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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have prospectively searched for IgA anti-transglutaminase antibodies by an enzyme-linked immunosorbent assay test in 20 untreated coeliacs and 21 patients with small bowel diseases other than coeliac disease consecutively referred to our Malabsorption Clinic. All the untreated coeliacs and one out of 21 disease controls turned out to be positive for the presence of these antibodies. The use of the enzyme-linked immunosorbent assay test for anti-transglutaminase antibodies could represent a new screening test for coeliac disease, in fact, this new enzyme-linked immunosorbent assay test has an absolute sensitivity and a satisfactory specificity and, in comparison to antiendomysial antibodies, is less expensive and avoids the ethical problems related to the use of monkey oesophagus.
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PMID:Tissue transglutaminase antibodies for coeliac disease screening. 983 5

Coeliac disease, a life-long gluten-sensitive disorder, characterized by malabsorption, villous atrophy and crypt hyperplasia, is well recognized. However, the disease is evidently underdiagnosed, and the classic forms constitute only the tip of the 'coeliac iceberg'. Patients with coeliac disease can have subtle symptoms, if any. Diagnostic difficulties may further emerge when minor mucosal changes are found. In coeliac screening and case-finding a novel test, the antitissue transglutaminase test, has proven promising with a sensitivity and specificity of over 95 %. Genetic and immunohistological research has taken a great leap forward. Coeliac disease is strongly associated with HLA-DQ2, coded by the DQA1*0501 and DQB1*02 alleles, or the DQ8 (DQA1*03, DQB1*0302 alleles). The disease is rare in patients who do not share these alleles, a circumstance which can be utilized in diagnostics. An increase in small bowel intraepithelial lymphocytes especially gammadelta+ T-cell receptor-bearing cells is typical, albeit not pathognomonic, for coeliac disease. Combining new symptoms, humoral immunity, genetics and immunohistological staining can today offer a greater diagnostic scope for coeliac disease, especially in cases where clinical presentation and small bowel biopsy findings remain doubtful.
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PMID:New diagnostic findings in coeliac disease. 1068 Aug 54

Celiac disease (CD) is an intestinal malabsorption characterized by intolerance to cereal proteins accompanied by immunological responses to dietary gliadins and tissue transglutaminase, an autoantigen located in the endomysium. Tissue transglutaminase belongs to the family of enzymes that catalyze protein cross-linking reactions and is constitutively expressed in many tissues as well as being activated during apoptosis. The role of gliadins in eliciting the immune response in CD and how transglutaminase is linked to the primary reaction are still unclear. In this work, we report the production and analysis of six phage Ab libraries from the peripheral and intestinal lymphocytes of three CD patients. We were able to isolate Abs to transglutaminase from all intestinal lymphocytes libraries but not from those obtained from peripheral lymphocytes. This is in contrast to Abs against gliadin, which could be obtained from all libraries, indicating that the humoral response against transglutaminase occurs at the local level, whereas that against gliadin occurs both peripherally and centrally. Abs from all three patients recognized the same transglutaminase epitopes with a bias toward the use of the V(H)5 Ab variable region family. The possible role of these anti-transglutaminase Abs in the onset of CD and associated autoimmune pathologies is discussed.
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PMID:Molecular dissection of the tissue transglutaminase autoantibody response in celiac disease. 1123 68

Coeliac disease is an intolerance to gluten that classically produces a chronic diarrhoea with a picture of malabsorption and a total villous atrophy. These elements regress completely in a sequential way under a prolonged strict gluten-free diet. The progress registered in the understanding of this affection depends on the individualization of the atypical forms (delayed isolated stature, constipation...) of asymptomatic forms thanks to the study of specific antibodies (anti-gliadin, anti-endomysium, and more recently anti-transglutaminase). The auto-immune nature of coeliac disease is well established. The diagnostic criteria are simplified allowing the commencement of a gluten-free diet which must be perfectly detailed. Finally, allergy to wheat flour merits individualization in the framework of coeliac disease (cf. article).
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PMID:[Celiac disease: clinical and subclinical forms]. 1201 89

Celiac disease is a permanent intolerance to dietary gluten. Its well known features are abdominal symptoms, malabsorption of nutrients, and small-bowel mucosal inflammation with villous atrophy, which recover on a gluten-free diet. Diagnosis is challenging in that patients often suffer from subtle, if any, symptoms. The risk of clinically silent celiac disease is increased in various autoimmune conditions. The endocrinologist, especially, should maintain high suspicion and alertness to celiac disease, which is to be found in 2-5% of patients with insulin-dependent diabetes mellitus or autoimmune thyroid disease. Patients with multiple endocrine disorders, Addison's disease, alopecia, or hypophysitis may also have concomitant celiac disease. Similar heredity and proneness to autoimmune conditions are considered to be explanations for these associations. A gluten-free diet is essential to prevent celiac complications such as anemia, osteoporosis, and infertility. The diet may also be beneficial in the treatment of the underlying endocrinological disease; prolonged gluten exposure may even contribute to the development of autoimmune diseases. The diagnosis of celiac disease requires endoscopic biopsy, but serological screening with antiendomysial and antitissue transglutaminase antibody assays is an easy method for preliminary case finding. Celiac disease will be increasingly detected provided the close association with autoimmune endocrinological diseases is recognized.
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PMID:Endocrinological disorders and celiac disease. 1220 61

Celiac disease is an intestinal malabsorption characterized by an intolerance to cereal proteins accompanied by immunological responses to dietary gliadins and an autoantigen located in the endomysium. The latter has been identified as the enzyme tissue transglutaminase which belongs to a family of enzymes that catalyze protein cross-linking reactions and is constitutively expressed in many tissues as well as being activated during apoptosis. In a recent paper, we described the selection and characterization of anti-transglutaminase Igs from phage antibody libraries created from intestinal lymphocytes from celiac disease patients. In this work, using transglutaminase gene fragments, we identify a region of tissue transglutaminase recognized by these antibodies as being conformational and located in the core domain of the enzyme. This is identical to the region recognized by anti-transglutaminase Igs found in the serum of celiac disease patients.
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PMID:The analysis of the fine specificity of celiac disease antibodies using tissue transglutaminase fragments. 1239 49

Gluten-sensitive enteropathy or, as it is more commonly called, celiac disease, is an autoimmune inflammatory disease of the small intestine that is precipitated by the ingestion of gluten, a component of wheat protein, in genetically susceptible persons. Exclusion of dietary gluten results in healing of the mucosa, resolution of the malabsorptive state, and reversal of most, if not all, effects of celiac disease. Recent studies in the United States suggest that the prevalence of celiac disease is approximately one case per 250 persons. Gluten-sensitive enteropathy commonly manifests as "silent" celiac disease (i.e., minimal or no symptoms). Serologic tests for antibodies against endomysium, transglutaminase, and gliadin identify most patients with the disease. Serologic testing should be considered in patients who are at increased genetic risk for gluten-sensitive enteropathy (i.e., family history of celiac disease or personal history of type I diabetes) and in patients who have chronic diarrhea, unexplained anemia, chronic fatigue, or unexplained weight loss. Early diagnosis and management are important to forestall serious consequences of malabsorption, such as osteoporosis and anemia.
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PMID:Gluten-sensitive enteropathy (celiac disease): more common than you think. 1250 63

Celiac disease is characterized by intestinal mucosal injury and malabsorption precipitated by dietary exposure to gluten of some cereals with a prominent role being played by gliadins, specific antigenic determinants found in wheat gluten. Patients suffering from celiac disease have serum antibodies recognizing gliadin, as well as the endomysial autoantigen tissue transglutaminase. Phage display antibody libraries have revealed ectopic production of anti-transglutaminase antibodies by intestinal lymphocytes with a biased use of the VH5 antibody gene family. Here we report a study on the pairing of VH and VL families in the antibodies to transglutaminase. Our results led to the construction of small phage display antibody libraries based on the amplification of the two genes in the VH5 family from intestinal lymphocytes. This method can be used for the rapid characterization of the anti-transglutaminase response in a potentially large number of subjects including asymptomatic patients whose serum antibodies may be undetectable.
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PMID:One-step cloning of anti tissue transglutaminase scFv from subjects with celiac disease. 1470 14

Celiac sprue (CS) is defined as a chronic small bowel malabsorption disorder caused by ingestion of gluten, affecting those genetically predisposed individuals. It is characterized by intestinal villi atrophy, increased number of intraepithelial lymphocytes and extense inflammatory infiltrate in the intestinal lamina propria. The role of gluten as responsible for the intestinal damage seen in CS patients is clear, however, the physiopathological mechanisms involved are still unknown. Several factors and theories have been proposed: 1) Genetic predisposition, based on the association to mendelian factors as well to the presence of particular major histocompatibility complex (MHC) haplotypes in CS patients; 2) Immunological factors, that consider the derangements that occur in the immune response of CS patients, and 3) Gliadin partial deamination by the tissular transglutaminase (tTG). In an effort to explain all these complex mechanisms, recently, all these theories have been unified, yielding one complex physiopathogenic mechanism that we tray to explain in the present review.
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PMID:[Current concepts on celiac disease physiopathology]. 1496 78

Intolerance of gluten, resposible for Coeliac disease, is essentially shown by an auto-immune enteropathy, even if the cutaneous manifestation (herpetiform dermatitis) and perhaps certain neurological signs (cerebral syndrome, peripheral neuropathy) may be independent as well as associated with the intestinal illness. This affection is of immunological nature, occuring in a genetic field that predisposes to the illness (familial form: concordance of 70% in homozygote twins; 90% of patients show an HLA molecule of type DQ2, DQ8 in almost all the other cases. The exogenous factor is the gluten content contained in wheat, rye and barley, more precisely by the intermediary "the prolamines" which are the "reactive" element that induces a the same time an inflammatory reaction of type TH11 locally (expressed by the histological aspect of a duodenal biopsy evolving as villous atrophy) and a humoral response with production of anti-gliadine and anti-transglutaminase antibodies (the role of the latter enzyme is intervention in the local transformation of antigens to make them antigenic). It is an illness of adults as well as children and this point must now be emphasized. Recent epidemiological studies insist on a high prevalence (1/300 in Europe). Clinical expression, at the start very polymorphic and so misleading, before the appearance of the more classical signs of malabsorption and development, always feared, towards a lymphoma. These signs are haematological (anemia of various types, hyper platelets by hyposplenism, haemorrhagic signs) cutaneous (herpetiform dermatitis, cutaneous vasculitis) mucosal (aphtose), hepatic (cytolysis), neurophysical (fatigue, troubles of behaviour, cerebral syndrome, neuropathy) and osteo-articulitis (osteopenia, arthralgias, diffuse pains). The association of certain auto-immune illnesses must be emphasized (diabetes, Hashimoto thyroiditis, Gougerot disease, primitive biliary cirrhosis). To think early of the possibility of intolerance to gluten, is to give the means of a very easy diagnosis (measurement of anti-gliadin, anti-endomysium and anti-transglutaminase, and secondarily duodenal biopsy if necessary), and it is early elimination of gluten food which will make the various clinical manifestations disappear and so prevent the risk of evolution to a tumoral pathology.
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PMID:[A great imitator for the allergologist: intolerance to gluten]. 1513 80


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