Filis Konstantinos, Kavantzas Nikolaos, Dalainas Ilias, Galyfos George, Karanikola Evridiki, Toutouzas Konstantinos, Tsioufis Constantinos, Sigala Fragiska
Division of Vascular Surgery, First Department of Propaedeutic Surgery, University of Athens Medical School, Hippokration Hospital, Athens, Greece.
First Department of Pathology, University of Athens Medical School, Athens, Greece.
Vasa. 2014 Jul;43(4):252-9. doi: 10.1024/0301-1526/a000360.
The factors contributing to superficial vein thrombosis (SVT) in patients with varicose vein disease are unclear. Differences in vein wall apoptotic activity could be associated with the pathogenesis of SVT. The aim of the study is to address the role of the programmed cell death in the vein wall by comparing varicose veins with history of SVT to uncomplicated varicose veins.
Vein segments from the proximal part of the great saphenous vein (GSV), the distal part of the vein and from a varicose tributary, from 16 patients with varicose vein disease and one episode of SVT, were evaluated for the immunohistochemical expression of pro-apoptotic (Bax, p53, Caspase 3, BCL-6, BCL-xs), anti-apoptotic (BCL-xl and BCL-2) and proliferation (Ki-67) markers. The results of this study were compared to the results from the evaluation of 19 patients suffering from uncomplicated varicose vein disease and 10 healthy GSVs as controls.
Overall, there was increased apoptosis in the distal part of GSV compared to the proximal part documented by increased expression of Bax (p < 0.01), Caspase 3 (p = 0.01), BCL-xs (p < 0.01). The comparisons of the markers' expression between patients with varicose veins and patients with a history of SVT showed significant differences among the three different anatomic locations. In the proximal GSV, only BCL-xs was higher in patients with SVT (p = 0.029). In the tributaries, Bax, BCL-xl and Ki-67 were higher in patients with SVT (p < 0.01). In the distal GSV, increased Bax, BCL-xs, BCL-xl and Ki-67 staining was observed in the thrombosis group compared to uncomplicated veins (p < 0.01).
The vein wall in SVT shows increased pro-apoptotic activity compared to uncomplicated disease and normal veins. Whether increased vein wall cell apoptosis is a causative factor for SVT in varicose veins disease or a repairing mechanism of the thrombosis itself needs further research.
导致静脉曲张疾病患者发生浅静脉血栓形成（SVT）的因素尚不清楚。静脉壁凋亡活性的差异可能与SVT的发病机制有关。本研究的目的是通过比较有SVT病史的静脉曲张与无并发症的静脉曲张，探讨程序性细胞死亡在静脉壁中的作用。
对16例有静脉曲张疾病且有一次SVT发作的患者，取其大隐静脉（GSV）近端、静脉远端及曲张属支的静脉段，评估促凋亡（Bax、p53、Caspase 3、BCL-6、BCL-xs）、抗凋亡（BCL-xl和BCL-2）及增殖（Ki-67）标志物的免疫组化表达。将本研究结果与19例无并发症的静脉曲张疾病患者及10条正常GSV作为对照的评估结果进行比较。
总体而言，与近端相比，GSV远端的凋亡增加，表现为Bax（p<0.01）、Caspase 3（p = 0.01）、BCL-xs（p<0.01）表达增加。静脉曲张患者与有SVT病史患者之间标志物表达的比较显示，在三个不同解剖位置存在显著差异。在近端GSV中，只有BCL-xs在有SVT的患者中较高（p = 0.029）。在属支中，有SVT的患者Bax、BCL-xl和Ki-67较高（p<0.01）。在远端GSV中，与无并发症的静脉相比，血栓形成组Bax、BCL-xs、BCL-xl和Ki-67染色增加（p<0.01）。
与无并发症的疾病和正常静脉相比，SVT中的静脉壁显示出增加的促凋亡活性。静脉壁细胞凋亡增加是静脉曲张疾病中SVT的致病因素还是血栓形成本身的修复机制，需要进一步研究。
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