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Since their introduction in clinical practice, antigliadin antibodies (AGA) have simplified the diagnostic iter of coeliac disease. In addition they have allowed us to recognize an even high number of new cases and also to identify new clinical forms. While AGA are widely used in the diagnostic phase, their determination during follow-up of the disease has been always limited. With the present work we observe the behaviour of AGA during the various phases of coeliac disease. The study was carried out on 288 coeliac children divided as follows: 96 at diagnosis, 136 on gluten-free-diet (75 diet adherent and 61 non adherent) and 56 on gluten-challenge. 145 healthy children were also studied as a control group. In all children AGA (IgA and IgG) were determined, with a micro-ELISA method, every two months in the children on gluten-free-diet and monthly in the children on gluten-challenge. Data obtained showed AGA behaviour strictly related to the diet. In fact while children with good compliance to the diet had AGA normalization within the 2nd and 6th month, respectively for IgA and IgG, children with poor adherence to diet had constantly positive AGA. Noteworthy was the AGA behaviour during challenge. Gluten introduction determined a rapid increase of IgA and a slow increase of IgG. Our results confirm the usefulness of AGA determination during the follow-up of coeliac children giving us the possibility to avoid one or more biopsies included in the ESPGAN protocol.

Recent antigliadin antibody (AGA) determination has become an important diagnostic tool in coeliac disease (CD). Although this test has high sensibility for the disease, it is less specific, especially for IgG class, because of its having been found in some acute and chronic common intestinal childhood diseases. We studied the behaviour of AGA, IgA and IgG, in 234 children affected by various gastrointestinal diseases, comparing the results with those obtained in 125 coeliac children and 788 normal children. The intestinal diseases were as follows: irritable bowel syndrome, cow's milk protein intolerance, acute infectious diarrhoea, parasitosis, lactase deficiency, recurrent abdominal pain, cystic fibrosis, chronic constipation, gastroesophageal reflux, intestinal lymphangiectasia, chronic intractable diarrhoea and nodular lymphoid hyperplasia. Our results showed that while AGA-IgA were absent in all children studied, with the exception of 3 cases of acute diarrhoea, a moderate percentage of AGA-IgG was observed in subjects with cow's milk protein intolerance, acute diarrhoea, irritable bowel syndrome, lactase deficiency, chronic intractable diarrhoea and in a low percentage of children with parasitosis, intestinal lymphangiectasia and nodular lymphoid hyperplasia. There was no antibody movement in subjects with cystic fibrosis, gastroesophageal reflux, recurrent abdominal pains and chronic constipation. The different behaviour of the two antibody classes could be explained by the fact that AGA-IgG were detected in diseases where scattered areas of mucosal damage could allow the permeability of the macromolecules inducing passage of gliadin through the mucosal barrier and immune system-induced antibody stimulation.