title: Haemostasis in inflammatory bowel diseases: clinical relevance.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Vrije Universiteit Medical Centre, Dept. of Gastroenterology, Amsterdam, The Netherlands. v.bodegraven@vumc.nl
authors.forename: A A
authors.initials: AA
authors.lastname: van Bodegraven
mesh_terms: D000925:Anticoagulants / Q000627:therapeutic use; D001779:Blood Coagulation Factors / Q000502:physiology; D006487:Hemostasis / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D015212:Inflammatory Bowel Diseases / Q000150:complications / Q000188:drug therapy / Q000235:genetics / Q000503:physiopathology*; D013917:Thrombin / Q000502:physiology; D013923:Thromboembolism / Q000188:drug therapy / Q000209:etiology / Q000235:genetics / Q000503:physiopathology*
chemical_list: D000925:Anticoagulants; D001779:Blood Coagulation Factors; D013917:Thrombin