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寻常型银屑病中瘦素基因多态性rs2060713的评估

Assessment of Leptin Gene Polymorphism rs2060713 in Psoriasis Vulgaris.

作者信息

Karpouzis Anthony, Tripsianis Gregory, Gatzidou Elisavet, Veletza Stavroula

机构信息

University Clinic of Dermatology, School of Health Sciences, Democritus University of Thrace, 68100 Alexandroupolis, Greece.

University Department of Medical Statistics, School of Health Sciences, Democritus University of Thrace, 68100 Alexandroupolis, Greece.

出版信息

ISRN Dermatol. 2014 Jan 28;2014:845272. doi: 10.1155/2014/845272. eCollection 2014.

Abstract

Psoriasis is a lifelong disorder characterized by approximately 8-fold reduction of the duration of normal skin keratinocyte cell cycle and 2-fold increase of the number of dividing cells. Multiple genes, several environmental factors, and immune system alterations are involved in the pathogenesis of psoriasis. Hyperleptinemia is associated with psoriasis and leptin acts as an angiogenic factor. Angiogenetic processes precede the epidermal hyperplasia in psoriasis, indicating possible involvement of leptin in the pathogenesis of psoriasis. Leptin gene polymorphisms and their association with psoriasis have been given very little attention. We present a study of the rs2060713C/T genetic polymorphism in the pathogenesis of psoriasis vulgaris in 263 vulgaris patients and 252 unrelated matched healthy controls. No statistically significant differences were observed between patients and controls. A statistically nonsignificant trend was observed in males with the early onset type of psoriasis (11.1% C/T in patients versus 5.6% in controls) and in females with the late onset type of the disease (12.8% C/T in patients versus 3.3% in controls). Still, there is no hard evidence on correlation of psoriasis vulgaris with this polymorphism. Possible association with specific forms of the disease and either gender needs further investigation in larger studies.

摘要

银屑病是一种终身性疾病,其特征为正常皮肤角质形成细胞的细胞周期持续时间缩短约8倍,分裂细胞数量增加2倍。多种基因、多种环境因素以及免疫系统改变均参与银屑病的发病机制。高瘦素血症与银屑病相关,且瘦素可作为一种血管生成因子。血管生成过程先于银屑病的表皮增生,这表明瘦素可能参与银屑病的发病机制。瘦素基因多态性及其与银屑病的关联很少受到关注。我们对263例寻常型银屑病患者和252例无亲缘关系的匹配健康对照进行了研究,探讨rs2060713C/T基因多态性在寻常型银屑病发病机制中的作用。患者与对照组之间未观察到统计学上的显著差异。在早发型银屑病男性患者(患者中C/T占11.1%,对照组中占5.6%)和晚发型银屑病女性患者(患者中C/T占12.8%,对照组中占3.3%)中观察到一种无统计学意义的趋势。然而,尚无确凿证据表明寻常型银屑病与这种多态性存在关联。银屑病特定类型与性别之间的可能关联需要在更大规模的研究中进一步探究。

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