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By screening the patient list of four Sicilian centers of gastroenterology and those with gluten-free product consumption, 1074 patients (607 females and 467 males) with celiac disease, diagnosed between 1975 and 1989, were identified. A maximum cumulative incidence rate by birth cohort was reached in 1986 (1.65/1000). When the incidence rate was adjusted for the years of follow-up, the actual standardized rate was 3 cases per 1000 live births. Growth failure and chronic diarrhea were the most common symptoms, but a diminishing trend for chronic diarrhea was observed when symptoms were distributed by year of diagnosis. Even though 61.1% of all cases were diagnosed within six months from the onset of symptoms, mean age at diagnosis showed an increasing trend, from less than two years to approximately four years of age. The results of our study showed an increasing incidence of celiac disease due to diagnosis of less typical cases at an older age and also to a steady increase in the rate of diagnosis of cases with a classic clinical picture.

Anti-endomysium antibodies (AEA) and Antigliadin antibodies (AGA) have been compared in a group of coeliac patients (17 with untreated coeliac disease, 56 after gluten free diet and 14 after gluten challenge), in 69 patients with various intestinal pathological conditions, and in 40 healthy children, in order to appreciate sensitivity and specificity of these tests in diagnosis of coeliac disease. AEA and AGA IgA were detected in 100% and AGA IgG were found in 94.1% of coeliacs with untreated disease; after gluten free diet AGA IgG were found in 27.7% of cases, while AGA IgA and AEA were absent in all coeliacs but one with non correct compliance to diet. After gluten challenge followed by villous atrophy, 78.5% of patients were positive for AGA IgA, 85.71% for AGA IgG and 100% for AEA. Anti-endomysium antibodies were absent both in healthy controls both in control disease patients, while sometimes antigliadin antibodies were present in patients with various intestinal pathology (AGA IgA in 1.44% and AGA IgG in 7.2% of cases). In our experience therefore AEA, because their sensitivity and high specificity, appear to disclose new prospects in diagnosis of coeliac disease.

The authors have studied the proceeding of anti endomysium antibodies (AEA-IgA) in a group of coeliac patients, in order to investigate new tests, not intrusive and easy repeatable, to employ in diagnosis and in follow up of coeliac disease. The research was carried out by an indirect immunofluorescent test on 65 sera of patients with age range 1-11 years; of those patients 14 show the coeliac disease at beginning, 16 were on Gluten Free Diet (GFD) from 3-5 months, 28 were on GFD from 1 year and 7 were on challenge with gluten from 2-4 months. We investigated AEA-IgA in sera of 71 gastroenterological and not-gastroenterological patients of analogous age to coeliacs how control subjects. All coeliac patients (14) with disease at beginning were positive for AEA-IgA. For the patients on GFD we observed an evident correlation between the term of diet and presence of AEA-IgA: 12 of 16 patients on GFD from 3-5 months were positive, but after 1 year of GFD all patients were negative; after 2-4 months from reintroduction of gluten in diet with the challenge we observed that all examined patients were positive for AEA-IgA. In 21 coeliac patients on free diet (14 with the disease at beginning and 7 after challenge) any reduction of percentage positivity was noted with the growth. The investigation of AEA-IgA in all examined control subjects was always negative. Our data suggest that the AEA-IgA investigation, for highly sensitivity and specificity, for easy repeatability and absence of intrusivity, is a diagnostic test that can be usefully combined to others (intestinal biopsy, dosage of anti gliadin antibodies) in diagnosis and in follow up of coeliac disease.

We studied the role of the immunoglobulin heavy-chain allotypes in the evolution of celiac disease. Particularly the Gm(fb) phenotype was investigated since this phenotype is able to determine the breadth of immune response against alpha-gliadin antigen. The results show that weight percentiles and intestinal absorption as assessed by xylose test are influenced by Gm(fb) phenotype suggesting that Gm(fb) genes contribute to the determination of clinical aspects and evolution of celiac disease.

The Authors have performed a study on the dietary habits of 74 celiac children and have analysed retrospectively the type of nursing (breast-feeding or bottle-feeding), the time and the age of gluten introduction. Then they related these data to the age of onset of symptoms. Children breast-fed for 3 months or more showed a marked delay in the onset of the disease and a longer latency time from gluten introduction when compared with bottle-fed children; on the contrary early gluten introduction was not positively correlated to risk of celiac disease. This observations induce to think that breast-feeding may be a protective factor towards coeliac disease, while the precocious gluten introduction is not an important factor of risk correlated to this disease.

The authors have studied the immunoglobulin heavy chain allotypes in 14 Sicilian patients with celiac disease (CD) and in 75 healthy controls. No association has been found between CD and Gm or Km phenotypes. When the role of Gm phenotypes in immune response against gliadin was analyzed, fb-positive CD patients on gluten-free diet for 1 year showed an increased antigliadin IgG response. Comparing the values of fb-positive subjects with those of negative ones, a significant difference was observed. These data, demonstrating that the presence or absence of a phenotype is able to define the breadth of immune response against alpha-gliadin antigen, are indicative of the role played by Ig allotypes in CD.

The authors have studied the HLA genotypes in 17 Sicilian coeliac children, in their parents and in their healthy brothers. A positive association has been found between coeliac disease (C.D.) and HLA antigens; this was strongest firstly for DQW2 and than for DR7 and DR3. Those antigens however do not result specific for C.D., because they were present in healty-control population too and because one coeliac patient was DQW2, DR7 and DR3 negative. A distortion of vertical transmission of HLA haplotypes has been observed in the studied patients, and this occurred for DR3/DQW2 that was transmitted mainly by paternal way. Moreover, in the healty brothers of our coeliac subjects a significant reduction of HLA antigens DQW2, DR7 and DR3 has not been found. Those observation and the finding that in our families the responsible gene for C.D. seems to have a low penetrance, should induce to search others genetic markers for coeliac disease.