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 teeth of 30 adult patients with dermatitis herpetiformis and 66 sex- and age-matched healthy controls were examined for dental enamel defects. Sixteen of the patients (53%) with dermatitis herpetiformis, opposed to only one (2%) of the healthy controls (p less than 0.001), were found to have coeliactype permanent-tooth enamel defects. The grades of these defects were milder than those described for severe coeliac disease. There was no correlation between the degree of enamel defects and jejunal villous atrophy. The present finding of frequent coeliactype dental enamel defects in adults with dermatitis herpetiformis suggests that these patients were already suffering from subclinical gluteninduced enteropathy in early childhood, at the time when the crowns of permanent teeth develop.
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PMID:Coeliac-type dental enamel defects in patients with dermatitis herpetiformis. 135 Jan 36

Although the proportion of gamma delta T-cell-receptor (TCR)-bearing intraepithelial lymphocytes is increased in the jejunum of patients with active coeliac disease, an abnormality thought to be specific among those with gluten-sensitive enteropathy, the factors influencing gamma delta TCR expression remain uncertain. We examined the relation between genetic factors associated with coeliac disease and intraepithelial gamma delta T lymphocyte distribution in both coeliac patients and their healthy first-degree relatives. 41% (45/109) of healthy relatives had an increased density of gamma delta T cells in their mucosa and 66% had an increased density of alpha beta T cells. By contrast with alpha beta T cells, the density of gamma delta cells was significantly associated with genetic markers for coeliac disease susceptibility (DR3, DQA, and DQB). We also found a dose effect of DQA and DQB genes on the number of intraepithelial gamma delta T cells. An increased density of gamma delta T cells in normal jejunal mucosa of a healthy individual with appropriate genetic determinants might be necessary for the development of the typical lesions of coeliac disease. Routine jejunal histological studies should include gamma delta T-cell counts, thus allowing early detection of coeliac disease latency.
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PMID:Intraepithelial gamma delta T-cell-receptor lymphocytes and genetic susceptibility to coeliac disease. 135 Nov 85

Epithelial adaptation clearly occurs during the course of intestinal cell-mediated immune responses to alloantigens. The adaptive response is similar to that seen in a number of enteropathies, namely villus atrophy, crypt hypertrophy, and crypt cell hyperplasia. In human fetal gut, polyclonal activation of lamina propria CD4+ T cells produces the same epithelial adaptive responses. Although these data provide overwhelming evidence that cell-mediated immune responses can cause enteropathy, the demonstration of antigen-specific T cells in the lamina propria of patients with enteropathy is still lacking, even in a disease as well-characterized as celiac disease. Epithelial adaptation in experimental and clinical situations, however, must involve a change in the mechanisms and mediators involved in normal intestinal homeostasis, such as epidermal growth factor and transforming growth factor-alpha and -beta, and in the interactions between epithelial cells and the underlying stromal cells.
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PMID:Cell-mediated immune injury in the intestine. 135 77

Bilateral occipital calcifications, occurring in celiac disease, are factors coming under a particular cerebral syndrome, which also includes epilepsy, migraine-like headache, visual troubles and mental deterioration. They seem to arise from hypofolatemia following gluten-induced enteropathy.
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PMID:Cerebral occipital calcifications in celiac disease. 140 90

Twenty-nine patients affected with dermatitis herpetiformis (HD), all of whom were on a diet including gluten, were investigated for symptoms of enteropathy. Of these patients, 71% presented severe intestinal lesions, indistinguishable from those found in coeliac disease (CD). However, there were little other clinical manifestations of this finding since only three children in this group had weight and height < or = P3. Of the remaining children, 18% had moderate intestinal atrophy and 10% had normal mucosa or mucosa with negligible changes. When changed to a gluten free diet, the intestinal lesions subsided, dermic lesions disappeared in 17 patients, improved in 8 others and remained the same in the other three patients that were still on variable diets. A study of human leukocyte antigens (HLA) class II showed a total association with Dqw2 and 85% association to DR3, which was identical to the coeliac disease control group. These findings lead one to conclude that HD and CD are different clinical expressions of the same sensitivity to gluten which is associated to an immunological disorder with a common genetic base linked to certain HLA molecules.
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PMID:[Dermatitis herpetiformis vs. celiac disease]. 144 40

The coeliac disease (CD) or gluten-sensitive enteropathy (GSE) is a permanent intolerance to wheat gliadin and to correlated proteins inducing malabsorption and typical damages of the jejunal mucosa (total or subtotal villous atrophy = SVA) in genetically-predisposed individuals ("DQW2"). A large amount of research has been devoted to CD pathogenesis: the most recent studies, thanks to sophisticated and experimental methods, support the pathogenetic immunological theory and the one of direct cytotoxicity. The correct diagnostic procedure for CD, established in 1970 by the European Society for Pediatric Gastroenterology and Nutrition (ESPGAN), suggested three small bowel mucosal biopsies. In the last years, because of the difficulties of such a practice, the necessity of non-invasive diagnostic approaches has developed; such approaches have been verified in absorption tests (one-hour blood xylose, intestinal permeability methods) and in immunogenetic tests (antibodies antigliadin, anti-reticulin, anti-endomysium, anti 90 KD glycoprotein, anti-human jejunum, HLA I/II antigens). The specific MHC antigens establish CD's incidence in several population and in particular situations, as in first-degree relatives and in diseases associated with CD (dermatitis herpetiformis (DH), insulin dependent diabetes mellitus (IDDM) and other auto-immune syndromes). The specific serum antibodies singly used as first level screening if estimated in combination with absorption tests, reach the highest levels of specificity and sensibility in CD diagnosis. It's anyway fundamental the comparison with at least a typical CD histological feature, caused by a challenge with a sufficient gluten to be carried in dubious cases and in non high auxological risk age (ESPGAN 1989). Adolescence is a period of frequent non compliance with a gluten-free diet and of particular psychological and physical problems: the apparent "gluten insensitivity", typical of teen-agers and adults, recalls the definitions of silent CD and latent CD (iceberg like). In the first case the jejunal mucosa is abnormal and the symptomatology isn't evident. In latent CD, genetically restricted, the mucosa is normal but there are minimal markers of inappropriate immunity to gliadin (at intestinal humoral immunity level) and a possible worsening of histological lesions to the third stage under environmental stimuli. This represents a two-stage model CD. That's why CD is still under-evaluated despite recent statistics reporting an increasing incidence (late and atypical forms). Prevalence rates between 1:300 and 1:4,000 and more are quoted in literature. The necessity of a strict gluten-free diet is confirmed by the evident frequency of lymphoma and by the increased risk of malignancy in untreated CD.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Celiac disease and its diagnostic evolution. Comparisons and experiences in a hospital pediatric department (1975-1992). I]. 152 93

The ultrastructural binding sites of endomysium antibodies, specific serological markers of gluten sensitive enteropathy, were investigated in the rabbit oesophagus using the immunogold technique. Endomysium antibodies from sera of patients with dermatitis herpetiformis and with coeliac disease bound in an identical manner in a non-fibrillar material closely associated with fine collagenous-reticulin fibrils and also with similar fibrils connecting smooth muscle cells and elastic tissue in the endomysial connective tissue. These observations suggest that IgA antibodies in sera from patients with dermatitis herpetiformis and coeliac disease recognise a common antigen in an amorphous component associated with the reticular connective tissue of oesophageal lamina muscularis mucosae and thus confirm the probable identity of IgA class endomysium and jejunal antibodies.
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PMID:Ultrastructural binding sites of endomysium antibodies from sera of patients with dermatitis herpetiformis and coeliac disease. 154 14

Gliadin antibodies of the IgG and IgA isotypes and IgG subclasses were measured in 200 adults who were randomly selected from the Icelandic National Register. Those with the highest gliadin antibody concentrations were invited with negative controls to participate in a clinical evaluation. Neither the study subjects nor the physicians who recorded and evaluated the clinical findings were aware of the antibody levels. Significantly higher proportion of the gliadin antibody positive individuals reported unexplained attacks of diarrhoea (p = 0.03), and IgA gliadin antibodies were associated with increased prevalence of chronic fatigue (p = 0.0037). The gliadin antibody positive group also showed significantly decreased transferrin saturation, mean corpuscular volume and mean corpuscular haemoglobin compared with the gliadin antibody negative controls. Serum folic acid concentrations were significantly lower in the IgA gliadin antibody positive individuals. On blind global assessment 15 of the 48 participants were thought to have clinical and laboratory features that are compatible with gluten sensitive enteropathy, and 14 of these were in the gliadin antibody positive group (p = 0.013). Complaints that have not been associated with gluten intolerance had similar prevalence in both groups with the exception of persistent or recurrent headaches that were more common in the gliadin antibody positive group. These findings raise the possibility that a subclinical form of gluten intolerance may be relatively common.
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PMID:Do adults with high gliadin antibody concentrations have subclinical gluten intolerance? 154 15

The finding in primary IgA nephropathy of increased levels of IgA to food antigens and particularly to gliadin prompted the hypothesis that a subgroup of these patients may have latent coeliac disease. The observation that gliadin may experimentally induce IgA mesangial deposits supported this hypothesis. We evaluated specific immunological markers of coeliac disease (antiendomysium antibodies) which parallel histological changes of gluten sensitive enteropathy, and an IgA immunofluorescent test for antigliadin antibodies in 18 patients with IgA nephropathy, in 56 untreated coeliac disease patients, in 254 controls (58 healthy and 196 disease controls). Antiendomysium antibodies were positive in 89.28% of coeliac patients, but negative in all IgA nephropathies and controls. IgA immunofluorescent test for antigliadin antibodies, negative in all IgA nephropathy patients, was positive in 76.78% of coeliac patients and in 4.91% of controls. ELISA IgA antigliadin antibodies were negative in controls, but positive in 22.22% of IgA nephropathy patients and in 60.71% of coeliac patients. Our data would suggest that in most patients with IgA nephropathy there is no evidence of latent coeliac disease.
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PMID:Do IgA antigliadin and IgA antiendomysium antibodies show there is latent coeliac disease in primary IgA nephropathy? 158 90

Intestinal disease might contribute to osteopenia. Measurements of IgA antibodies to gliadin have been established as an accepted screening procedure for detection of coeliac disease. When we applied these measurements to 92 patients with verified osteoporosis, 11 subjects (12%) were found to have elevated levels. This is markedly higher than the incidence in healthy subjects (3%). However, the patients with raised levels of IgA antibodies displayed no clinical symptoms and no laboratory evidence of calcium malabsorption. Thus their values for serum calcium, phosphate, parathyroid hormone (PTH), alkaline phosphatase and osteocalcin, as well as the fasting urinary excretion of hydroxyproline and calcium, were similar to those found in other patients with osteoporosis. Intestinal biopsy verified coeliac disease in three patients and was normal in another three. This gives an incidence of verified coeliac disease in this patient group that is approximately tenfold higher than that in the healthy population. Subclinical coeliac disease appears to be unusually over-represented among patients with idiopathic osteoporosis, and screening for gliadin antibodies might therefore be a valuable addition to the routine assessment of the osteopenic patient. The mechanisms underlying the relationship are not clear, but calcium malabsorption is not evident.
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PMID:Screening for antibodies against gliadin in patients with osteoporosis. 158 66


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