunologically intact subjects, including histologically normal jejunal (n = 10) and large bowel (n = 10) mucosa and stomach mucosa with slight chronic gastritis (n = 8). The total mucosal population of immunoglobulin-producing cells per 500 microns gut length unit was only slightly decreased in IgA deficiency because of an increased number of IgG (30%) and especially IgM (71%) immunocytes. The IgG1 immunocyte proportion in the proximal gut (median 87%) was higher than that in the comparable controls (gastric 69%, jejunal 66%). A similar trend was seen in the distal gut (69%) compared with controls from the large bowel mucosa (55%). Conversely, IgG2 and IgG3 cell proportions were significantly decreased compared with the respective controls from the proximal gut. The same was true for IgG4, which also was significantly reduced in jejunal mucosa. Paired staining for cytoplasmic J chain and immunoglobulin isotype showed 71% positivity for jejunal IgG-producing cells in IgA deficiency, which was somewhat reduced compared with comparable controls (89%). J chain appeared to be preferentially expressed by IgG1 cells (75%), but was also found in IgG2 (70%), IgG3 (32%) and IgG4 cells (33%). IgM-producing cells showed a J-chain positivity (99%) in IgA deficiency similar to normal (100%). Our results suggested that the block in mucosal B cell differentiation to IgA expression in the proximal gut is mainly located immediately upstream to the CH alpha 1 gene, giving excessive terminal maturation of J-chain-positive IgG1 immunocytes.
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PMID:Subclass composition and J-chain expression of the 'compensatory' gastrointestinal IgG cell population in selective IgA deficiency. 173 87

Oral contraceptive steroids (OCS) are well absorbed from the gastrointestinal tract in humans. However, while the progestogens are almost completely bioavailable, ethinylestradiol (EE2) is subject to extensive first pass metabolism consisting chiefly of conjugation with sulfate in the gut wall. Both EE2 and progestogens are well absorbed in patients with an ileostomy or with diseases such as cystic fibrosis or Crohn's disease. However in patients with celiac disease (gluten-sensitive enteropathy) the gut wall is less able to conjugate EE2 and thus its bioavailability is increased. The bioavailability returns to control values as the disease is improved following gluten withdrawal. Other drugs that are conjugated with sulfate, such as vitamin C and paracetamol, compete for available sulfate when coadministered with OCS leading to high plasma levels of EE2. Enzyme-inducing agents such as rifampicin, phenobarbitone, phenytoin and carbamazepine reduce blood levels of the OCS leading to contraceptive failure. In the case of anticonvulsants (but not rifampicin) this can be easily overcome by increasing the dose of OCS used. Broad-spectrum antibiotics are reported to cause failure of contraception by interfering with the enterohepatic circulation of EE2 but limited systematic studies show no evidence of such an interaction. Nevertheless practitioners are advised to recommend the use of alternative contraceptive precautions for women receiving broad-spectrum antibiotics concurrently with their OCS preparation.
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PMID:Oral contraceptive steroids--pharmacological issues of interest to the prescribing physician. 177 56

Gamma/delta T cells are increased in the gut epithelium of patients with coeliac disease compared with normal controls. The aim of this study was to determine whether the increase in gamma delta intraepithelial lymphocytes (IEL) is specific for coeliac disease, in which case it could be of diagnostic importance. Biopsies were obtained from children with no intestinal disease, coeliac disease, cow-milk-sensitive enteropathy/post-enteritis syndrome (CMSE PES) and miscellaneous other enteropathies (n = 67). Intraepithelial CD3+ and gamma delta T cells were identified in frozen sections using peroxidase immunohistochemistry. In normal biopsies there were 0-7 gamma delta IEL/100 cells in the epithelium. In untreated coeliac patients this increased to 9-22 gamma delta IEL/100 cells in the epithelium (P = 0.000004). Of 27 patients with morphologic intestinal damage which was not due to coeliac disease, four with CMSE/PES had gamma delta IEL/100 cells in the epithelium in the same range as the patients with coeliac disease. Of these, two had high densities of CD3+ IEL in the epithelium and were indistinguishable from patients with untreated coeliac disease. The other two could be excluded as possible coeliacs because their CD3+ IEL/100 epithelial cells were in the normal range. Thus an increase in gamma delta IEL is not specific for coeliac disease. However, enumeration of both of gamma delta IEL and CD3+ IEL densities will be useful in the exclusion of coeliac disease as a diagnosis in some children.
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PMID:Gamma/delta T cells and the diagnosis of coeliac disease. 182 88

Immunohistochemistry with monoclonal antibodies to the T cell receptor V beta regions 5, 6, 8 and 12 was used to determine whether normal intestinal lymphocytes that are potentially exposed to many bacterially derived superantigens show any preferential expression of particular V beta regions compared with the blood. No difference between V beta expression in the mucosa and the blood was observed, suggesting that they share a common pool of alpha beta T cells and that there is no expansion of alpha beta T cells in response to bacterial "superantigens" in the gut. The T cell receptor V beta expressed by the activated T cells in the lamina propria of bowel from patients with Crohn's disease was also studied. There was no increase in V beta 8 expression in these cells, suggesting that the increase in V beta 8 observed in the blood and mesenteric nodes of patients with Crohn's disease is not of primary importance in the aetiology of the disease. Finally, V beta expression by mucosal T cells in coeliac disease was studied. There was no difference in V beta use by T cells in coeliac disease and those in the blood and normal jejunum.
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PMID:T cell receptor V beta expression by mucosal T cells. 183 73

Bacteriologic cultures were taken from the mesenteric lymph nodes, biliary tract, blood, liver, spleen and pancreas of opossums (Didelphis virginiana) obtained directly from the wild for use as research animals. The overall incidence of salmonellosis outside the intestinal tract was 61% among 18 opossums. Salmonella was recovered from the gallbladder of six (33%) animals, indicating chronic biliary tract infection. Among these six animals, translocation of Salmonella to regional lymph nodes was observed in five animals, bacteremia in three animals, and spread to liver or spleen in five animals, respectively. The biliary tract was sterile in 12 opossums (67%). In these 12 animals, bacteria were isolated from the celiac and superior mesenteric lymph nodes of five animals, the blood of two animals, and the liver and spleen of one animal, respectively. Bacteriologic cultures were obtained from the intestinal tract and from extraintestinal sites in nine opossums. Salmonella were found in the small bowel of two animals, both of which had biliary salmonellosis. In addition, Salmonella was isolated from extraintestinal organs of three animals with negative cultures from the gut. All isolates identified were: S. enterica subsp houtenae. These data establish the biliary tract of wild opossums as a reservoir for Salmonella enterica subsp houtenae which may be particularly important when opossums are used in research laboratories.
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PMID:Salmonella infection of the biliary and intestinal tract of wild opossums. 184 88


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