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No evidence of activated blood coagulation in Crohn's disease

Background: Thromboembolism seems to be a significant and serious complication in Crohn's disease (CD), and multifocal microvascular infarction of the intestinal mucosa may be an important effector mechanism in the pathogenesis of CD. Therefore, it has been hypothesized that an increased activation of the blood coagulation system may favour thromboembolic complications. Objectives: To assess the activity of blood coagulation as a potential index of thromboembolic risk in CD using thrombin‐antithrombin III complex (TAT). Design: Prospective evaluation of TAT. Setting: Out‐patients at the gastroenterological department of a university hospital. Patients: Eighty patients with CD, 47 with inactive (Crohn's disease activity index (CDAI) <150) and 33 with active disease, and 80 healthy controls were investigated in this study. Methods: TAT and fibrinogen were used as parameters of blood coagulation. C‐reactive protein and orosomucoid were used as serum inflammatory parameters. Results: Fibrinogen was significantly higher in patients with active CD (median 535 mg/dl; interquartile range 402‐620mg/dl) than in patients with inactive CD (357 mg/dl; 300‐467mg/dl) or controls (268mg/dl; 231‐299mg/dl). Fibrinogen correlated with CDAI, C‐reactive protein and orosomucoid. TAT did not show any difference between patients with active CD (3.2 ng/ml; 2.5‐4.6 ng/ml), inactive CD (3.0 ng/ml; 2.4‐3.9 ng/ml) and controls (3.1 ng/ml; 2.3‐3.6 ng/ml). Correspondingly, TAT correlated neither with serum inflammatory parameters and CDAI nor with fibrinogen. Conclusion: We could not find evidence of activation of the blood coagulation system as determined by TAT plasma levels in CD, not even in patients with active disease. TAT is not, therefore, a potential index of thromboembolic risk in CD and of microvascular infarction as an effector mechanism in the pathogenesis of CD.