Journal of Clinical Gastroenterology and Hepatology Open Access

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Involvement of coagulation and hemostasis in inflammatory bowel diseases

14th International Conference on Gastro Education
September 06-07, 2018 London, UK

Antoni Stadnicki

Medical University of Silesia, Poland

Scientific Tracks Abstracts: J Clin Gastroenterol Hepatol

Abstract:

Inflammatory bowel diseases (IBD); Crohn’s disease and ulcerative colitis (UC), are idiopathic, intestinal and systemic inflammatory disorders which are immunologically mediated with activation of plasma proteolytic cascades. Activation of coagulation in IBD is related to activity and colonic extension of the disease, but may be still persistent in quiescent stage. Factor XIII seems to be as much coagulation factor as connective tissue factor which may contribute to intestinal healing. Fibrinolytic capacity is reduced in general circulation of IBD patients, but a role of recently recognized thrombin – activatable fibrinolytic inhibitor is unclear. Platelets activation is a feature of IBD and contribute to pathogenic inflammatory sequel. There are evidences that in turn coagulation activation may mediate and amplify inflammatory cascades in IBD especially via activating PARs related pathways. The etiology of thromboembolism in IBD is likely multifactorial but largely attributable to coagulation activation, and platelet aggregation during systemic inflammation. Thromboembolic (TE) complications in both Crohn’s disease and UC appear to have at least 3-4 fold increased risk of developing compared to control patients. Currently no single TE laboratory marker has predictive value, but recently developed endogenous thrombin potential test may predictive potential value in IBD. At present no interaction between IBD and inherited factors of thrombophilia was found. An efficacy of heparin treatment in UC is still controversial and not established, although heparin is safe in UC flare. Prophylactic anticoagulation against TE is currently defined, moderate and high-risk patients should be considered for using moderate dose of heparin.

Biography :

Dr. Antoni worked in Thrombosis Research Center, Temple University Medical School, Philadelphia, USA, having faculty position, investigated a role of plasma and intestinal tissue kallikrein kinin system in experimental IBD, in collaboration with Prof. Dr. RB Sartor, NC, and Chapel Hill, US. Currently working as Professor, Silesian Medical University doing research, medical practice, and teaching students. He has supervised two large research projects founded by Polish Ministry of Sciences related to pathogenesis and treatment of human IBD. He also continued IBD coagulation study to evaluate link of coagulation-inflammation in joints and gut diseases, and anti - platelets agents (Clopidogrel) interactions with proton pump inhibitors. My recent projects were also related to the tissue kallikrein kinin system, and kinin receptors in colorectal polyps, and colorectal cancer as well as a significance of angiogenesis related to kinins and grow factors in ulcerative colitis.

E-mail: astadnic@wp.pl