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العنوان
Efficacy of Allergen Specific Immunotherapy for Treatment of Allergic Rhinitis: A systematic review and meta-analysis /
المؤلف
Adly, Madonna Nader,
هيئة الاعداد
باحث / مادونا نادر عدلى
مشرف / مجدى عيسى سعفان
مشرف / محمود فؤاد عبد العزيز
مشرف / محمود فوزى مندور
الموضوع
E.N.T.
تاريخ النشر
2020.
عدد الصفحات
p 142. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الحنجرة
تاريخ الإجازة
13/9/2020
مكان الإجازة
جامعة طنطا - كلية الطب - E.N.T
الفهرس
Only 14 pages are availabe for public view

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from 169

Abstract

Abstract Background: Allergic rhinitis is an inflammatory disease of nasal mucosa, induced by an immunoglobulin E (IgE)-mediated reaction caused by house dust mite (HDM) in allergene sensitized subject. HDM is one of the commonest AR allergen in the world and the most common organisms are Dermatophagoides Pteronyssinus and dermatophagoides Farinae the two types are different from each other to some extent but AR patients are cosensetized to both species. AR is characterized by sneezing, rhinorrhea, nasal congestion and nasal pruritus, which are often accompanied by ocular pruritus, redness and/or lacrimation. Allergic rhinitis (AR) is a common airway disease which is reported prevelance of 10-30%. Although AR is not a serious illness, it is clinically relevant because it underlies many and productivity at work or school. Current treatment modalitis include allergen avoidance, antihistamine, nasal steroid and allergen specific immunotherapy (SIT). Comparing to the symptom-releasing options (eg. antihistamine and nasal steroid), SIT (subcutaneous or sublingual route) represent the only immunemodifying and curative available option for the treatment of AR patients. Novel data demonstrate the efficacy of SCIT also as a preventive strategy to reduce onset of new sensitization to non-related allergens, progression from AR to asthma. Immunotherapy modulates immune system function and is currently considered to be the only option with a potential long‑term post treatment effect on allergic diseases. The molecular and cellular mechanisms of AIT include mast cell and basophil desensitization effects, regulation of T‑ and B‑cell responses, regulation of IgE and IgG4 production, and inhibition of