Farag Azza G A, Hammam Mostafa A, Khaled Hesham N, Soliman ShimaE, Tayel Nermin Reda, El-Shamendy Amira A, Shehata Wafaa A
Department of Dermatology, Andrology and STDs, Faculty of Medicine, Menoufia University, Shebin ElKom, Egypt.
Department of Biochemistry, Faculty of Medicine, Menoufia University, Shebin ElKom, Egypt.
J Cosmet Dermatol. 2020 Nov;19(11):2929-2935. doi: 10.1111/jocd.13338. Epub 2020 Feb 28.
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.
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.
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).
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.
背景/目的：特应性皮炎（AD）是一种炎症性慢性皮肤病。AD的病因尚未完全明确。因此，本研究旨在通过调查抵抗素rs3745367单核苷酸多态性（SNP）和抵抗素血清水平，以及它们与埃及特应性皮炎患者样本中白细胞计数的关系，来阐明抵抗素在AD发病机制中的潜在作用。
本病例对照研究纳入了45例AD患者和40例对照。评估SCORAD指数以评估AD的严重程度。分别进行全血细胞计数（CBC）、酶联免疫吸附测定（ELISA）和聚合酶链反应-限制性片段长度多态性分析（PCR-RFLP）以检测白细胞计数、抵抗素血清水平和抵抗素rs3745367 SNP。
特应性皮炎患者血清抵抗素浓度显著降低（P = 0.036），白细胞增多症的发生率显著升高（P = 0.003）。抵抗素血清水平低与AD疾病严重程度（P < 0.001）和白细胞增多症的存在（P < 0.001）显著相关。抵抗素rs3745367 GG基因型（P = 0.030）及其G等位基因（P = 0.019）与AD的发生显著相关，且分别使AD风险增加3倍和2倍。抵抗素rs3745367 GG基因型与抵抗素血清水平低（P < 0.001）、AD阳性家族史（P = 0.015）和白细胞增多症的存在（P < 0.001）显著相关。
抵抗素rs3745367基因多态性可能与AD的发生有关。抵抗素可能在AD发病机制中具有免疫调节活性，这可能通过其抗炎作用介导。从这项工作中，我们可以提出抵抗素作为一种新的治疗方法来减轻AD中发现的促炎环境。
