Background/Objectives Atopic dermatitis (AD) is an inflammatory chronic skin disorder. The etiology of AD is not fully understood. Therefore, we aimed by this study to shed light on the potential role of resistin in an etiopathogenesis of AD through investigation of resistin rs3745367 single nucleotide polymorphism (SNP) and resistin serum levels, and their relation to leukocytic count in a sample of Egyptian patients having atopic dermatitis. Methods This case‐control study included 45 patients having AD and 40 controls. SCORAD index was assessed to evaluate the severity of AD. CBC, ELISA, and PCR‐RFLP were performed to detect leukocytic count, resistin serum level, and resistin rs3745367 SNP, respectively. Results Atopic dermatitis patients had significant low serum resistin concentrations (P = .036) and a significantly high frequency of leukocytosis (P = .003). Low resistin serum levels were significantly related to AD disease severity (P < .001) and the presence of leukocytosis (P < .001). Resistin rs3745367 GG genotype (P = .030), as well as its G allele (P = .019), was expressively associated with AD development, and both increased the risk of AD by 3‐ and 2‐fold, respectively. Resistin rs3745367 GG genotype was significantly linked to low resistin serum levels (P < .001), AD‐positive family history (P = .015), and the presence of leukocytosis (P < .001). Conclusions Resistin rs3745367 gene polymorphism may contribute to the development of AD. Resistin may have an immune‐modulating active character in the AD etiopathogenesis that could be mediated through its anti‐inflammatory effect. From this piece of work, we may suggest resistin as a new therapy to mitigate the pro‐inflammatory environment found in AD.

Background: Atopic dermatitis (AD) is a recognized T helper (Th)2, allergic, skin disease. Galectin-9 (gal-9) is a member of galectin family. It alters T-cell balance resulting in Th2 polarization. These Th2 cells yield various cytokines that may influence E selectin expression. Therefore, we hypothesized that gal-9 may have an active role in AD and this role could be mediated through E selectin. Objective: To assess this hypothesis, immunohistochemical expression of gal-9 and E selectin was investigated in skin lesions, from atopic dermatitis patients, and compared. Methods: Twenty-two atopic dermatitis patients and ten controls were included in this casecontrol study. SCORAD score was used to evaluate atopic dermatitis severity. Biopsies from skin lesions of AD patients and matched sites of controls were taken and stained immunohistochemically by gal-9 and E selectin polyclonal antibodies. Results: Compared to controls, atopic dermatitis patients exhibited a significant increased gal-9 H score, percent of expression, cellular localization (P˂0.001) and intensity (P=0.04) as well as dermal cellular infiltrate (P˂0.001). Also, there were significant elevations in E selectin H score (P=0.002), percent of expression (P=0.001) and cellular localization (P<0.001) as well as dermal inflammatory infiltrates in AD cases than controls. In AD, 20 cases showed co expression of both gal-9 and E selectin in the epidermis with insignificant correlation between their H scores. Study Limitations: This study only included a small number of studied subjects. Conclusion: Galectin-9 and E selectin participates independently in atopic dermatitis pathogenesis, that may help in development of new therapeutic agents in atopic dermatitis management program.

Background: Keloids represent chronic fibroproliferative skin disorders in which there is deposition of extracellular components, especially type 1 collagen, fibronectin and elastin, in excessive amounts. NEDD4 is associated with fibrosis found in abnormal wound healing through increased fibroblast proliferation and regulation of type 1 collagen expression. The exact etiology of keloid formation is undefined, but the role of genetic factors was demonstrated. Objective: To investigate the polymorphism of the NEDD4 gene rs8032158 in a sample of Egyptian patients who have keloids. Methods: The current case-control study was conducted in 160 unrelated subjects; 100 keloid patients and 60 ages and sex coincided with apparently healthy controls. All subjects underwent a complete history, and weight and length were measured to calculate body mass index (BMI). The Vancouver Scar Scale (VSS) was used to assess keloid severity. An analysis of the polymorphism of the NEDD4 gene rs8032158 T/C was performed using taqman allelic discrimination (real-time PCR). Results: The rs8032158 CC genotype was observed significantly in keloid patients and increased the risk of keloid development by approximately 2 times (p = 0.003, OR = 1.80). The C allele significantly increased the risk of keloid development by approximately 2 times (P = 0.002, OR = 2.08). The carriers of the CC genotype were significantly associated with severe keloid form and with the highest VSS values. Conclusion: The polymorphism of the NEDD4 gene rs8032158 could participate in the formation of keloids in the Egyptian population. The NEDD4 rs8032158 CC genotype may have a role in keloid severity.

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