The highly sensitive tests Anti-Gliadin (GAF-3X) ELISA serve for the determination of the celiac disease related fraction of gliadin antibodies in the serological diagnosis of gluten-sensitive enteropathy (celiac disease, non-tropical sprue) and Duhring’s dermatitis herpetiformis. Celiac disease is an autoimmune disease which occurs in predisposed individuals as a reaction to gluten sensitivity. After absorption in the lamina propria of the intestinal mucosa gliadin is deamidated by tissue transglutaminase (tTG). In this process particular glutamine residues are replaced by glutamic acid residues. In individuals with a genetic predisposition pieces (peptides) of gliadin modified (reconstructed) in this way bind to e.g. HLADQ2/8 molecules of the antigen presenting cells and are presented to helper T cells. An extensive immune reaction is triggered, causing pathological tissue changes, particularly damage to the small intestine. Components of this immune reaction are antibodies against endomysium or tTG and against the deamidated gliadin generated by tTG. The frequency of diagnosed coeliac disease amounts to around 1:300 in western Ireland, Italy, the USA, the Middle East, India and Cuba, around 1:1,000 in Germany and Austria and around 1:2,000 to 1:4,500 in other European countries. The clinical symptoms comprise fatigue (78%), borborygmus (72%), abdominal pain (64%), diarrhoea (56%), effects of malabsorption (44%) with weight loss, anaemia and growth retardation in children, vomiting (16%), constipation (12%) and bone pains (12%). Some patients with glutensensitive enteropathy also suffer from Duhring's dermatitis herpetiformis (10%), a chronic skin disease accompanied by the formation of blisters. In a prolonged course, mainly in adults, the risk of melanoma, particularly intestinal T-cell lymphoma, is about 10%

The determination of antibodies against gliadin is also suitable for use in monitoring the course of therapy and for control of a gluten-free diet or a gluten loading test. A characteristic rise or fall in titers of antibodies against gliadin can spare the patient an additional biopsy of the small intestine. The prevalence of specific antibodies in children with coeliac disease under gluten-free diet depends on the patient’s compliance with the diet and amounts to around 15-30% according to literature. If a relapse takes place under gluten loading, the level of IgA and IgG antibodies against gliadin rises within a few days. During the acute phase of a gluten-sensitive enteropathy, antibodies of class IgA against endomysium/tTG and/or gliadin are almost always detected. IgA-negative coeliac disease patients show a higher incidence of latent forms (around 13%), recurrent infections (around 30%) and atopic diseases (around 13%) than IgA-positive patients. Furthermore, it has been observed that a selective IgA antibody deficiency against gliadin is associated with a very high titer of class IgG anti-gliadin antibodies in almost 100% of cases. IgM antibodies against gliadin are detected occasionally, but generally only when antibodies of classes IgA and IgG against gliadin are also present. Anti-gliadin IgM plays therefore almost no diagnostic role. During the course of therapy by means of a gluten-free diet, the concentration of IgA antibodies against gliadin falls more rapidly and against endomysium more slowly to a low value within a few months. Permanently elevated IgA gliadin-antibody levels are indicative of non-compliance with a gluten-free diet. If IgA antibodies against gliadin are detected in healthy infants and small children with a normal, glutencontaining diet, the IgA antibody level should be investigated after three months. If a gluten-sensitive enteropathy is suspected, but the levels of IgA antibodies against gliadin or endomysium are low, the possibility of an IgA deficiency should be considered and the total IgA concentration determined. Antibodies against Gliadin (GAF-3X) are formed exclusively in patients with coeliac disease and not in healthy people.