Elevated markers of thrombin generation and fibrinolysis in patients with active and quiescent ulcerative colitis

2009 
Prothrombotic abnormalities within the coagulation system, the presence of microvascular thrombi in intestinal mucosa, and the increased risk of thromboembolic complications in patients with Inflammatory bowel disease, suggest that a hypercoagulable state may be an important contributing factor in disease pathogenesis. The activation of the coagulation system in a cohort of ulcerative colitis patients was investigated. Markers of coagulation activation in blood (thrombin-antithrombin complex, TAT; prothrombin fragments 1 and 2, F1+2; and D-dimers) and markers of inflammation (erythrocyte sedimentation rate, ESR; C-reactive protein, CRP; and fibrinogen) were measured in 38 patients with active and 13 patients with long-standing quiescent ulcerative colitis. Disease activity was assessed by clinical, endoscopic, and histological criteria. The markers of coagulation activation were also measured in 28 healthy volunteers. There were no differences in TAT, F1+2, and D-dimer plasma levels between active and inactive ulcerative colitis. D-dimer and F1+2 levels were significantly higher in the active ulcerative colitis patients than in the healthy controls. Plasma levels of TAT, F1+2, and D-dimers did not differ between inactive ulcerative colitis patients and healthy controls. However, both active and inactive ulcerative colitis patients had significantly higher proportions of elevated (above-normal) values of coagulation markers than the healthy controls. Correlation analyses revealed strong correlation between ESR, fibrinogen, and D-dimers, which also correlated with the severity and extent of ulcerative colitis. A chronic low-grade activation of coagulation exists in ulcerative colitis, regardless of disease activity, and it might be implicated in disease pathogenesis.
    • Correction
    • Source
    • Cite
    • Save
    • Machine Reading By IdeaReader
    31
    References
    11
    Citations
    NaN
    KQI
    []