Atopy spectrum and its relationship with clinical characteristics in asthmatic children under 4 years of age / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the atopy spectrum and the influence of clinical characteristics upon it in asthmatic children under 4 years of age.</p><p><b>METHODS</b>Clinical data of 62 asthmatic children under 4 years of age, including age, sex, the age of first wheezing attack, the total times of wheezing attack, the duration of history of wheezing, and the allergic history of both children and parents, were collected. The screening tests on allergens (fx5E, mx2 and Phadiatop) were conducted by fluoroenzyme-immunometric assay using the UniCAP100 system. The total serum IgE level was also measured. Logistic regression was used to analyze the effect of clinical characteristics on allergic sensitization.</p><p><b>RESULTS</b>The positive rates of fx5E, mx2 and Phadiatop were 40.3%, 14.5% and 14.5% respectively, and the total allergic sensitization screening test rate was 46.8%. The sensitization rate to inhalant allergens was 24.2%. The allergic history of parent (s), the sensitization to food allergens, the age of first wheezing attack and total serum IgE level were main factors influencing the sensitization to inhalant allergens.</p><p><b>CONCLUSIONS</b>About a quarter of asthmatic children under 4 years of age showed sensitization to inhalant allergens. The asthmatic history of parent (s), the sensitization to food allergens, the age of first wheezing attack greater than 2 years and the significantly higher total serum IgE level may increase the possibility of sensitization to inhalant allergens in asthmatic children under 4 years of age.</p>

Effects of budesonide on chronic airway inflammation in guinea pigs sensitized with repeated exposure to allergen / 中华儿科杂志

<p><b>OBJECTIVE</b>Inhaled glucocorticosteroids (ICS) remains the first line controller medication for chronic airway inflammation in asthma till now. If the impact of allergen could not be eliminated, how would the improvement of airway inflammation be achieved with inhaled glucocorticosteroids therapy? What was its effect on airway remodeling? In this study, an animal model of asthma was established and the effects of budesonide on airway allergic inflammation and extracellular matrix (ECM) deposition in sensitized guinea pigs with repeated exposure to allergen were investigated.</p><p><b>METHODS</b>Thirty-two male Hartley guinea pigs were randomly divided into four groups with 8 in each group: (A) Group of repeated exposure to ovalbumin (OVA), (B) Group of repeated exposure to OVA plus budesonide (BUD) intervention, (C) Group of stopping repeated exposure to OVA plus stopping BUD intervention, (D) Control group. At 24 h after the last OVA challenge (8 weeks after the first OVA challenge), bronchoalveolar lavage fluid (BALF) was collected from each animal. Total and differential leukocyte counts in BALF was performed on cell suspension smear stained with May-Grünwald-Giemsa (MGG) method. The upper lobe of right lung was removed and regularly fixed, then paraffin embedded lung tissues sections were prepared. The count of eosinophils infiltrated in the airway wall was performed on H&E stained lung tissue sections with LEICA Q500IW computerized image analysis system. Fibronectin and collagen type III (Col-III) deposited in the airway wall were detected by immunohistochemical staining on the paraffin embedded lung tissues sections. The intensity of positive reaction of fibronectin or Col-III deposited in the airway wall was analyzed with LEICA Q500IW computerized image analysis system.</p><p><b>RESULTS</b>The count of eosinophils in BALF (x 10(5)/ml) of group A and B were higher than that of group C and D (35.70 +/- 25.22, 11.49 +/- 5.51 vs. 1.00 +/- 0.90, 1.02 +/- 0.78, P < 0.01), the difference between group A and B, group B and C was significant. The count of eosinophils infiltrated at each level of airway wall in group A and B were higher than that of group C and D (large airway: 6.95 +/- 2.28, 1.54 +/- 1.09 vs. 0.76 +/- 0.45, 0.88 +/- 0.25; medial airway: 9.22 +/- 3.89, 3.99 +/- 2.3 vs. 1.25 +/- 1.20, 0.64 +/- 0.36; small airway: 11.56 +/- 4.02, 2.67 +/- 1.15 vs. 1.32 +/- 0.83, 0.43 +/- 0.24, P < 0.01), the difference between group A and B, group B and C was significant. The gray values of fibronectin deposited in medial and small airway of group A and B were lower than those of group C and D (medial airway 122 +/- 22, 174 +/- 23 vs. 219 +/- 34, 229 +/- 20; small airway 135 +/- 29, 165 +/- 41 vs. 236 +/- 20, 220 +/- 16, P < 0.05), the difference between group A and B, group B and C was significant. The gray values of Col-III deposited in medial and small airway of group A and B were lower than those of group C and D (medial airway 153 +/- 21, 174 +/- 22 vs. 189 +/- 14, 200 +/- 18; small airway 133 +/- 23, 176 +/- 20 vs. 191 +/- 14, 198 +/- 20, P < 0.05), the difference between group A and B was significant.</p><p><b>CONCLUSION</b>Inhaled budesonide could partially inhibit allergic inflammation and ECM deposition in airway wall in guinea pig chronic asthma model with repeated exposure to allergen. Early inhaled budesonide combined with avoidance of OVA exposure could completely inhibit allergic inflammation and ECM deposition. These results suggest that the inhibitory effect on airway allergic inflammation and airway remodeling of inhaled glucocorticosteroids would be limited when the allergen factor could not be avoided.</p>