Thrombosis and inflammatory bowel disease: A call for improved awareness and prevention

Abstract

Thrombotic complications in patients with inflammatory bowel disease (IBD) are common and require improved awareness and prevention. In this review the interface between IBD and thrombosis is discussed, with emphasis on risk assessment and data to aid clinical decision making. Thromboembolic complications are 3-fold more likely in IBD patients than controls and the relative risk exceeds 15 during disease flares. Improved assessment of thrombosis risk for an individual patient includes thorough personal and family history and awareness of prothrombotic medications and lifestyle choices. Patients with the highest risk of thrombosis are those with active colonic disease, personal or strong family history of thrombosis, and those with significant acquired risk factors. Combined risk factors or hospitalization should prompt mechanical thromboprophylaxis. Indications for prophylactic anticoagulation are not defined currently by clinical studies, especially in pediatric patients, although some groups now advocate prophylactic anticoagulation for all hospitalized IBD patients and even some outpatients with disease flares. Thrombosis management requires a multidisciplinary therapeutic approach to balance anticoagulation and bleeding risk. While bleeding may occur with anticoagulation in IBD, data and experience indicate that therapeutic heparin is safe and bleeding manifestations can be managed supportively in most patients. Until prospective trials of prophylactic anticoagulation are published, management of thrombotic risk and prophylaxis in IBD will remain a clinical challenge.

Prognosis After First-Time Myocardial Infarction in Patients With Inflammatory Bowel Disease According to Disease Activity

“…For example, local target organ (artery or bowel) infiltration and activation of cells from both the innate and the adaptive immune response is associated with both conditions as are elevated circulating levels of high-sensitive C-reactive protein, platelet activation, and atherogenic lipid abnormalities. 4,8,27 Our finding of an increased all-cause mortality in patients with post-MI and IBD parallels recent observations of a moderately increased all-cause mortality and cardiovascular mortality among Danish patients with IBD when compared with a random sample of the Danish population. 28 However, we here considerably expand this observation by demonstrating that the increased mortality in patients with MI and IBD was present exclusively during active disease stages, whereas quiescent IBD did not carry any increased mortality risk.…”

“…[3][4][5][6] IBD is associated with increased risk of venous thrombosis, and the risk is particularly high at flares, consistent with previous findings of a prothrombotic state during active inflammation. [7][8][9] Recent studies also indicate an increased risk of atherothrombotic events in patients with IBD, and we have demonstrated this risk to be present solely during active IBD stages and not in quiescent IBD, which suggests a role of shared pathophysiological inflammatory mechanisms. [10][11][12][13] However, the focus of existing studies has been on the risk of new onset cardiovascular disease in patients with IBD and not on the significance of coexistent IBD on the prognosis after such events.…”

Inflammatory Bowel Disease Is Associated With an Increased Risk of Hospitalization for Heart Failure

“…[4][5][6][7][8][9] Research has provided evidence that inflammatory activation plays a role in the development and progression of HF, and the prothrombotic state associated with inflammation has been suggested as a causal link between IBD and atherothrombosis. [10][11][12][13][14][15][16][17] In addition, intestinal inflammation in IBD, especially during flares, may contribute to the development of HF by translocation of bacterial lipopolysaccharides from the bowel to the circulatory system that elicit production of proinflammatory mediators and tissue injury including myocardial damage. 10,11 However, whether IBD is associated with an increased risk of HF has not been explored previously.…”

Acute renal artery occlusion following infliximab infusion

“…Immobilization of in-patients, surgery, indwelling catheters, and hyperhomocysteinemia associated with folate or vitamin B12 deficiencies or bleeding disorders may be part of the explanation in some patients. However, systemic inflammation is probably the main culprit through activation of the coagulation cascade with increased thrombin and platelet activation [8] . The formation of immune complex might also have contributed to the occurrence of TEE.…”