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. 1. Introduction Psoriasis is a lifelong genetic disorder, whose appearance is influenced by both multiple genes and environmental factors. Genome-wide association studies have been carried out in order to establish causative genes of psoriasis vulgaris [1]. Genetic studies on psoriasis, performed with classical major histocompatibility complex alleles, indicated a strong association of early onset psoriasis with the HLA-Cw6, tightly linked to PSORS1. Genetic linkage analyses identified over 20 possible loci associated with psoriasis vulgaris. Association of the disease with genetic polymorphisms in specific candidate genes suggested their possible involvement in psoriasis vulgaris pathogenesis [1]. Leptin is a 16-kilodalton hormone, produced by adipocytes, in both subcutaneous and visceral fat, circulating in the serum, in either free or bound form. Leptin acts through the leptin receptor, a single-trans-membrane receptor detected in several tissues. The human leptin gene is situated on chromosome 7. By fluorescence in situ hybridization, this gene was mapped to 7q31.3 [2]. Skin leptin upregulates the hypoxia-inducible factor-1a that in turn influences several genes encoding key regulators of angiogenesis and
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