ArticleDigestive diseases and sciences1997
Activation of plasma contact and coagulation systems and neutrophils in the active phase of ulcerative colitis.
Article in Digestive diseases and sciences, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 54 citations in OpenAlex.
- Molecular determinants of thromboinflammatory activation in inflammatory bowel disease.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Anti-HK antibody inhibits the plasma contact system by blocking prekallikrein and factor XI activation in vivo.Blood advances · 2023Article
- Venous and arterial thromboembolism in patients with inflammatory bowel diseases.World journal of gastroenterology · 2021Review
- The Plasma Kallikrein-Kininogen Pathway Is Critical in the Pathogenesis of Colitis in Mice.Frontiers in immunology · 2018Article
- Factor XII-Driven Inflammatory Reactions with Implications for Anaphylaxis.Frontiers in immunology · 2017Review
- Inhibition of plasma kallikrein by a highly specific active site blocking antibody.The Journal of biological chemistry · 2014Article
- Thrombosis and inflammatory bowel disease-the role of genetic risk factors.World journal of gastroenterology · 2008Review
- The relevance of kinin B1 receptor upregulation in a mouse model of colitis.British journal of pharmacology · 2008Article
- Deletion of murine kininogen gene 1 (mKng1) causes loss of plasma kininogen and delays thrombosis.Blood · 2008Article
- Immunolocalization and expression of kallistatin and tissue kallikrein in human inflammatory bowel disease.Digestive diseases and sciences · 2003Article
- Anti-cardiolipin and anti-beta2-glycoprotein I antibodies in patients with inflammatory bowel disease.Digestive diseases and sciences · 1998Article
- Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.