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Query: UMLS:C0007570 (celiac disease)
 13,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One of the most reliable sero-diagnostic tests for coeliac disease (CD) is the measurement, by ELISA, of serum IgA antibodies to tissue transglutaminase (tTG) adsorbed to the wells of microtitre plates. In spite of its reliability, however, some discrepancies exist with the results obtained by the antiendomysium histological assay (EMA) and by biopsy the accepted gold standard. Among the reasons for these differences in titres between the ELISA and the last 2 mentioned assays are the conformational changes that proteins undergo on adsorption and the importance of conformational epitopes on tTG for diagnosing CD. To address this problem, a novel procedure was developed using guinea-pig tTG (gptTG) free in solution to interact with IgA antibodies in the sera of CD patients. Any immune complexes so formed are then captured by anti-tTG antibodies preadsorbed to the wells of microtitre plates. This immunocapture method was optimized for the amount of soluble gptTG needed to interact with all the IgA's anti-tTG present in fixed dilutions of serum samples, the amount of rabbit IgG anti-gptTG used to coat the wells of microtitre plates and the order of addition of the reaction components. Comparison of the IgA titres obtained by immunocapture with those by EMA and ELISA (adsorbed tTG) on 9 highly positive and 6 weakly positive sera from clinically characterized CD patients and 5 negative sera from non-CD control subjects revealed that the IgA titres by the immunocapture procedure were well correlated with those obtained by EMA, whereas the titres on ELISA showed discrepancies with both immunocapture and EMA.
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PMID:Development of an immunocapture method for measuring IgA antibodies to tissue transglutaminase in the sera of patients with coeliac disease. 1654 71

We report the case of a 77-year-old Japanese man with natural killer (NK)-like T cell lymphoma of the small intestine diagnosed after an emergency laparotomy for perforated peritonitis. Immunohistochemical staining of the tumor showed that the patient had CD3+ CD8+ CD30- CD56+ CD68- CD79a- UCHL-1+ EMA- LMP-1 NK-like T cell lymphoma. The patient had a history of hepatocellular carcinoma (HCC) and was also diagnosed with T cell non-Hodgkin's lymphoma associated with T cell receptor (TCR) reconstruction in the Jgamma chain. Intestinal T cell lymphoma is uncommon and very few cases of CD56+ T cell lymphoma, otherwise known as NK-like T cell lymphoma, have been reported. The patient did not have a history of gluten-sensitive enteropathy (celiac disease). Multiple lesions appeared within months after the initial operation and his condition deteriorated rapidly. We think that this patient probably had NK-type granular lymphocyte-proliferative disorder (NK-GLPD) because the percentage of CD16+ CD56+ cells among peripheral blood mononuclear cells was elevated, at 21%. We report this case to help elucidate the relationship between underlying digestive organ disease and the development of intestinal NK-like T cell lymphoma. An accumulation of other such cases is needed to determine the etiology of this disease.
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PMID:Natural killer-like T cell lymphoma of the small intestine: report of a case. 1663 56

Anti endomysial and anti transglutaminase (EMA/TTG) antibodies measurements in large population groups, show that celiac disease is significantly more common than previously thought and 0.5-1% of the population suffer this condition. The recognition of atypical clinical presentations by active screening of high risk groups is a successful global initiative. In Chile there is little awareness of the enormous changes occurred in this field. Available national information on typical presentation of the disease shows that it is found in 1:1836 live births, figure that is comparable to European societies. Two urgent tasks are required in our country. First, to asses the Chilean population using EMA and/or TTG. Second, to improve the legal aspects that regulate consumer information about gluten content in processed foods. We here review the most relevant aspects to be considered to improve the management of celiac patients and the tasks that require the participation of health authorities for their implementation.
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PMID:[Improving the management of celiac disease: an urgent challenge]. 1667 11

Celiac disease is an immune mediated enteropathy initiated by ingestion of gluten, in genetically susceptible individuals. With changing epidemiology, celiac disease initially thought to affect only Europeans, has been increasingly reported from other parts of the world including India. However, its true prevalence in India is still not known, as the diagnosis is being missed. The gold standards for diagnosis have been characteristic small intestinal mucosal changes on gluten and a full clinical remission on its removal from the diet. Presence of serological antibodies, which disappear on gluten free diet further confirms the diagnosis. The understanding of the histopathology of celiac disease has changed over the years. The small bowel mucosal lesion of celiac disease is an evolutionary process with normal mucosal architecture and an increase in intraepithelial lymphocytes at one end of the spectrum and classical flat mucosa at the other. In the Indian subcontinent celiac disease has a heterogeneous histological presentation and the diagnosis may be missed if it is based only on severe mucosal changes or the serology is not considered when moderate or mild mucosal changes are present. The last two decades have shown that antiendomysical (Anti EMA) and anti tissue transglutaminase antibodies (anti-tTGA) have a sensitivity and specificity of more than 95% to diagnose celiac disease. Anti EMA tests being operator dependent are more liable to errors and anti- tTGA may be preferred for large scale screening. However, the different source of tTGA antigen, varied techniques of production and the use of arbitrary units by different commercial kits can influence the diagnostic accuracy of the anti-tTGA assay. There is a strong genetic association of celiac disease with HLA-DQ2 or DQ8. The presence of HLA-DQ2 hetrodimer in more than 97% of a group of North Indian patients with celiac disease indicates that this population has a similar genetic risk for the disease. HLA DQ2 typing can be used for ruling out celiac disease where the diagnosis is equivocal as it has a negative predictive value of greater than 95%. Given the protean clinical manifestation and the heterogeneous histology a standard algorithm for diagnosis of celiac disease is important.
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PMID:Diagnosis of celiac disease. 1693 66

Histological confirmation of infiltrative lesions via small bowel biopsy is the gold standard for diagnosing celiac disease. Four serum antibody assays may serve as a first-step diagnostic tool to identify biopsy candidates: immunoglobulin A tissue transglutaminase (IgA tTG), IgA endomysial antibody (IgA EMA), IgA antigliadin antibody (IgA AGA), and IgG antigliadin antibody (IgG AGA). IgA tTG and IgA EMA offer the best diagnostic accuracy. Patients with selective IgA deficiency may have falsely negative IgA assays (strength of recommendation [SOR]: B, based on a systematic review, multiple small cross-sectional studies, and expert opinion).
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PMID:Clinical inquiries: What blood tests help diagnose celiac disease? 1713 49

Clinical studies have estimated a 10- to 20-fold increased risk for celiac disease (CD) in patients with selective IgA deficiency (SIgAD). For this reason, screening for CD is mandatory in SIgAD patients, but it represents a special challenge since the specific IgA class antibodies against gliadin (AGA), endomysium (EMA), and tissue-transglutaminase (tTG) are not produced in patients with CD. IgG class counterparts of these antibodies may be informative; in particular IgG EMA has been demonstrated to be a valid marker for diagnosing CD in SIgAD cases, but it is not used much in clinical laboratories, because it is cumbersome and involves some technical difficulties. Even if it was widely used in clinical laboratories, the measuring of IgG AGA has shown a less-than-optimum diagnostic accuracy, so that now it tends to be substituted by tests for anti-tTG IgG, for which the few available studies have shown diagnostic performances superior to AGA. Since it is not known whether various available methods for measuring IgG anti-tTG antibodies offer similar diagnostic performances, we have compared the results obtained from nine second-generation commercial methods (D-tek, Phadia, Immco, Orgentec, Radim, Euroimmun, Inova, Aesku, Generic Assays), measuring IgG anti-tTG antibodies in 20 patients with CD and SIgAD and in 113 controls (9 patients with SIgAD without CD, 54 patients with chronic liver disease, and 50 healthy individuals). Diagnostic sensitivity, calculated by means of ROC plot analysis, ranged between 75% and 95%, and specificity ranged from 94% to 100%. In the same population, the diagnostic sensitivity and specificity of AGA IgG were 40% and 87%, respectively. Even though they perform differently, all IgG anti-tTG methods evaluated are reliable serological assays for the diagnosis of CD in SIgAD patients, with diagnostic accuracy superior to the AGA IgG method. The methods that use a mix of tTG and gliadin peptides as the antigenic preparation have a specificity slightly lower than that of the methods that use only tTG.
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PMID:Diagnostic accuracy of IgA anti-tissue transglutaminase antibody assays in celiac disease patients with selective IgA deficiency. 1778 8

This review of the current scenario of celiac disease (CD) in India covers both pediatric and adult CD. CD is primarily reported from northern India with isolated case reports from the rest of the country. CD cases among Indian children are associated with multiple DR3-DQ2 haplotypes. Delay in diagnosis is contributed by multiple factors including atypical presentations. Use of serological tests, IgA EMA and anti-tTG antibodies, along with modified ESPGHAN criteria provides a definitive diagnosis of CD. Dietary management is often difficult due to non-availability of labeled and marketed gluten-free foods. A majority of children with CD show normalization of nutrition, substantial improvement in growth parameters and attainment of healthy percentile curves on gluten-free diet. Small bowel histology remarkably improves but does not normalize even after 2-3 years on gluten-free diet. The true burden of the disease should be addressed by large epidemiological studies.
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PMID:Celiac disease in India. 1897 75

In 1997, a German group demonstrated that the antigen of the biomarker EMA (endomysial antibodies) in coeliac disease is a calcium-dependent thiol enzyme, transglutaminase type 2 (TG2). This most important discovery opened up an exciting field of research aimed at a better understanding of the pathogenesis of coeliac disease, a T-cell-driven autoimmune disorder with a prevalence of about 1%. The accidental activation of TG2, possibly caused by a stress-induced local deficiency of zinc in the intestinal wall, might play a key role where the enzyme catalyzes an atypical deamidation of specific glutamine residues of food gliadins. The genetic contribution is HLA DQ2 or DQ8, which can form a complex with the TG2-modified gliadin residues, resulting in an immune response with the formation of antibodies against both gliadin and the enzyme. Indeed, the immunopathogenesis of coeliac disease can now be recognized partly at the molecular level. Progress has already improved the opportunities for laboratory diagnostics and, hopefully, new ways of treating and preventing coeliac disease will become available. These exciting developments might stimulate research within other fields of autoimmune disorders. With its focus on TG2, this review highlights some of the intriguing mechanisms of the pathogenesis of coeliac disease, such as the structure of the neo-antigen, the involvement of calcium and zinc, and the effects of coeliac antibodies on TG2 activity. Moreover, the many pitfalls due to dubious laboratory practice are addressed, as is the potential when a fundamental biological mechanism is understood at the molecular level.
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PMID:Transglutaminase and the pathogenesis of coeliac disease. 1824 2

The association of chronic idiopathic thrombocytopenic purpura (cITP) and thyroid autoimmune diseases (TAD) is a known but an uncommon condition. Celiac disease (CD), which is characterized by malabsorption and villous atrophy that occur as a consequence of the ingestion of wheat gluten may also be related to other autoimmune disorders. In this study, we investigated the prevalence of thyroid anti-microsomal (TAMA) and anti-thyroglobulin (TATA) auto antibodies, anti-gliadin (AGA) IgG, IgA, anti-endomisium (EMA) IgG and IgA antibodies in 74 patients with cITP and in 162 healthy controls. TATA positivity was found in 29, and TAMA positivity in 19 out of 74 patients; and in 16 and 18 out of 162 controls respectively (p < 0.0001 and p = 0.005, respectively). TAD was diagnosed in 29 of cITP patients. AGA IgG positivity was found in 17, and IgA was present in five out of 74 patients; and AGA IgG was found in 19, and IgA was detected in 4 out of 162 controls (p = 0.032 and p = 0.143, respectively). EMA IgG positivity was found in six out of 74 patients and in nine out of 162 control subjects (p = 0.566). EMA IgA positivity was found in two out of 74 patients and in one out of 162 controls (p = 0.232). We showed that the prevalence of TAD and related autoantibodies are higher in patients with cITP. We suggest that, patients with cITP should be followed up for development of TAD. In addition, all CD related auto antibodies were found to be more frequent in patients with cITP, but only the AGA IgG reached to the clinical significance. None of the CD related auto antibody positive patients developed clinically manifested CD. Large-scale designed studies are needed to clarify the long-term impact and importance of these CD related auto antibodies in patients with cITP.
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PMID:Thyroid and celiac diseases autoantibodies in patients with adult chronic idiopathic thrombocytopenic purpura. 1856 60

We are reporting ten recently diagnosed children with celiac disease who presented neither undernutrition nor symptoms suggesting malabsortion syndrome. All showed IgA, EMA and just eight tTG2 autoantibodies. Biopsies allowing histopathologic diagnosis were taken after detailed endoscopic examina- tion from proximal duodenum. Samples from distal duodenum were within normal histologic range. The findings are particularly interesting in order to explain cases with aparent disagreements between clinical, laboratory and histopathologic data.
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PMID:[Celiac disease, a paradigmatic disease]. 1866 Oct 42


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