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炎症性肠病中组织因子暴露的微粒。

Tissue factor exposing microparticles in inflammatory bowel disease.

机构信息

Department of Internal Medicine III, Division of Gastroenterology and Hepatology; Medical University of Vienna, Vienna, Austria.

出版信息

J Crohns Colitis. 2013 Apr;7(3):222-9. doi: 10.1016/j.crohns.2012.05.016. Epub 2012 Jun 15.

DOI:10.1016/j.crohns.2012.05.016
PMID:22705067
Abstract

BACKGROUND

Circulating procoagulant microparticles (MPs) are thought to be involved in the pathogenesis of venous thromboembolism in patients with inflammatory bowel disease (IBD). However, the exposure of tissue factor, the primary initiator of coagulation activation, on microparticles (TF(+)MPs) and its association with hemostasis activation has not yet been studied in IBD patients.

METHODS

In this case-control study 49 IBD patients (28 Crohn's disease, 21 ulcerative colitis) and 49 sex- and age-matched, healthy controls were included. Clinical disease activity (Crohn's Disease Activity Index and Clinical Activity Index, respectively) was assessed and IBD-related data were determined by chart review. Numbers, cellular origin and procoagulant activity of TF(+)MPs in plasma were determined using flow cytometry and a chromogenic activity assay. D-dimer and high-sensitive C-reactive protein (CRP) served as markers for coagulation activation and inflammation, respectively. The primary endpoint was the number of TF(+)MPs in IBD patients compared to controls.

RESULTS

Median number (interquartile range) of TF(+)MPs was higher in IBD patients than in controls (14.0 (11.9-22.8)×10(3)/mL vs. 11.9 (11.9-19.1)×10(3)/mL plasma, P=0.029). This finding was due to generally higher plasma levels of MPs from platelets and leukocytes in IBD patients. However, the number of TF(+)MPs was neither correlated with their procoagulant activity and D-dimer nor with disease activity and CRP.

CONCLUSIONS

Increased numbers of circulating TF(+)MPs represent a new facet of hemostatic abnormalities in IBD. However, the lack of association with activation of the coagulation system and disease activity questions their pathogenetic role for venous thromboembolism in this patient group.

摘要

背景

循环促凝血微粒(MPs)被认为参与了炎症性肠病(IBD)患者静脉血栓栓塞的发病机制。然而,组织因子(凝血激活的主要启动子)在微粒上的暴露(TF(+)MPs)及其与止血激活的关联在 IBD 患者中尚未得到研究。

方法

在这项病例对照研究中,纳入了 49 名 IBD 患者(28 名克罗恩病,21 名溃疡性结肠炎)和 49 名性别和年龄匹配的健康对照者。通过图表回顾确定临床疾病活动(分别为克罗恩病活动指数和临床活动指数)和与 IBD 相关的数据。使用流式细胞术和显色活性测定法测定血浆中 TF(+)MPs 的数量、细胞起源和促凝血活性。D-二聚体和高敏 C 反应蛋白(CRP)分别作为凝血激活和炎症的标志物。主要终点是与对照组相比,IBD 患者的 TF(+)MPs 数量。

结果

与对照组相比,IBD 患者的 TF(+)MPs 中位数(四分位距)更高(14.0(11.9-22.8)×10(3)/mL 比 11.9(11.9-19.1)×10(3)/mL 血浆,P=0.029)。这一发现是由于 IBD 患者的血小板和白细胞来源的 MPs 血浆水平普遍较高。然而,TF(+)MPs 的数量既与它们的促凝血活性和 D-二聚体无关,也与疾病活动和 CRP 无关。

结论

循环 TF(+)MPs 数量的增加代表了 IBD 中止血异常的一个新方面。然而,缺乏与凝血系统激活和疾病活动的关联,使得它们在该患者群体中对静脉血栓栓塞的发病机制作用受到质疑。

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