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The authors have performed a clinical and epidemiological study on 162 immunocompetent children with herpetic gingivostomatitis, during 1982-1991. They have observed a peak age of incidence between 9 and 28 months, absence of sex differences and seasonal variations, and a prevalence of patients of lower social status. HSV I was the most frequent aetiological agent and it was not always possible to recognize the source of contagion. The patients have been graded in three classes (severe, moderate and mild disease), according to clinical manifestations of gingivostomatitis, and the severe form was the most frequent with a prevalent orolabial involvement. The prognosis of the disease was satisfactory in all patients, even if more favourable in acyclovir treated children because of fast regression of the symptoms.

The alimentary habits have been analyzed in 440 infant with acute and chronic disease of nutrition. It has been observed a high incidence of dietetic mistakes, whether qualitative or quantitative. These mistakes appeared in correlation with the poor cultural and socio-economic conditions of the population. The Authors compare the observed pathology with the wrong alimentary habits conditioned by low social context and suggest an adequate prophylaxis of infant's nutrition disease, thorough better alimentary habits in childhood and better life conditions of the population.

The authors report about four children with Schönlein-Henoch purpura in whom the clinical picture has been characterized by an unusual localization, the testicular involvement. The main clinical aspects of this feature are illustrated and the approach to its diagnosis and its management is discussed.

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.

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.