Haemostasis in Inflammatory Bowel Diseases: Clinical Relevance
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Background: In inflammatory bowel disease (IBD), many alterations of haemostasis have been reported. Furthermore. IBD is associated with thromboembolic disease.
Methods: Literature on new insights into the physiology of haemostasis. the interaction between haemostasis and inflammation, plasmatic and mucosal changes in haemostasis in IBD, and haemostasis-interfering therapy in patients with IBD are reviewed.
Results: Haemostasis is a vascular-bed-specific, locally regulated, physiological phenomenon aimed at the maintenance of fluidity of blood, and not a simple cascade-shaped chain of reactions. Coagulation activation is part of the inflammatory response, but coagulation activation induces pro-inflammatory effects at the same time. Coagulation and fibrinolysis are activated in the course of IBD. but sometimes in a misbalanced way. Overall, this may induce a state of plasmatic hypercoagulation, irrespective of disease activity. Thromboembolic disease is a common extra-intestinal manifestation of IBD. Established treatment of thromboembolism is similarly useful in IBD patients: concurrent aggressive treatment of exacerbations is recommended. Intractable gastrointestinal bleeding seldom occurs, and has mainly been reported in patients with untreated active IBD. Thrombophilic genetic background does not seem to be responsible for either the increased risk of thromboembolism, or the prevalence of IBD. Haemostasis-interfering therapy to alter the course of IBD is experimental.
Conclusion: Thromboembolism is an extraintestinal manifestation of IBD, partly because of the associated state of plasmatic hypercoagulation. Thrombophilic genetic background does not contribute to prevalence or course of IBD: genetic investigations may be restricted to patients with clinically proven thrombophilia. Anticoagulant therapy can normally be given to patients. but not as an established therapy against IBD.
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Meher L, Dalai S, Panda S, Hui P, Nayak S J Clin Diagn Res. 2016; 10(5):OD35-6.
PMID: 27437291 PMC: 4948467. DOI: 10.7860/JCDR/2016/20105.7883.
Thrombosis in inflammatory bowel diseases: what's the link?.
Giannotta M, Tapete G, Emmi G, Silvestri E, Milla M Thromb J. 2015; 13:14.
PMID: 25866483 PMC: 4393581. DOI: 10.1186/s12959-015-0044-2.
Inflammatory bowel disease and thromboembolism.
Zezos P, Kouklakis G, Saibil F World J Gastroenterol. 2014; 20(38):13863-78.
PMID: 25320522 PMC: 4194568. DOI: 10.3748/wjg.v20.i38.13863.
Induction of apoptosis by thrombin in the cultured neurons of dorsal motor nucleus of the vagus.
Wu X, Zhang W, Li J, Chai B, Peng J, Wang H Neurogastroenterol Motil. 2010; 23(3):279-85, e123-4.
PMID: 21143557 PMC: 3079207. DOI: 10.1111/j.1365-2982.2010.01641.x.
Assessment of thrombophilic abnormalities during the active state of inflammatory bowel disease.
Maher M, Soloma S Saudi J Gastroenterol. 2009; 14(4):192-7.
PMID: 19568537 PMC: 2702936. DOI: 10.4103/1319-3767.41743.