Activation of plasma contact and coagulation systems and neutrophils in the active phase of ulcerative colitis

Dig Dis Sci. 1997 Nov;42(11):2356-66. doi: 10.1023/a:1018891323205.


We have shown that the contact (kallikrein-kinin) system is involved in the pathogenesis of experimental enterocolitis. We now investigate activation of the contact and coagulation pathways, platelets, and neutrophils in active and inactive ulcerative colitis patients as compared to normal controls. In active ulcerative colitis patients, a significant decrease of plasma prekallikrein, high molecular weight kininogen, and C1 inhibitor levels was observed as compared with controls, as well as prekallikrein activation on western blots. Significant elevation of prothrombin fragment (F1 + 2), which indicates thrombin generation, and elastase-alpha 1-antitrypsin complexes, reflecting neutrophil activation, were found in patients with active disease. Plasma beta-thromboglobulin, a marker of platelet activation, was elevated in both active and inactive disease and appears to be a feature of ulcerative colitis. Activation of contact and coagulation pathways, as well as neutrophils, may mediate inflammation in the active phase of ulcerative colitis.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adult
  • Blood Coagulation / physiology
  • Blotting, Western
  • Colitis, Ulcerative / physiopathology*
  • Female
  • Fibrinolysis / physiology
  • Humans
  • Kallikrein-Kinin System*
  • Male
  • Neutrophil Activation*
  • Platelet Activation*
  • Prekallikrein / analysis
  • beta-Thromboglobulin / analysis


  • beta-Thromboglobulin
  • Prekallikrein