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)

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

The value of proximal intestinal mucosal biopsy was reviewed in 381 children presenting with chronic diarrhoea over an eight year period. An enteropathy was detected in 44% of cases and was more frequently seen in those aged less than 6 months. A diagnosis was established in 91% of cases. The most common diagnosis was the postenteritis syndrome where the presence of an enteropathy indicated those requiring treatment with a cows' milk free diet. Other conditions where a biopsy facilitated diagnosis or treatment included giardiasis, enteropathogenic Escheriichia coli, crytosporidiosis, autoimmune enteropathy, and microvillous atrophy. Coeliac disease was considered in 55% of children and established in 8%, clearly identifying those requiring a gluten free diet. This also emphasises the important role of the biopsy procedure in the exclusion of specific diseases. Proximal small intestinal mucosal biopsy is an essential investigation in children with chronic diarrhoea in whom an enteropathy is suspected.
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PMID:The value of proximal small intestinal biopsy in the differential diagnosis of chronic diarrhoea. 843 6

Adult coeliac disease has a broad clinical spectrum and remains undetected for years. Among subclinical deficiency states, attributable to coeliac enteropathy, combined iron and folic acid malabsorption is predominant. An unexplained recurrent iron anaemia is an indication for small intestinal biopsy. Gastro-intestinal disorders are present in only 50% of the cases. Coeliac disease is frequently associated with other major histocompatibility complex (MMC)-linked diseases which are mediated by immunological mechanisms: dermatitis herpetiformis, oral ulcerations, IgA nephropathy, rheumatoid arthritis, sarcoidosis. Dermatitis herpetiformis is a useful model for examination of the spectrum of mucosal changes that typify gluten sensitivity and subliminal lesions without villous atrophy. An increased interest is devoted to the intra-epithelial T-lymphocyte population, not only in the small intestine, but at the level of the stomach and the colon. A "rectal challenge" test has been proposed for detecting gluten sensitivity in coeliac patients. Such a test could be an original method of screening, reducing so the need of small intestinal biopsy. The preliminary results are to be confirmed. Until now, jejunoscopy remains mandatory for the diagnosis and the survey of intestinal lesions related to coeliac disease.
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PMID:[Celiac disease in adults: clinical aspects--role of endoscopy]. 163 35

HLA-DR, DQ, and DP restriction fragment genotyping was undertaken in 23 dermatitis herpetiformis patients and 53 healthy control subjects. HLA-DQw2 was present in 100% of patients with dermatitis herpetiformis (23 of 23) versus 40% of control subjects (21 of 53). Significant secondary associations occurred with HLA-DR3 (91% of patients versus 28% of control subjects) and DPw1 (39% of patients versus 11% of control subjects). Dermatitis herpetiformis and coeliac disease thus share an identical HLA class II association. It is likely that HLA class II genes directly influence the immune responses leading to mucosal damage in both diseases. The strongest candidate for disease susceptibility to dermatitis herpetiformis is DQw2. The HLA molecule most likely to be involved in coeliac disease is a specific DQ alpha/DQ beta heterodimer, encoded in cis arrangement in DR3 haplotypes or in trans arrangement in a DR5, 7 genotype. Our data on dermatitis herpetiformis patients fits this model perfectly. All these patients are capable of expressing this molecule, which may be responsible for the gluten sensitive enteropathy seen in a subgroup of patients with dermatitis herpetiformis and coeliac disease.
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PMID:HLA association with dermatitis herpetiformis is accounted for by a cis or transassociated DQ heterodimer. 167 26

We identified and purified six human noncollagenous protein molecules that specifically bind to serum IgA from patients with coeliac disease, and which as a combination can act as true antigen to reticulin antibodies. In affinity chromatography, the purified human protein molecules removed antibodies against reticulin and endomysium from serum samples of coeliac disease patients. We postulate that an autoimmune mechanism operates in generating the jejunal damage in gluten-sensitive enteropathy and that the human protein molecules described here act as self-antigens in the disease.
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PMID:Reaction of human non-collagenous polypeptides with coeliac disease autoantibodies. 167 69

Celiac disease (CD) is a permanent gluten-sensitive enteropathy appearing in individuals genetcally predisposed. Its incidence varies according to the authors, but is situated about 1/1.500 alive newborn infants (ANI). Recently, a decreased in the incidence of the disease as well as a delay in the onset of symptoms have been reported in several countries. The incidence of the disease in Spain is unknown so we have studied it in our population. In the period 1976-1987, 117 patients were suspected to have CD in the different centers performing intestinal biopsies in Vizcaya. Diagnosis was confirmed in 87 cases, thus implying an incidence of 1/2.151 ANI. Age onset has been stable along the years, and most cases continue to be diagnosed during the first 2 years of life.
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PMID:[Incidence of celiac disease in Vizcaya]. 176 52

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

Recurrent aphthous stomatitis (RAS) or canker sores occur in 20-60% of all persons. The lesion occurs because of increased viscosity of oral submucosal extracellular matrix (ECM). The lesions begin in the second decade and peak in the third decade. Sex hormones are an important influence on fibroblasts, especially in the early phase of exposure. Sex hormones are known to concentrate, to a degree, in the bucal mucosa in animals. Lesions of RAS localize clinically and experimentally at sites of trauma. In the skin, edema is known to trigger early cellular inflammation. Increased viscosity of ECM heightens the response. The histopathology of the ulcerated lesions is similar to that which occurs under sites of acute inflammation in the skin. Systemic corticosteroids completely supress the lesions. Caustics, such as silver nitrate and phenol, stop the growth and pain of lesions. Irritants are known to break ECM viscosity. The oral mucosa exerts some control on underlying ECM. Substances such as lectins influencing the mucosa could influence ECM. Soluble substances in food or organisms could also penetrate to influence ECM. A number of different foods have been incriminated as trigger agents in individual cases. This includes gluten in patients with gluten sensitive enteropathy. Gluten is known to alter the mucosa of the small intestine in persons with celiac disease.
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PMID:Aphthous stomatitis (canker sores): a consequence of high oral submucosal viscosity (the role of extracellular matrix and the possible role of lectins). 180 53

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

In 43 children with neglected coeliac disease (NCD) the growth and nutritional status (NS) were followed-up and analysed in the period between the age of 3 and 9 years in which prolonged exposure to gluten resulted in the persistent enteropathy. The significant "weight for age" and "height for age" deficits without concomitant "weight for height" deficits were observed at each yearly interval in the monitored period. The significant positive correlation between the percentage of children with the deficient NS and the duration of the exposure to gluten was found for the total examined period. There was also evidenced the significant bone age v. height age deficit. The linear growth retardation observed in NCD may be considered as the result of the progressive deficiency of NS.
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PMID:Growth, bone age and nutritional status in neglected coeliac disease. 184 3


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