BACKGROUND: Activation of coagulation and fibrinolysis occurs in patients with inflammatory bowel disease. Our aim was to study the course of a marker for activation of the coagulation cascade, prothrombin fragment 1 + 2 (F1+2), and fibrinolysis, fibrin degradation products (FbDP), in patients with ulcerative colitis and Crohn's disease before and during therapy with glucocorticoids. METHODS: Twenty-seven patients with active ulcerative colitis and 42 with active Crohn's disease treated with glucocorticoids were studied. Plasma samples were drawn before, during, and at end of therapy or at time of treatment failure. F1+2 and FbDP were measured with commercially available enzyme immunoassays. RESULTS: Mean base-line concentrations of F1+2 were significantly increased in patients with ulcerative colitis (4.77 +/- 0.50 nmol/l; P < 0.0001) and in Crohn's disease (4.66 +/- 0.59 nmol/l; P < 0.0001) compared with healthy controls (1.57 +/- 0.09 nmol/l). Mean base-line concentrations of FbDP were significantly increased in patients with ulcerative colitis (1264 +/- 161 microg FE/l; P < 0.0001) and in Crohn's disease (491 +/- 51 microg FE/l; P < 0.0001) compared with healthy controls (194 +/- 21 microg FE/l). During treatment with glucocorticoids the plasma concentrations of FbDP decreased in patients with Crohn's disease achieving remission and in patients with ulcerative colitis avoiding surgery but remained unchanged in patients not responding to therapy. In contrast, F1+2 remained increased in patients with Crohn's disease and ulcerative colitis irrespective of outcome. CONCLUSION: The present data support the concept that coagulation cascade and fibrinolysis is activated in patients with active inflammatory bowel disease. F1+2 and FbDP correlate poorly with the clinical disease activity and acute-phase reactants. The clinical response to treatment with glucocorticoids is accompanied by a decrease in plasma concentrations of FbDP but not in F1+2. FbDP may emerge as a new marker in the assessment of disease activity in patients with inflammatory bowel disease.
BACKGROUND: Activation of coagulation and fibrinolysis occurs in patients with inflammatory bowel disease. Our aim was to study the course of a marker for activation of the coagulation cascade, prothrombin fragment 1 + 2 (F1+2), and fibrinolysis, fibrin degradation products (FbDP), in patients with ulcerative colitis and Crohn's disease before and during therapy with glucocorticoids. METHODS: Twenty-seven patients with active ulcerative colitis and 42 with active Crohn's disease treated with glucocorticoids were studied. Plasma samples were drawn before, during, and at end of therapy or at time of treatment failure. F1+2 and FbDP were measured with commercially available enzyme immunoassays. RESULTS: Mean base-line concentrations of F1+2 were significantly increased in patients with ulcerative colitis (4.77 +/- 0.50 nmol/l; P < 0.0001) and in Crohn's disease (4.66 +/- 0.59 nmol/l; P < 0.0001) compared with healthy controls (1.57 +/- 0.09 nmol/l). Mean base-line concentrations of FbDP were significantly increased in patients with ulcerative colitis (1264 +/- 161 microg FE/l; P < 0.0001) and in Crohn's disease (491 +/- 51 microg FE/l; P < 0.0001) compared with healthy controls (194 +/- 21 microg FE/l). During treatment with glucocorticoids the plasma concentrations of FbDP decreased in patients with Crohn's disease achieving remission and in patients with ulcerative colitis avoiding surgery but remained unchanged in patients not responding to therapy. In contrast, F1+2 remained increased in patients with Crohn's disease and ulcerative colitis irrespective of outcome. CONCLUSION: The present data support the concept that coagulation cascade and fibrinolysis is activated in patients with active inflammatory bowel disease. F1+2 and FbDP correlate poorly with the clinical disease activity and acute-phase reactants. The clinical response to treatment with glucocorticoids is accompanied by a decrease in plasma concentrations of FbDP but not in F1+2. FbDP may emerge as a new marker in the assessment of disease activity in patients with inflammatory bowel disease.
Authors: Nathalie Vergnolle; Laurie Cellars; Andrea Mencarelli; Giovanni Rizzo; Sunita Swaminathan; Paul Beck; Martin Steinhoff; Patricia Andrade-Gordon; Nigel W Bunnett; Morley D Hollenberg; John L Wallace; Giuseppe Cirino; Stefano Fiorucci Journal: J Clin Invest Date: 2004-11 Impact factor: 14.808