Derangement of hemostasis in rheumatoid arthritis: association with demographic, inflammatory and metabolic factors
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  • 作者:Theodoros Dimitroulas (1) (5)
    Karen M. J. Douglas (1)
    Vasileios F. Panoulas (1)
    Tracey Toms (1)
    Jacqueline P. Smith (1)
    Gareth J. Treharne (2)
    Peter Nightingale (3)
    James Hodson (3)
    George D Kitas (1) (4)
  • 关键词:Blood coagulation ; Cardiovascular disease ; Fibrinolysis ; Rheumatoid arthritis
  • 刊名:Clinical Rheumatology
  • 出版年:2013
  • 出版时间:September 2013
  • 年:2013
  • 卷:32
  • 期:9
  • 页码:1357-1364
  • 全文大小:184KB
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  • 作者单位:Theodoros Dimitroulas (1) (5)
    Karen M. J. Douglas (1)
    Vasileios F. Panoulas (1)
    Tracey Toms (1)
    Jacqueline P. Smith (1)
    Gareth J. Treharne (2)
    Peter Nightingale (3)
    James Hodson (3)
    George D Kitas (1) (4)

    1. Department of Rheumatology, Dudley Group of Hospitals, NHS FT, Dudley, West Midlands, DY1 2HQ, UK
    5. Department of Rheumatology, Russells Hall Hospital, Dudley Group of Hospitals, DY1 2HQ, Dudley, West Midlands, UK
    2. Department of Psychology, University of Otago, Dunedin, New Zealand
    3. Wolfson Computer Labaratory, University Hospitals of Birmingham, Birmingham, NHS FT, UK
    4. Arthritis Research UK Epidemiology Unit, School of Translational Medicine, University of Manchester Rutherford House, Manchester Science Park 40 Pencroft Way, Manchester, M15 6SZ, UK
文摘
Disturbance of fibrinolysis is common in rheumatoid arthritis (RA), and it may be associated with the increased cardiovascular risk observed in this population. We aimed to assess coagulation derangement and investigate whether abnormalities are influenced by demographic, inflammatory or metabolic factors in patients with RA. Levels of tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI-1), fibrinogen, prothrombin fragment 1-- (PF1--), thrombomodulin (TM), protein C and Von Willebrand factor (vWF) were compared between 141 RA patients and 50 healthy hospital controls. Within RA, coagulation factors were assessed alongside several demographic, inflammation and metabolic indicators. RA patients had higher levels of coagulation factors than controls. After correction for age and sex, having RA predicted increased tPA (B--.15, P-lt;-.001), PAI-1 (B--.21, P-lt;-.001), fibrinogen (B--.86, P-lt;-.001), PF1-- (B--.20, P-lt;-.001), and TM (B--.01, P--.03) levels. CRP correlated positively with tPA (P-lt;-.05), fibrinogen (P-lt;-.001), TM (P-lt;-.05), PF1-- (P-lt;-.001) and vWF (P-lt;-.001). Metabolic factors linked with coagulation factors were hypertriglyceridaemia (tPA, P-lt;-.05; PAI-1, P-lt;-.05; protein C, P-lt;-.05) and insulin resistance (tPA, P-lt;-.01; PAI-1, P-lt;-.01; vWF, P-lt;-.05). Imbalance of coagulation and fibrinolytic mechanisms is common in RA and associates with age, inflammation, and metabolic factors. Further studies may determine whether these abnormalities are the consequence of acute inflammation or markers of vascular dysfunction.

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