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No evidence of activated blood coagulation in Crohn's disease

G Novacek1, S Kapiotis, G Moser

  • 1Department of Internal Medicine IV, Gastroenterology and Hepatology, University of Vienna, Austria.

Insights

Thromboembolism is a complication in Crohn's disease (CD). This study found no evidence of blood coagulation activation, measured by thrombin-antithrombin III complex (TAT), suggesting TAT is not a reliable indicator of thromboembolic risk in CD patients.

Area of Science:

  • Gastroenterology
  • Hematology
  • Immunology

Background:

  • Thromboembolism is a serious complication in Crohn's disease (CD).
  • Microvascular infarction of the intestinal mucosa is a potential mechanism in CD pathogenesis.
  • Increased blood coagulation activation is hypothesized to contribute to thromboembolic complications in CD.

Purpose of the Study:

  • To assess blood coagulation activity as a potential index of thromboembolic risk in CD.
  • To evaluate thrombin-antithrombin III complex (TAT) as a marker for thromboembolic risk in CD.

Main Methods:

  • Prospective evaluation of TAT plasma levels in 80 CD patients (47 inactive, 33 active) and 80 healthy controls.
  • Fibrinogen, C-reactive protein, and orosomucoid were measured as parameters of blood coagulation and inflammation.
  • Correlations between TAT, fibrinogen, inflammatory markers, and Crohn's Disease Activity Index (CDAI) were analyzed.

Main Results:

  • Fibrinogen levels were significantly higher in active CD patients compared to inactive CD patients and controls.
  • Fibrinogen levels correlated with CDAI and inflammatory markers.
  • No significant difference in TAT levels was observed between active CD patients, inactive CD patients, and controls.

Conclusions:

  • No evidence of blood coagulation system activation, as indicated by TAT plasma levels, was found in CD patients, even in those with active disease.
  • TAT is not a suitable index for assessing thromboembolic risk in CD.
  • TAT does not appear to reflect microvascular infarction as a pathogenic mechanism in CD.
Abstract

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