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慢性静脉性腿部溃疡患者的血栓形成倾向——一项针对有或无血栓后综合征患者的研究。

Thrombophilia in patients with chronic venous leg ulcers-a study on patients with or without post-thrombotic syndrome.

机构信息

Department of Dermatology, Venereology and Allergology, University of Göttingen, Göttingen, Germany.

出版信息

J Eur Acad Dermatol Venereol. 2011 Dec;25(12):1432-9. doi: 10.1111/j.1468-3083.2011.04001.x. Epub 2011 Mar 11.

DOI:10.1111/j.1468-3083.2011.04001.x
PMID:21392126
Abstract

BACKGROUND

Chronic venous leg ulcers (CVU) cause considerable burden of disease for the patients as well as enormous costs for health care systems. The pathophysiology of CVU is complex and not entirely understood. So far reliable pathogenic and/or prognostic parameters have not been identified.

OBJECTIVES

We studied the role of thrombophilia in patients referred to a University dermatology department for treatment of CVU.

PATIENTS AND METHODS

A cohort of 310 patients with active chronic venous leg ulcers (CEAP 6) was stratified into two comparably large groups according to the presence or absence of post-thrombotic syndrome (PTS+; PTS-) as determined using duplex scan and/or phlebography. In addition, several thrombophilia parameters were assessed.

RESULTS

The prevalence of protein S deficiency and factor V Leiden mutation was significantly higher in PTS+ patients compared with the PTS- group. However, patients in both subgroups revealed high prevalences of thrombophilia (antithrombin deficiency, protein C deficiency, protein S deficiency, activated protein C resistance, factor V mutation or elevated homocysteine).

CONCLUSION

Based on these data, it is conceivable that thrombophilia contributes to the pathogenesis of CVU, possibly through induction of microcirculatory dysregulations.

摘要

背景

慢性静脉性腿部溃疡(CVU)给患者带来了相当大的疾病负担,也给医疗保健系统带来了巨大的成本。CVU 的病理生理学很复杂,尚未完全了解。迄今为止,尚未确定可靠的病因和/或预后参数。

目的

我们研究了血栓形成倾向在因 CVU 到大学皮肤科就诊的患者中的作用。

患者和方法

根据双功能超声扫描和/或静脉造影确定的存在或不存在血栓后综合征(PTS+;PTS-),将 310 例活动性慢性静脉性腿部溃疡(CEAP 6)患者分为两组,每组人数相当。此外,还评估了几种血栓形成倾向参数。

结果

与 PTS- 组相比,PTS+ 患者的蛋白 S 缺乏和因子 V Leiden 突变的患病率明显更高。然而,两个亚组的患者均存在较高的血栓形成倾向(抗凝血酶缺乏、蛋白 C 缺乏、蛋白 S 缺乏、活化蛋白 C 抵抗、因子 V 突变或同型半胱氨酸升高)。

结论

基于这些数据,可以想象血栓形成倾向通过诱导微循环失调而促进 CVU 的发病机制。

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