Abstract
Atopic Dermatitis is an itchy, inflammatory skin condition with a predilection for the skin flexures. Studies have found the expression of IL-4 and decreased IFN-γ expression was more pronounced in allergen-specific T cells stimulated by various allergens. A comparative descriptive study cover 21 case of AD and 16 control individuals. The mean level of INF-γ was higher among the control than the cases of AD but there was no significant difference between the mean INF-γ level (P = 0.261). There was no significant difference in age between cases and control (P = 0.053). Keywords : Atopic dermatitis, INF- γ, Family history, Children DOI : 10.7176/JHMN/64-01 Publication date :July 31 st 2019
Highlights
Atopic Dermatitis (AD) is an itchy, inflammatory skin condition with a predilection for the skin flexures [1]
A possible mechanism is that Langerhans cells, which are surface IgE positive, present antigen to T cells leading to their activation and release of cytokines, IL-1, IL-6, IFN-γ and Tumor Necrosis Factor-a (TNF-a) [8]
There was no significant difference in age between cases and control
Summary
Atopic Dermatitis (AD) is an itchy, inflammatory skin condition with a predilection for the skin flexures [1] It is characterized by poorly defined erythema with edema, vesicles, and weeping in the acute stage and skin thickening (lichenification) in the chronic stage. 70% of cases of AD start in children under five years of age [2], 10% of cases seen in hospital settings start in adults [3]. The prevalence of symptoms of AD in children six or seven years of age during a one-year period varied from less than 2% in Iran and China to approximately 20% in Australia, England, and Scandinavia [4]. Pathogenesis: Genetic and environmental factors induce a complex series of cellular interactions leading to the symptoms and signs of AD [7]. A possible mechanism is that Langerhans cells, which are surface IgE positive, present antigen to T cells leading to their activation and release of cytokines, IL-1, IL-6, IFN-γ and Tumor Necrosis Factor-a (TNF-a) [8]
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