الفهرس 
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Abstract
Our study was carried out in Pediatric departments, Faculty of Medicine, Ain-Shams University. It included seventy five subjects who were divided into three groups and were crossly matched with age and socioeconomic level.
These groups were:
Group I: It included 25 normal apparently healthy children and free from any disease that interferes with this study.
Group (II) ( atopic bronchial asthma):
This group comprised 25 patients with atopic bronchial asthma.
Group (III)( non atopic bronchial asthma) :
This group comprised 25 patients with nonatopic bronchial asthma.
All groups were subjected to the following:
1. A complete personal and medical history.
2. Full clinical examination to exclude other diseases that may interfere with the studied parameters including renal function tests, liver enzymes, and urine and stool analysis.
3. Complete blood picture to count blood eosinophils.
4. Skin prick test for common 12 areoallergens.
5. Lung function tests (peak expiratory volume).
6. Assessment of studied parameters:
a) Total IgE level by ELISA.
b) Analysis of IL-13 receptor alpha 1 gene polymorphism (A1398G allele) by PCR according to (Heinzmann et al., 2000)
Our results were tabulated and statistically analyzed. They showed a non significant association of IL-13 Rα1 (A+1398G) gene polymorphism between groups II and III as compared to control group.
Regarding serum IgE, it was significantly increased in group II as compared to control group. Also there was a significant increase of serum IgE level in group II as compared to group III and there was no statistically significant difference between III and control group.
There was a significant increase in the serum level of total IgE towards heterozygous AG and homozygous GG than homozygous AA in atopic asthma and non atopic asthma patients but not in control group.
There was a significant increase in the serum level of total IgE towards homozygous GG than heterozygous AG in atopic asthma and non atopic asthma patients but not in control group.
The significant association of hetero- or homozygosity for the risk allele of IL-13Rα1 A+1398G with increased total IgE levels in children with asthma, especially atopic asthma. This may suggest that this non-coding polymorphism of IL-13Rα1 has a functional consequence for the binding of IL-13, or alternatively that the IL-13Rα1 A+1398G polymorphism is in linkage disequilibrium with as yet unidentified polymorphisms in the regulatory or coding regions of the gene encoding IL-13Rα1.
In conclusion the study showed a non significant association of IL-13 Rα1 (A+1398G) gene polymorphism between asthmatic groups as compared to control group.Regarding serum IgE concentration, it was significantly increased in asthmatic group as compared to control group.