Hemostatic imbalance in active and quiescent ulcerative colitis

OBJECTIVE: In healthy conditions, factors inducing or inhibiting coagulatio n and factors inducing or inhibiting fibrinolysis are in balance. In ulcera tive colitis, hypercoagulation is presumed, which may explain part of the c linical features of this disease. Therapy strategies affecting hemostasis m ay improve the course of ulcerative colitis. This study was conducted to ev aluate the balance of coagulation and fibrinolysis in the course of treatme nt of active ulcerative colitis. METHODS: Patients with active ulcerative colitis were stud led by serial de termination of markers of the coagulation cascade (thrombin-antithrombin co mplexes and fibrin degradation products [FbDP]) and the fibrinolytic cascad e (fibrinogen degradation products [FgDP]). Parameters of inflammation were also measured (C-reactive protein [C:RP], erythrocyte sedimentation rate [ ESR], albumin, platelet count, and fibrinogen). Disease activity was assess ed by endoscopic and histopathological scores. Follow-up measurement was pe rformed in the course of treatment at the third or fourth month after basel ine. Measurements were compared with healthy controls. RESULTS: Thirty-three patients and 22 healthy controls were included. Durin g active ulcerative colitis, inflammatory parameters (CRP, ESR, platelet co unt) and hemostatic parameters (thrombin-antithrombin complexes, fibrinogen , FgDP, and FbDP) were elevated in comparison with healthy controls. Albumi n was decreased and antithrombin-III remained unchanged. During treatment, disease activity decreased significantly endoscopically and histopathologic ally (p = 0.001). CRP, ESR, platelet count, and fibrinogen also decreased s ignificantly. The hemostatic balance, expressed as the ratio between the pl asmin-dependent generation of FgDP and coagulation-dependent generation of FbDP, increased from 0.69 to 1.12 during treatment, mainly because of a dec rease of FbDP. In healthy controls, this ratio was 1.33. CONCLUSIONS: The coagulation and fibrinolytic cascades were activated in ac tive ulcerative colitis, with a hemostatic imbalance in favor of coagulatio n. This hypercoagulability persisted in 20% (7/33) of patients with ulcerat ive colitis in remission. The decrease of FbDP and the increase in the FgDP /FbnP ratio during reconvalescence of ulcerative colitis showed that the co agulation cascade was more activated than the fibrinolytic cascade in activ e disease. (C) 2001 by Am. Cell. of Gastroenterology.