Figure 4.
Figure 4. Proposed mechanisms of thrombosis in IBD. IBD predisposes to thrombosis by inducing episodes of acute and chronic intestinal inflammation, leading to a systemic prothrombotic state characterized by upregulation of tissue factor, an elevated platelet count, and impaired fibrinolysis as a result of decreased expression of tissue plasminogen activator (t-PA) and decreased expression of plasminogen activator inhibitor-1 (PAI-1). Clinical risk factors, such as dehydration, malnutrition, and placement of central venous catheters also contribute to thrombotic risk in patients with IBD.

Proposed mechanisms of thrombosis in IBD. IBD predisposes to thrombosis by inducing episodes of acute and chronic intestinal inflammation, leading to a systemic prothrombotic state characterized by upregulation of tissue factor, an elevated platelet count, and impaired fibrinolysis as a result of decreased expression of tissue plasminogen activator (t-PA) and decreased expression of plasminogen activator inhibitor-1 (PAI-1). Clinical risk factors, such as dehydration, malnutrition, and placement of central venous catheters also contribute to thrombotic risk in patients with IBD.

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