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Coagulation Systems and Neutrophils in the Activation of Plasma Contact and Active Phase of Ulcerative Colitis

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Abstract

We have shown that the contact (kallikrein-kinin) system is involved in the pathogenesis ofexperimental enterocolitis. We now investigateactivation of the contact and coagulation pathways,platelets, and neutrophils in active and inactiveulcerative colitis patients as compared to normalcontrols. In active ulcerative colitis patients, asignificant decrease of plasma prekallikrein, highmolecular weight kininogen, and C1 inhibitor levels was observedas compared with controls, as well as prekallikreinactivation on western blots. Significant elevation ofprothrombin fragment (F1 + 2), which indicates thrombin generation, and elastase-α1-antitrypsincomplexes, reflecting neutrophil activation, were foundin patients with active disease. Plasmabeta-thromboglobulin, a marker of platelet activation,was elevated in both active and inactive disease and appearsto be a feature of ulcerative colitis. Activation ofcontact and coagulation pathways, as well asneutrophils, may mediate inflammation in the activephase of ulcerative colitis.

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Stadnicki, A., Gonciarz, M., Niewiarowski, T.J. et al. Coagulation Systems and Neutrophils in the Activation of Plasma Contact and Active Phase of Ulcerative Colitis. Dig Dis Sci 42, 2356–2366 (1997). https://doi.org/10.1023/A:1018891323205

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