In our study the efficacy on symptom control and lung function of the combination of a long-acting bronchodilator with inhaled corticosteroid is equal to doubling the dose of the inhaled corticosteroid in children still symptomatic on a moderate dose of inhaled corticosteroid.

We present the clinical, radiological, and pathological findings of open lung biopsies from monozygotic prematurely born male twins with respiratory distress at ages 6 and 8 weeks postnatally. Radiological examination showed a reticular nodular interstititial pattern on chest radiography. High-resolution computed tomography (HRCT) revealed ground-glass opacification and thickened interstitial septae in both infants. Lung biopsies showed a similar histology. There was diffuse interstitial thickening of the alveolar septa by mesenchymal cells, without prominent hyperplasia of type 2 pneumocytes, and without airspace exudates. Sections were periodic acid-Schiff (PAS)-positive within the cytoplasm of interstitial cells, indicating the presence of glycogen. Thus the diagnosis of pulmonary interstitial glycogenosis was made. Both infants were treated with glucocorticoids and had a favorable outcome. We speculate that pulmonary interstitial glycogenosis could be a histopathological form of chronic lung disease (CLD) of infancy. Pediatr Pulmonol. 2005; 40:362-366. ß 2005 Wiley-Liss, Inc.

In the present investigation we have tested the hypothesis that children with a high IgG antibody response to foods have an increased risk of developing IgE antibodies to inhalant allergens. Sera from 106 children with an increased risk of developing IgE-mediated allergy were analysed. During the follow-up, in 54 of these children IgE antibodies to inhalant allergens appeared. A positive/negative IgG1 and IgG4 anti-food score was determined as described previously: sera from age-clustered unselected children were tested for the levels of IgG1 and IgG4 antibodies to common foods. For each IgG RAST and each age group, the 75-percentile was chosen as cut-off value. Each antibody level was thus converted into a positive (higher than the 75-percentile of the age group) or negative value. The number of positive tests was used as the score. High-risk children with a high IgG1 anti-food score more often developed inhalant-specific IgE antibodies than high-risk children with low IgG1 titres: 50% of the children with a high IgG1 anti-food score developed IgE antibodies to grass pollen. Fifty per cent of the children with a high and 14% of the children with a low IgG1 anti-food score developed IgE antibodies to cat dander. For the prediction of the development of IgE anti-mite (house dust mite), the IgG4 anti-food scores appeared less useful than the IgG1 anti-food scores; 46% of the IgG4 high responders versus 22% of the IgG4 low responders acquired IgE anti-mite, whereas for IgG1 these percentages were 73 and 19, respectively.

To obtain reference levels for subsequent investigations, we analysed the IgG1 and IgG4 antibody levels to common foods in the sera of 213 unselected children (age 3 months to 14 years). The children were clustered into five age groups and tested on a broad screening panel of common foods. We used the IgG1 and IgG4 RAST with Sepharose-coupled antigens: cows' milk, hens' egg white, banana, legumes (a mixture of soybean and peanut), grains (a mixture of wheat and rice), potato, orange and pork. In all age groups and all antigens, a considerable variability in the antibody response was found. As for some assays more than half of the sera were negative or borderline, statistics based on interval or ordinal scaling were considered inappropriate and we resorted to nominal classification. We decided to use, for each of the assays, the 75-percentile of the age group as a cut-off level. Each antibody titre was thus converted into positive (more than the 75-percentile of that age group) or negative; the number of positive tests was used as the score. This resulted in a sigma G1-score and a sigma G4 score (summed scores for IgG1 and IgG4 antibodies, respectively). The results of the present study indicate that children with a high response to one food tend to have elevated responses to other non-related foods, possibly explained by a defective mucosal barrier and/or a hyperactive immune system. This suggests that a high-food responder phenotype may exist.