慢性不愈合伤口:腿部溃疡会遗传吗?

Ulcers Pub Date : 2013-03-10 DOI:10.1155/2013/219257
N. Nagy, N. Nagy, G. Szabad, G. Szolnoky, Zsuzsanna Kiss-László, E. Dósa-Rácz, Z. Bata-Csörgő, Z. Bata-Csörgő, L. Kemény, L. Kemény, M. Széll, M. Széll
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引用次数: 0

摘要

背景。一些已知的获得性和假定的遗传性病因因素有助于腿部静脉性溃疡(VLU)的发展。的目标。在这项研究中,我们着手对可能导致VLU发展的遗传和后天因素进行荟萃分析。方法。根据获得性病因将VLU患者分为3个亚组。测定4个遗传因子的频率:F5基因的R506Q (Leiden)突变、F2(凝血酶原)基因的G20210A突变、成纤维细胞生长因子受体2 (FGFR2) 3 ' UTR的2451 A/G SNP和肿瘤坏死因子α (TNFA)启动子的- 308 G/A SNP。结果。- 308 TNFA SNP在无已知获得性易感因素的VLU患者中比在有血栓或软组织感染病史的患者中出现的频率更高(Fisher)。结论。本研究表明,VLU患者的遗传易感因素具有异质性。需要进一步的大规模研究来描述关于VLU发展的遗传和获得性病因之间的联系,并将已知遗传因素的后果整合到VLU的管理中。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Chronic Nonhealing Wounds: Could Leg Ulcers Be Hereditary?
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.
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