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)

In coeliac disease, gluten, or one of its fractions, combines with a gut-wall macrophage or lymphocyte to form a lymphoid cell which is recognised by the host as foreign. It is proposed that this cell, rather than being eliminated as the target of a cell-mediated attack by the host, becomes autonomous and initiates a graft-versus-host (GvH)-like reaction. The reaction is largely confined to the gut wall and its associated lymphoid tissue. The severe cachexy and the peripheral lymph-node and splenic atrophy may be explained as features of chronic GvH disease. or a "runting" syndrome. Untreated coeliac disease may lead to lymphomatous transformation indistinguishable from the lymphoma of experimental chronic GvH disease
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PMID:Coeliac disease: a graft-versus-host-like reaction localised to the small bowel wall? 611 75

Deficiency of either folic acid or vitamin B12 may interfere with DNA synthesis and result in megaloblastic anemia or other conditions. These 2 vitamins have dissimilar molecular structures and are present in different foods; they are also absorbed and metabolized differently. In 201 consecutive cases of megaloblastic anemia, for 90% the cause was alcoholism and poor diet; 0.5% (1 case) was related to oral contraceptives (OCs). Megaloblastic anemia due to folate deficiency has occasionally been reported in patients with inflammatory bowel disease and has been attributed to poor diet, impaired absorption, and increased tissue utilization of folate. Sulfasalazine, a compound containing a sulfa drug and a salicylate that is broken down to its active components by the gut flora, is widely used in the treatment of inflammatory bowel disease and has been shown to impair the absorption of folic acid, polyglutamyl folate, and methyl-tetrahydrofolic acid in patients with these disorders. There is also evidence suggesting an interaction between anticonvulsant drugs and folate balance. A number of cases of megaloblastic anemia due to folate deficiency have been reported in women taking OCs. While in some cases no apparent cause for the megaloblastic anemia other than contraceptive therapy was demonstrated, in many patients other underlying disorders that were likely to disturb folate balance such as celiac disease, decreased dietary vitamin intake, and the administration of other drugs known to affect folate status have also been present. There is no convincing evidence that sex steroids affect folate absorption; about 20% of women taking OCs were found to have mild megaloblastic changes on Papanicolaou smears. These changes disappered after folic acid therapy, suggesting that OCs may cause an increased demand for folate limited to the reproductive system. Another finding is of low serum cobalamin levels in women using OCs; this appears however to be a laboratory abnormality of uncertain cause and of no clinical significance.
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PMID:Drugs and vitamin B12 and folate metabolism. 613 2

Regulation of pancreatic exocrine secretion is comprised of a complex interplay between hormonal and nervous mechanisms. Stimulatory gut hormones which act via the circulation include secretin, CCK, gastrin and bombesin, while VIP operates through peptidergic nervous release. Pancreatic polypeptide and glucagon are two examples of circulating inhibitory hormones while inhibition by somatostatin is through a paracrine release mechanism. Although the effects of vagal cholinergic nerves have been previously thought to be indirect through hormone release evidence is now accumulating for a direct role. Altered hormone release has been noted in chronic pancreatic insufficiency, cystic fibrosis and coeliac disease and may contribute in an important way to the pathophysiology of these malabsorptive disorders.
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PMID:Neuro-hormonal control of pancreatic function in man and its failure. 613 50

Mannose-rich 90 kD glycoprotein, a constituent of skin and small-bowel mucosa, was identified as antigen in circulating IgG-type immune complexes in dermatitis herpetiformis and coeliac disease by means of an enzyme-linked immunosorbent assay. High levels of 90 kD glycoprotein-IgG complexes were found in 7 out of 12 patients with dermatitis herpetiformis and in 10 out of 20 patients with coeliac disease but in only 2 out of 20 patients with systemic lupus erythematosus. The highest levels of 90 kD antigen-IgG complexes were found in patients with dermatitis herpetiformis. The amount of these complexes did not correlate with the degree of jejunal villous atrophy. The 90 kD glycoprotein-containing immune complexes with targets in skin and gut may be involved in the pathogenesis of dermatitis herpetiformis and coeliac disease.
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PMID:Demonstration of tissue 90 kD glycoprotein as antigen in circulating IgG immune complexes in dermatitis herpetiformis and coeliac disease. 614 20

Sprague-Dawley rats were exposed to lectins, either concanavalin A (Con A) or wheat germ agglutinin (WGA). The lectins were instilled into a ligated segment of the distal small intestine together with permeability markers, fluoresceinated dextran (MW 3,000) or a mixture of differently sized polyethylene glycols (MW 400, 600 and 1,000). WGA-treated rats showed a decreased permeability to small molecules (MW less than 600) of polyethylene glycol but an increase for a larger dextran molecule (MW 3,000). These effects as well as the morphological findings might mimic the situation in patients with food allergy or celiac disease. Con A-treated rats had decreased intestinal permeability to the larger dextran molecules (MW 3,000), whereas the passage of small molecules was unaffected and the ultrastructural effects were minute. The Con A-induced changes could result from a mucotractive effect, associated with a low-grade gut allergy. These observations suggest that lectins can affect both the ultrastructure and the permeability of the intestine, in a way assumed to mimic allergic reactions to food constituents.
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PMID:The effect of concanavalin A and wheat germ agglutinin on the ultrastructure and permeability of rat intestine. A possible model for an intestinal allergic reaction. 620 12

Autoantibodies reacting with endocrine cells in the gastrointestinal mucosa were found by indirect immunofluorescence in 22 out of 268 sera (8.2%) obtained from patients with coeliac disease, Crohn's disease, ulcerative colitis, irritable bowel syndrome, and from subjects without bowel disease. A double immunofluorescence technique showed that the autoantibodies reacted with cells secreting gastric inhibitory polypeptide (glucose dependent insulinotropic polypeptide, GIP), secretin, somatostatin or enteroglucagon. Most sera contained antibodies against more than one cell type. Neither the presence of a particular antibody nor the pattern of antibody combinations appeared to be specific for any diagnostic category. The mean plasma GIP concentrations, however, both fasting and two hours after a test meal, were significantly lower in subjects with GIP cell autoantibodies. Thus gut hormone cell autoantibodies may be markers of impaired hormone secretion.
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PMID:Autoantibodies to gut hormone secreting cells as markers of peptide deficiency. 634 Nov 78

Previous reports suggest that prolactin could be one of the factors controlling intestinal mucosal growth. Therefore plasma levels of prolactin have been measured at the time of jejunal biopsy performed for suspicion of celiac disease. One hundred eighty-seven biopsies from 166 children have been reviewed according to histology, age, diagnosis, and plasma prolactin. No difference in the plasma prolactin could be detected among a group of 117 normal biopsies (9.4 +/- 0.4 ng/ml, mean +/- SEM), 31 biopsies with partial atrophy of various degree (9.0 +/- 0.9 ng/ml), and 39 biopsies with flat mucosa (9.1 +/- 0.7 ng/ml), nor could we demonstrate an increase in prolactin according to age and diagnosis (celiac disease before and after treatment, cow's milk protein intolerance, isolated postenteritic syndrome, selective sugar intolerance, and functional gut problems). Prolactinlike material has been detected by immunoperoxidase in the jejunal mucosa. The intracellular granules are located in the infranuclear portion of isolated epithelial cells mainly in the crypts. This material could not be correlated with the corresponding prolactinemias, whatever the histological appearance of the mucosa. These results would suggest that plasma prolactin is not a marker of jejunal regeneration in children. The nature and function(s) of this prolactinlike material remain to be established.
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PMID:Prolactin and the gut: a controversy. 638 57

Coeliac disease is a permanent condition of gluten intolerance associated with characteristic gluten-sensitive changes in the jejunal mucosa. In Edinburgh and the Lothians Region of Scotland, the prevalence of the disease is one in 1637 (61/100,000) with considerable variation in age, and sex-specific prevalence and incidence. Several lines of evidence indicate an immunologic basis for the gluten-sensitive enteropathy in coeliac disease. Animal models of intestinal T cell-mediated reactions in the gut have shown pathologic features similar to those of coeliac disease. These include changes in villus and crypt architecture with crypt hyperplasia, and increased numbers of intraepithelial lymphocytes and of intraepithelial lymphocyte mitosis. Experimental CMI reactions also influence differentiation of goblet cells and expression of Ia antigen on epithelial cells, but these factors have not yet been reported for the coeliac mucosa. In addition to this circumstantial evidence, based on animal work, other factors which suggest that CMI reactions rather than antibodies are relevant to coeliac disease include the findings of antigliadin antibodies in a proportion of normal individuals, patients without gastrointestinal disease (seen in hospital), and patients with jejunal Crohn's disease. In addition, there is a well documented patient with adult onset primary hypogammaglobulinaemia and coeliac disease. The underlying pathogenesis in coeliac disease can be envisaged as failure of the normal inhibition of immune responses to this particular food antigen in the gut. Manipulation of immunoregulatory mechanisms would provide a new approach to treatment or cure of this disease and of other food protein-sensitive enteropathies.
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PMID:Gluten intolerance (coeliac disease). 639 Dec 93

The recently described IgA anti-endomysial antibodies (IgA-EmA) are directed against the intermyofibril substance of the smooth muscle, which may correspond either to a reticulin-like structure or a surface component of smooth muscle fibrils. These antibodies occurred in about 80% of sera of thirty-eight patients with dermatitis herpetiformis (DH), in about 70% of twenty-eight patients with coeliac disease and in about 20% of nine patients with other enteropathies. IgG class anti-gliadin antibodies (AGA) also occur in each of these diseases. Both antibodies were detected on monkey oesophagus by immunofluorescence. The IgA-EmA could not be detected in 122 control sera from patients with other gut or skin diseases, including fifteen cases with ulcerative colitis and fifteen cases with linear IgA bullous dermatosis (LABD). The presence and the titre of IgA-EmA and AGA paralleled the severity of the jejunal changes in patients with coeliac disease.
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PMID:IgA anti-endomysium antibody. A new immunological marker of dermatitis herpetiformis and coeliac disease. 643 66

Forty-eight gut mucosa specimens from 27 children with celiac disease, diagnosed by means of conventional serial biopsies taken at different dietary conditions, were studied by means of scanning electron microscopy (SEM). The observations were correlated with those made by concomitant dissection microscope (DM), light microscope (LM), and transmission electron microscope (TEM) examinations. Five children with constitutional short stature served as controls. The results of the SEM analyses were in good conformity with the observations made by DM, LM, and TEM. In addition, SEM was found to offer further structural variables to be analyzed. In active celiac disease and after challenge with dietary gluten, which is necessary to establish the diagnosis of children, the lesions specifically observed by SEM were (1) a strikingly uniform destruction of the villi and a distortion of the enterocytes but with preserved extrusion zones, and (2) a decrease and disruption of the glycocalyx of the enterocytes with marked irregularity of the microvilli. After successful dietary treatment and despite a normalization of the gut mucosa by routine LM, SEM often disclosed persisting lesions of the enterocytes. It was concluded that by inclusion of SEM in the routine assessments of gut biopsy specimens in children with celiac disease, the diagnostic precision becomes increased.
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PMID:Surface ultrastructure of the small intestine mucosa in children with celiac disease. I. Untreated disease and effects of long-term gluten elimination and challenge. 648 22


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