Implications of von Willebrand Factor in Inflammatory Bowel Diseases: Beyond Bleeding and Thrombosis

• Published in: Inflammatory bowel diseases 2024-12, Vol.30 (12), p.2500-2508
• Main Authors: Lagrange, Jérémy, Ahmed, Muhammad Usman, Arnone, Djésia, Lacolley, Patrick, Regnault, Véronique, Peyrin-Biroulet, Laurent, Denis, Cécile V
• Format: Article
• Language: English
• Subjects: Gastrointestinal Hemorrhage - etiology; Hematology; Human health and pathology; Humans; Inflammatory bowel disease; Inflammatory Bowel Diseases - complications; Inflammatory Bowel Diseases - metabolism; Life Sciences; Risk Factors; Thrombosis - etiology; von Willebrand Factor - metabolism
• ISSN: 1078-0998; 1536-4844; 1536-4844
• DOI: 10.1093/ibd/izae142

Inflammatory bowel disease (IBD) displays an increased venous and arterial thrombotic risk despite the common occurrence of intestinal bleeding. While some of the mechanisms leading to these thrombotic complications have been studied, other specific changes in the hemostasis profile of IBD patients have been less explored. One such example relates to von Willebrand factor (VWF) whose plasma levels have been reported to be modulated in IBD. Von Willebrand factor is a plasma glycoprotein crucial for hemostatic functions via roles both in platelet function and coagulation. High plasma VWF is a known risk factor for venous thromboembolism. In addition to its canonical roles in hemostasis, VWF is known to be directly or indirectly involved in other vascular processes such as maintenance of endothelial barrier integrity or proliferation of vascular smooth muscle cells. The purpose of this review is to recapitulate and update the existing data about VWF biology in IBD and to highlight its role both in the existing procoagulant phenotype and in vascular alterations that may occur in IBD. Lay Summary Inflammatory bowel disease (IBD) displays an increased thrombotic risk. Von Willebrand factor (VWF) is increased in IBD and is a risk factor for venous thromboembolism. This review purposes to recapitulate and update the existing data about VWF biology in IBD.