Poredos P, Jezovnik M K
Department for Vascular Disease, University Medical Centre, Ljubljana, Slovenia.
Int Angiol. 2007 Dec;26(4):306-11.
During the last decade, the role of inflammation in the etiopathogenesis of arterial thrombosis has been elucidated. However, little is known about the relationship between inflammation and venous thrombosis. Recently, inflammation has been accepted as a possible mechanism through which different risk factors trigger thrombus formation in veins. The data indicate that inflammation of the vessel wall initiates thrombus formation in an intact vein and that inflammation and coagulation systems are coupled by a common activation pathway. The first event in thrombus formation is most probably activation of endothelial cells, platelets and leucocytes, with initiation of inflammation and formation of microparticles that trigger the coagulation system through the induction of a tissue factor. Therefore, the key event in the initiation of venous thrombus formation is most probably vein wall inflammation. However, expected relationship between inflammatory markers as indicators of inflammatory process and clinical venous thromboembolism (VTE) has not yet been elucidated. C-reactive protein does not appear to be useful in predicting future venous thrombosis or to be useful in the diagnosis of VTE. Recently, it was demonstrated that probable association between VTE and several other markers of inflammation such as: interleukin (IL)-6, IL-8 and tumor necrosis factor-a exists. While these markers of inflammation were studied during or after acute venous thrombosis, further prospective studies are needed to determine the predictive value of inflammatory markers for VTE. The identification and elucidation of inflammatory markers relevant to venous thrombosis could provide targets for future therapy. That inflammation is the basic etiopathogenetic process of VTE is also supported by the relation of some risk factors to both arterial and venous thrombosis: age, increased body mass index, hypercholesterolemia, hypertension, lupus anticoagulant and hyperhomocysteinemia. A relation was also found between preclinical and clinical atherosclerotic disease and VTE. Also in line with these arguments are the preventive effects of aspirin and statins in both arterial and venous disease.
在过去十年间，炎症在动脉血栓形成的病因发病机制中的作用已得到阐明。然而，关于炎症与静脉血栓形成之间的关系却知之甚少。最近，炎症已被公认为是不同风险因素触发静脉血栓形成的一种可能机制。数据表明，血管壁炎症在完整静脉中启动血栓形成，且炎症和凝血系统通过一条共同的激活途径相互关联。血栓形成的首个事件很可能是内皮细胞、血小板和白细胞的激活，伴随着炎症的启动以及通过诱导组织因子触发凝血系统的微粒的形成。因此，静脉血栓形成起始的关键事件很可能是静脉壁炎症。然而，作为炎症过程指标的炎症标志物与临床静脉血栓栓塞症（VTE）之间的预期关系尚未阐明。C反应蛋白似乎无助于预测未来静脉血栓形成，也无助于VTE的诊断。最近，已证实VTE与其他几种炎症标志物之间可能存在关联，如白细胞介素（IL）-6、IL-8和肿瘤坏死因子-α。虽然这些炎症标志物是在急性静脉血栓形成期间或之后进行研究的，但仍需要进一步的前瞻性研究来确定炎症标志物对VTE的预测价值。识别和阐明与静脉血栓形成相关的炎症标志物可为未来治疗提供靶点。一些风险因素与动脉和静脉血栓形成均有关联，如年龄、体重指数增加、高胆固醇血症、高血压、狼疮抗凝物和高同型半胱氨酸血症，这也支持了炎症是VTE基本病因发病过程的观点。在临床前期和临床动脉粥样硬化疾病与VTE之间也发现了关联。阿司匹林和他汀类药物在动脉和静脉疾病中的预防作用也与这些观点相符。
