Background: There is a large variation in the magnitude of the response to asthma medications. Pharmacogenetics is responsible for a significant part of this variation. We aimed at studying the effect of the Glucocoricoid receptors NR3C1 BCLI single nucleotide polymorphism (SNP) on the susceptibility to bronchial asthma in children and to evaluate its effect on the response to inhaled corticosteroids (ICS). Method: Seventy five asthmatic children and a control group of 66 non asthmatic children were included in the study. The level of asthma symptom control and pulmonary function tests were measured initially and 3 months after treatment with inhaled corticosteroids. The genotypes were studied using PCR-RFLP method. Results: No statistically significant difference was found between asthmatic group and the control group as regard the studied genotype. Among asthmatic children, The CC genotype was statistically associated with controlled asthma symptoms 3 months after treatment and the GG genotype was associated with poor asthma symptom control. Also, FEV1% after 3 months of treatment was statistically lower in children with the GG genotype as compared to children with the CG and CC genotypes. Conclusion: glucocorticoid receptor NR3C1 SNP was not associated with asthma susceptibility in the studied group. However, the presence of the GG genotype was associated with decreased response to ICSs among asthmatic children as regards asthma symptom control and FEV1% response.

Background: Mycoplasma pneumoniae (M. pneumoniae) is an important cause of pediatric community acquired pneumonia (CAP). Aim: The aim of this study was to determine the incidence of M. pneumoniae in pediatric community acquired pneumonia and to determine the most frequent clinical findings of M. pneumoniae CAP. Methods: A total of 83 pediatric CAP patients were subjected to history taking, clinical examination, chest X-ray, CBC, CRP and serum antimycoplasma pneumonia IgM and IgA by ELISA. Results: Twenty-nine (34.9%) out of 83 patients were positive for M. pneumoniae Ig M while 2 (3.4%) patients were positive for M. pneumoniae IgA. There was more infection (54%) in age group (5-9 years; p value <0.001). Mycoplasma pneumoniae pneumonia infected patients were presented with cough (29/29; 100%), fever (29/29; 100%), malaise (18/29; 43.8%), headache (16/29; 33.8%), wheeze (21/29; 52.5%), chest discomfort (13/29; 44.8%), sore throat (13/29; 46.4%), rhinitis (8/29; 27.5%) and pharyngitis (6/29; 24%). The most frequent X ray findings in M. pneumoniae pneumonia was air space pneumonia (71%); segmental more than lobar form (p-value < 0.0001). Conclusions: The findings of this study highlight the clinical significance of M pneumoniae in pediatric community acquired pneumonia.

Background: Asthma is a global health problem affecting millions of adults and children. Pathogenesis of asthma is multifactorial and the genetic component is of particular importance. Objectives: To assess the role of ADRB2 Thr164Ile gene polymorphism in asthma risk, severity and response to β2 agonist therapy in Egyptian children. Methodology: The study enrolled 50 asthmatic and 50 control children. Pulmonary function tests and serum levels of IgE of asthmatic children were measured. The Thr164Ile genotypes were detected for all study subjects by Amplification Refractory Mutation System- Polymerase Chain Reaction (ARMS-PCR). Results: Serum IgE levels were significantly higher on comparing mild to moderate and severe cases (P=0.002& 0.02, respectively). The Ile/Ile genotype of Thr164Ile SNP was significantly present in asthmatic subjects (P=0.039). The Thr164Ile SNP was associated with lowered response to β2 agonist inhalation (P<0.001) but there was no association between the studied SNP and asthma severity. Conclusion: The Thr164Ile SNP can be linked to asthma risk and lowered response to β2 agonist treatment but not to asthma severity in asthmatic children.

Background: Loss of Treg cell suppressive activity due to FOXP3 gene disruption is the leading hypothesis for the development of allergy disorders. Thus, asthma susceptibility appears to be determined by host genetic variables affecting FOXP3. A number of research have looked at the role of polymorphisms in the FOXP3 gene in relation to allergy susceptibility. Objective: We aimed at studying the association between FOXP3 gene single nucleotide polymorphism (SNP) and bronchial asthma, asthma severity as well as atopy in Egyptian children. Patients and Methods:The study comprised 101 children with asthma and a control group of 101 children without asthma. Subgroup analyses revealed that there were 44 "atopic" a nd 57 "non-atopic" asthmatics in the total asthmatic group. Polymerase chain reaction sequence specific primers (PCR-SSP) were used to investigate the FOXP3 genotypes (rs3761548, rs2232365). Results: There was no significant difference in the genotypes tested between the asthmatic group and the control group. The AC of rs3761548 and the GG (rs2232365) polymorphisms were the most frequent genotype among the studied children. And only C allele of (rs3761548) was more frequent among asthmatic cases compared to control group. Moreover, no statistically significant difference was found among atopic asthmatic children as regards FOXP3 genotypes (rs3761548, rs2232365) and degree of asthma severity. Conclusions: No link between FOXP3 gene polymorphism (rs3761548 and rs2232365) and asthma susceptibility was found in Egyptian children with asthma. The severity of atopic asthma in children was not shown to be correlated with FOXP3 polymorphism in the present study.

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