الفهرس 
Introduction and aim of the workOnly 14 pages are availabe for public view
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Abstract
Atopic dermatitis is the commonest chronic cutaneous disease of childhood in the first years of life. AD has been reported to affect more than 10% of children in most countries. AD results from strong genetic and environmental interactions. Most patients with AD have elevated numbers of circulating eosinophils and increased immunoglobulin E (IgE) levels. There is evidence of enhanced LT production in the pathogenesis of AD. Leukotrienes are generated from arachidonic acid. Montelukast is one of LT receptor antagonists, which is safe and effective drug as a combined systemic and topical treatment regimen for treatment of moderate-to-severe AD. Researches were carried out on montelukast in Europe and Asia and were effective.
The present study has been carried out to investigate the effect of montelukast treatment on total IgE levels and eosinophils counts in atopic dermatitis patients. The study was extended to evaluate the effect of montelukast on filaggrin mutation (R501X and 2282del4) gene in atopic dermatitis Egyptiant patients.
In the current study, a total of (48) subjects of Kafr El sheikh residents, (32) patients with AD (aged 2.5 - 45 years; 16 male and 16 female), and 16 healthy non-AD volunteers with no allergic disease (aged 5 - 32 years; 6 male and 10 female) were enrolled in this study. AD was diagnosed according to criteria of Hanifin classification. Cases were categorized into mild (< 20 points), moderate (20–40 points) or severe (> 40 points). A total 32 atopic dermatitis patients were given 1 tablet / day of (Kokast) each tableted contain montelukast sodium 4 mg for 2 weeks.
Total IgE level was measured in all subjects by ELISA. Eosinophils counts were done by blood film. DNA extraction and PCR amplification were done to (26 patients and 8 controls) using a commercial DNA isolation kit and primers of FLG variants R501X and 2282del4 then PCR product was visualized.
SCORAD significantly (P < 0.05) improvement was marked upon treatment with montelukast. No significant difference based on gender or age was detected.
Montelukast treatment showed significant (P < 0.05) reduction of the IgE levels and number of eosinophils counts compared to AD patients group. No significant difference was detected based on sex or age. Although, total IgE levels tend to be higher in adult than children and in male than female, no significant difference was detected based on sex or age.
In this study, FLG mutation R501X was not detected in patients or control. The FLG mutation 2282del4 was detected in 20 patients from 26 genotyped patients and was absent in healthy non AD controls. FLG mutation 2282del4 was detected in this study and its prevalence was 76.9%. Recovery in FLG mutation 2282del4 of genotyping patients was 20%. Significant (P < 0.05) correlation between FLG mutation 2282del4 and AD disease was detected. Montelukast treatment showed significant (P < 0.05) improvement in SCORAD and total IgE compared to AD patients with FLG. Similar pattern were detected between recovered and non-recovered FLG AD patients.
Data indicated high responsiveness in FLG 2282del4 modulation by decreasing IgE levels and SCORAD using montelukast treatment as a leukotriene receptor antagonist
from the present study, montelukast succeed in treatment AD patients by improving epidermal barrier and its ability to modulate FLG mutation 2282del4 in AD patients. However, further studies are needed to know the mechanism by which montelukast modulate of FLG mutation 2282del4 in AD patients.