Background: 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.

Material/methods: 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.

Results: 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.

Conclusions: A chronic low-grade activation of coagulation exists in ulcerative colitis, regardless of disease activity, and it might be implicated in disease pathogenesis.

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