Thrombosis in inflammatory bowel diseases: What's the link?

被引：100
作者：
Giannotta M. [1 ]
Tapete G. [1 ]
Emmi G. [2 ]
Silvestri E. [2 ]
Milla M. [1 ]
机构：
[1] AOU Careggi Regional Referral Center for Inflammatory Bowel Disease, Gastroenterology Department, Florence
[2] University of Florence and Patologia Medica Unit, AOU Careggi, Department of Experimental and Clinical Medicine, Florence
来源：
Thrombosis Journal | / 13卷 / 1期
关键词：
Crohn's disease; Inflammatory bowel disease; Thrombosis; Ulcerative colitis;
D O I：
10.1186/s12959-015-0044-2
中图分类号：
学科分类号：
摘要：
Inflammatory bowel disease affects more than 2 million people in Europe, with almost 20% of patients being diagnosed in pediatric age. Patients with inflammatory bowel disease are at increased risk of thromboembolic complications which may affect patients' morbidity and mortality. The risk of the most common thromboembolic events, such as deep venous thrombosis and pulmonary embolism, are estimated to be three-fold increased compared to controls, but many other districts can be affected. Moreover, patients with ulcerative colitis and Crohn's disease experience thromboembolic events at a younger age compared to general population. Many factors have been investigated as determinants of the pro-thrombotic tendency such as acquired risk factors or genetic and immune abnormalities, but a unique cause has not been found. Many efforts have been focused on the study of abnormalities in the coagulation cascade, its natural inhibitors and the fibrinolytic system components and both quantitative and qualitative alterations have been demonstrated. Recently the role of platelets and microvascular endothelium has been reviewed, as the possible link between the inflammatory and hemostatic process. © Giannotta et al.
引用
收藏
相关论文
共 112 条
[31]  
Guedon C., Cam-Duchez V., Lalaude O., Menard J.F., Le- rebours E, Borg JY. Prothrombotic inherited abnormalities other than factor V Leiden mutation do not play a role in venous thrombosis in inflammatory bowel disease, Am J Gastroenterol, 96, pp. 1448-1454, (2001)
[32]  
Jackson L.M., O'Gorman P.J., O'Connell J., Cronin C.C., Cotter K.P., Shanahan F., Thrombosis in inflammatory bowel disease: Clinical setting, procoagulant profile and factor V Leiden, Q J Med, 90, pp. 183-188, (1997)
[33]  
Thompson N.P., Wakefield A.J., Pounder R.E., Inherited disorders of coagulation appear to protect against inflammatory bowel disease, Gastroenterology, 108, pp. 1011-1015, (1995)
[34]  
Danese S., Sans M., Fiocchi C., Inflammatory bowel disease: The role of environmental factors, Autoimmun Rev, 3, pp. 394-400, (2004)
[35]  
Koutroubakis I.E., Therapy insight: Vascular complications in patients with inflammatory bowel disease, Nat Clin Pract Gastroenterol Hepatol, 2, pp. 266-272, (2005)
[36]  
Magro F., Soares J.B., Fernandes D., Venous thrombosis and prothrombotic factors in inflammatory bowel disease, World J Gastroenterol, 20, 17, pp. 4857-4872, (2014)
[37]  
Oussalah A., Gueant J.L., Peyrin-Biroulet L., Meta-analysis: hyperhomocysteinaemia in inflammatory bowel diseases, Aliment Pharmacol Ther, 34, pp. 1173-1184, (2011)
[38]  
Vecchi M., Sacchi E., Saibeni S., Meucci G., Tagliabue L., Duca F., Et al., Inflammatory bowel diseases are not associated with major hereditary conditions predisposing to thrombosis, Dig Dis Sci, 45, pp. 1465-1469, (2000)
[39]  
Mahmood A., Needham J., Prosser J., Mainwaring J., Trebble T., Mahy G., Et al., Prevalence of hyperhomocysteinaemia, activated protein C resistance and prothrombin gene mutation in inflammatory bowel disease, Eur J Gastroenterol Hepatol, 17, pp. 739-744, (2005)
[40]  
Saibeni S., Vecchi M., Faioni E.M., Franchi F., Rondonotti E., Borsi G., Et al., Val34Leu factor XIII polymorphism in Italian patients with inflammatory bowel disease, Dig Liver Dis, 35, pp. 32-36, (2003)
12345678910