Background. A number of well-known acquired and putative inherited etiological factors contribute to the development of venous leg ulcer (VLU). Aim. In this study we set out to perform a meta-analysis of putative genetic and acquired factors predisposing to VLU development. Methods. VLU patients ( ) were divided into three subgroups in accordance with their acquired etiological factors. The frequencies of four genetic factors were determined: the R506Q (Leiden) mutation of the F5 gene, the G20210A mutation of the F2 (prothrombin) gene, the 2451？A/G SNP of the fibroblast growth factor receptor 2 (FGFR2) 3′ UTR, and the ？308？G/A SNP of the tumor necrosis factor α (TNFA) promoter. Results. The ？308 TNFA SNP exhibited a higher frequency among VLU patients without known acquired predisposing factor in their history, than among patients with thrombosis or soft tissue infection in their history (Fisher ). Conclusions. This study has demonstrated that the group of VLU patients is heterogeneous in their genetic predisposing factors. Further large-scale studies are needed to delineate the associations among genetic and acquired etiological factors with regard to VLU development and to integrate the consequences of the already known genetic factors to the management of VLU. 1. Introduction Venous leg ulcer (VLU) is multifactorial disease with well-known acquired and putative inherited predisposing factors [1–15]. Besides the characteristic acquired etiological factors, such as venous insufficiency, obesity, and deep vein thrombosis, case-control studies suggest putative inherited etiological factors, which may also contribute to the mechanism of delayed or pathological wound healing and hence to the development of leg ulcer. A delineation of the genetic susceptibility factors relating to pathological wound healing would therefore promote a better understanding of the molecular background of VLU and that could provide opportunities for developing causative treatment of therapy-resistant forms [1, 2]. The difficulties involved in such investigations are increased by the fact that these inherited factors form a complex multifactorial genetic background which does not follow the rules of Mendelien inheritance. Moreover, each genetic component contributes differently to the pathogenesis of VLU, and assessment of its individual relevance in the development of the disease is difficult. To investigate the putative genetic factors and to minimize statistical bias, we set out to form subgroups of VLU patients which were homogeneous in their clinical characteristics and to
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