Venous thrombosis and prothrombotic factors in inflammatory bowel disease

作     者：Fernando Magro Jo?o-Bruno Soares Dália Fernandes 

作者机构：Gastroenterology Department of Centro Hospitalar S?o Jo?o4200-319 PortoPortugal Institute of Pharmacology and TherapeuticsFaculty of MedicineUniversity of Porto4200-319 PortoPortugal IBMCInstitute for Molecular and Cell BiologyUniversity of Porto4150-180 PortoPortugal Gastroenterology Department of Hospital de Braga4710-243 BragaPortugal Gastroenterology Department of Centro Hospitalar da Cova da Beira6200-251 Covilh?Portugal 

出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)

年 卷 期：2014年第20卷第17期

页      面：4857-4872页

核心收录：

学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

主　　题：Acquired Genetic Prothrombotic Venous thrombosis Risk of venous thrombosis Inflammatory bowel disease 

摘      要：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.