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1、Thromboembolic and cardiovascular risk in rheumatoid arthritis: role of the haemostatic systemI A M van den Oever,1N Sattar,2M T Nurmohamed1,3,4Handling editor Tore K Kvien1Department of Rheumatology,Jan van Breemen Research Institute/Reade, Amsterdam, The Netherlands 2BHF Glasgow CardiovascularRese
2、arch Centre, University of Glasgow, Glasgow, UK 3Departments of InternalMedicine, VU University Medical Centre, Amsterdam, The Netherlands 4Department of Rheumatology,VU University Medical Centre, Amsterdam, The NetherlandsCorrespondence to Dr Inge A M van den Oever, Department of Rheumatology, Jan
3、van Breemen Research Centre/Reade, PO Box 58271, Amsterdam, The Netherlands; i.vd.oeverreade.nlReceived 16 October 2013 Accepted 2 January 2014 Published Online First 14 January 2014To cite: van den Oever IAM, Sattar N, Nurmohamed MT. Ann Rheum Dis 2014;73: 954957.ABSTRACT Circumstantial evidence su
4、ggests that the innate immune system and coagulation system share a common evolutionary origin, which explains the extensivecrosstalk between inflammatory cytokines and coagulation factors, with many components being important for both systems. This crosstalk has been extensively studied in sepsis,
5、an acute state of high-grade inflammation. However, rheumatoid arthritis (RA) as well as many other autoimmune diseases can also be considered as a prothrombotic state. More and more studies show that autoimmune diseases, including RA, are a risk factor for cardiovascular disease, and also for venou
6、s thromboembolic events, such as pulmonaryembolism and deep vein thrombosis. Inflammation and its effect on the haemostatic system is probably the link between these diseases. This viewpoint gives an update of the current literature on thromboembolic risk in RA, but also documents important knowledg
7、e gaps. This viewpoint will therefore help to focus on further research topics to improve diagnostic and therapeutic optionswhich may relieve both the proinflammatory and the prothrombotic burden of autoimmune diseases.INTRODUCTIONRheumatoid arthritis (RA), an autoimmune inflam- matory disease, is a
8、ssociated with a substantially reducedlifeexpectancy.Epidemiologicaland pathophysiological studies to date have focused mainly on arterial atherosclerotic manifestations and their precursors, such as myocardial infarction and increased carotid artery wall thickness, as targets for diagnostic and the
9、rapeutic interventions to increase the life expectancy of patients with RA.1However, data on the risk of venous thrombo- embolic events (VTEs), such as deep vein throm- bosis and pulmonary embolism in RA are scarce, although pulmonary embolism is a potentially lethal complication with a death rate o
10、f 15% inthe first 3 months after diagnosis.2As a number of studies have shown, the risk of VTE seems to be increasedinautoimmunedisorders,including RA.3 4A recently published study demonstrated a more than twofold increased risk of VTE in a population-based inception cohort of 813 patients with RA i
11、n comparison with a cohort of non-RA subjects from the same population base, matched for age and sex.5Inflammationcanincreasetherisk ofboth venousandarterialthromboembolisminRA through several mechanisms. In this viewpoint we will focus on the thromboembolic risk in auto- immune diseases, like RA, a
12、nd the close link between the immune system and the coagulation system. With this update of the current literatureon thromboembolic risk in RA we provide insightinto interesting research fields and knowledge gaps. This can help to focus on further research topics to improve diagnostic and therapeuti
13、c options whichcan relieve both the proinflammatory and the pro- thrombotic burden of autoimmune diseases.THE LINK BETWEEN COAGULATION AND INFLAMMATION Circumstantialevidencesuggeststhatinnate immunity and coagulation share a common evolu- tionary origin, which explains the extensive cross- talkbetw
14、eeninflammatorycytokinesand coagulation factors, with many components beingimportant for both systems. The inflammatory cytokine network, when activated, induces several prothrombotic conditions such as endothelial dys- function, tissue factor (TF) expression and coagula-tion activation, inhibition
15、of fibrinolysis and the protein C system.6Also, indirectly, there may be alink between adiposity, insulin resistance, inflamma- tion and coagulation, since cytokines like tumour necrosis factor (TNF) and interleukin 6 (IL-6) are released in adipose tissue and play a large part in all the above pheno
16、mena.7Activation of coagula-tion and fibrin deposition can be viewed as a part of the host defence of the body against infectious agents in an attempt to contain the invading entity,and the consequent inflammatory response, to a limited area. In addition, activation of the extrinsiccoagulation system and impairment of the fibrino- lytic pathway may help to perpetuate and amplifythe inflammatory response.8 Other factors that also contribute to a hypercoa- gulable state are activated platele
