title: [Relevance of anti-tissue transglutaminase antibodies in coeliac disease diagnosis].
abstract: Coeliac disease is precipitated upon exposure to the dietary wheat gluten. Definitive diagnosis relies on intestinal biopsy and regression of clinical and histological disorders with adherence to a gluten-free diet. Coeliac disease is usually associated with a malabsorption syndrome. However, both atypical and silent clinical forms have been recently described and prevalence of the disease may be under-estimated. Serological tests have been developed in order to select candidates for intestinal biopsy, but these biological parameters are not suitable for screening in the general population. Indeed, antigliadin IgG antibodies have a poor specificity. antigliadin IgA antibodies a poor sensitivity. The detection of antiendomysial IgA antibodies (EmA) by immunofluorescence, although considered as the "gold standard" of serological coeliac disease markers, could not be automated, depends on a subjective fluorescence display, and may be limited by the degree of training of the observer. In year 1997, tissue transglutaminase (tTg) has been identified as the main autoantigen recognized by EmA. On this basis, solid-phase enzyme-linked immunosorbent assays (Elisa) have been developed in order to potentially replace the EmA assay. Several commercial kits are now available but their diagnostic performances have not yet been compared. We selected 75 sera, including sera from 26 patients with coeliac disease in order to evaluate five commercial anti-tTG Elisa kits. For all patients, treated or not, detection of anti-tTG antibodies with four of the five tested kits correlates with EmA test. Kits using human tTG have the highest specificity, equivalent to the value of EMA test, and widely better than antigliadin antibodies. Anti-tTG Elisa kits using human tTG may be used as an alternative way to the EmA assay in the next future, and may supplant IgA anti-gliadin antibodies for coeliac disease screening.
authors.affiliation: Laboratoire d'immunologie, CHRU de Lille, 1 Place de Verdun, 59045 Lille cedex.
authors.forename: S
authors.initials: S
authors.lastname: Lepers
authors.forename: F
authors.initials: F
authors.lastname: Soula
authors.forename: S
authors.initials: S
authors.lastname: Fily
authors.forename: E
authors.initials: E
authors.lastname: Fontaine
authors.forename: S
authors.initials: S
authors.lastname: Vuye
authors.forename: J-F
authors.initials: JF
authors.lastname: Colombel
authors.forename: D
authors.initials: D
authors.lastname: Guimber
authors.forename: L
authors.initials: L
authors.lastname: Prin
authors.forename: S
authors.initials: S
authors.lastname: Dubucquoi
mesh_terms: D000293:Adolescent; D000328:Adult; D001323:Autoantibodies / Q000097:blood*; D001324:Autoantigens / Q000276:immunology*; D015415:Biomarkers / Q000097:blood*; D016022:Case-Control Studies; D002446:Celiac Disease / Q000097:blood / Q000175:diagnosis* / Q000453:epidemiology / Q000276:immunology; D002648:Child; D002675:Child, Preschool; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods* / Q000592:standards; D005260:Female; D005455:Fluorescent Antibody Technique / Q000379:methods / Q000592:standards; D005602:France / Q000453:epidemiology; D019204:GTP-Binding Proteins / Q000276:immunology*; D005903:Gliadin / Q000276:immunology; D006801:Humans; D007070:Immunoglobulin A / Q000276:immunology; D007074:Immunoglobulin G / Q000276:immunology; D007223:Infant; D008297:Male; D008875:Middle Aged; D000091345:Protein Glutamine gamma Glutamyltransferase 2; D012680:Sensitivity and Specificity; D011503:Transglutaminases / Q000276:immunology*
chemical_list: D001323:Autoantibodies; D001324:Autoantigens; D015415:Biomarkers; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D005903:Gliadin; D000091345:Protein Glutamine gamma Glutamyltransferase 2; D011503:Transglutaminases; D019204:GTP-Binding Proteins