title: Venous thrombosis and prothrombotic factors in inflammatory bowel disease.
abstract: Patients with inflammatory bowel disease (IBD) may have an increased risk of venous thrombosis (VTE). PubMed, ISI Web of Knowledge and Scopus were searched to identify studies investigating the risk of VTE and the prevalence of acquired and genetic VTE risk factors and prothrombotic abnormalities in IBD. Overall, IBD patients have a two- to fourfold increased risk of VTE compared with healthy controls, with an overall incidence rate of 1%-8%. The majority of studies did not show significant differences in the risk of VTE between Crohn's disease and ulcerative colitis. Several acquired factors are responsible for the increased risk of VTE in IBD: inflammatory activity, hospitalisation, surgery, pregnancy, disease phenotype (e.g., fistulising disease, colonic involvement and extensive involvement) and drug therapy (mainly steroids). There is also convincing evidence from basic science and from clinical and epidemiological studies that IBD is associated with several prothrombotic abnormalities, including initiation of the coagulation system, downregulation of natural anticoagulant mechanisms, impairment of fibrinolysis, increased platelet count and reactivity and dysfunction of the endothelium. Classical genetic alterations are not generally found more often in IBD patients than in non-IBD patients, suggesting that genetics does not explain the greater risk of VTE in these patients. IBD VTE may have clinical specificities, namely an earlier first episode of VTE in life, high recurrence rate, decreased efficacy of some drugs in preventing further episodes and poor prognosis. Clinicians should be aware of these risks, and adequate prophylactic actions should be taken in patients who have disease activity, are hospitalised, are submitted to surgery or are undergoing treatment.
authors.affiliation: Fernando Magro, Gastroenterology Department of Centro Hospitalar São João, 4200-319 Porto, Portugal.
authors.forename: Fernando
authors.initials: F
authors.lastname: Magro
authors.affiliation: Fernando Magro, Gastroenterology Department of Centro Hospitalar São João, 4200-319 Porto, Portugal.
authors.forename: João-Bruno
authors.initials: JB
authors.lastname: Soares
authors.affiliation: Fernando Magro, Gastroenterology Department of Centro Hospitalar São João, 4200-319 Porto, Portugal.
authors.forename: Dália
authors.initials: D
authors.lastname: Fernandes
mesh_terms: D000818:Animals; D000925:Anticoagulants / Q000627:therapeutic use; D001777:Blood Coagulation / Q000187:drug effects / Q000235:genetics; D001779:Blood Coagulation Factors / Q000235:genetics / Q000378:metabolism*; D003093:Colitis, Ulcerative / Q000097:blood / Q000150:complications* / Q000188:drug therapy / Q000235:genetics; D003424:Crohn Disease / Q000097:blood / Q000150:complications* / Q000188:drug therapy / Q000235:genetics; D020022:Genetic Predisposition to Disease; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D010641:Phenotype; D012307:Risk Factors; D020246:Venous Thrombosis / Q000097:blood / Q000209:etiology* / Q000235:genetics / Q000517:prevention & control
chemical_list: D000925:Anticoagulants; D001779:Blood Coagulation Factors; D018836:Inflammation Mediators
keywords: Acquired; Genetic; Inflammatory bowel disease; Prothrombotic; Risk of venous thrombosis; Venous thrombosis