Abstract

The aim of the present paper was to determine the mechanism by which the level of coagulation factor XIIIA declines during the active phase of Crohn's disease. The relationship between the activity of Crohn's disease and factor XIIIA was observed in 31 patients with Crohn's disease prospectively. The relationship between factor XIIIA and thrombin-antithrombin III complex (TAT), factor XIIIA expressed on the surface of peripheral monocytes, was also evaluated. During the first year, there were 11 patients with Crohn's disease in the active phase and 20 patients who remained in remission. The average of the lowest level of factor XIIIA among the patients in the active phase was 60.1%. The average of the lowest level of factor XIIIA in patients who remained in remission was 78.1% (P = 0.049). Among the 20 patients who remained in remission for 1 year, eight patients had factor XIIIA levels below 70%. Six of them required surgical enterectomies, on average 2 years and 1 month later. However, none of the 12 patients who remained in remission for 1 year and who never had factor XIIIA levels <70% had a surgical enterectomy during follow up of 4 years and 6 months (P = 0.002). The decline of factor XIIIA was not due to increased consumption secondary to blood coagulation (TAT), nor was it due to a decline in the function of monocytes that produce factor XIIIA. Factor XIIIA declines during the active phase of Crohn's disease because it might be consumed in the repair of injured tissue.

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