Venous and arterial disease in inflammatory bowel disease

• Published in: Journal of gastroenterology and hepatology Vol. 28; no. 7; pp. 1095 - 1113
• Main Authors: Tan, Victoria P, Chung, Alvin, Yan, Bryan P, Gibson, Peter R
• Format: Journal Article
• Language: English
• Published: Australia Blackwell Publishing Ltd 01-07-2013
• Subjects: arteriosclerosis; atherosclerosis; Atherosclerosis - etiology; Atherosclerosis - prevention & control; Chronic Disease; deep venous thrombosis; Humans; Inflammatory Bowel Diseases - complications; Ischemia - etiology; Ischemia - prevention & control; MEDLINE; Mesenteric Arteries; Myocardial Ischemia - etiology; Myocardial Ischemia - prevention & control; prevention; Pulmonary Embolism - etiology; Pulmonary Embolism - prevention & control; pulmonary embolus; Risk; thromboembolism; Venous Thromboembolism - etiology; Venous Thromboembolism - prevention & control
• ISSN: 0815-9319; 1440-1746
• DOI: 10.1111/jgh.12260

Awareness is increasing that risk of venous thromboembolism and development of atherosclerosis is elevated in patients with some chronic inflammatory diseases. This review aimed to examine the risk of vascular disease in patients with inflammatory bowel disease (IBD) and to identify potential pathogenic mechanisms and therapeutic approaches. An extensive literature search was conducted using MEDLINE database, Cochrane Library and international conference s for studies pertaining to venous and arterial thromboembolism in adult IBD patients. There is a 1.1–3.6 fold risk of venothromboembolism in IBD, affecting 0.55–6.15% of patients. Risks are increased during a flare or with chronically active inflammation. Evidence is building that there may be a modestly increased risk of arterial disease overall, despite evidence that traditional risk factors may be reduced. Multiple pathogenic factors have been identified including endothelial dysfunction, inflammation‐mediated calcium deposition in the media of arteries, hyperhomocysteinemia, platelet activation, and altered coagulation and fibrinolysis. The key to active and preventive therapy is to effectively treat inflammation. Recommendations for prophylaxis of venothromboembolism have followed guidelines where they exist and have been extrapolated from studies of other at‐risk conditions, as have those for arterial disease, where screening for risk factors and actively treating abnormalities is encouraged. In conclusion, patients with IBD are at considerably increased risk of venothromboembolism and probably of arterial disease, in particular mesenteric ischemia and ischemic heart disease. Increased penetration of gaps between this knowledge and clinical therapeutic action to prevent thromboembolic events into IBD clinical practice is needed.