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Review
. 2011 Feb 7;17(5):594-608.
doi: 10.3748/wjg.v17.i5.594.

Haemostatic system in inflammatory bowel diseases: new players in gut inflammation

Franco Scaldaferri  1 , Stefano Lancellotti, Marco Pizzoferrato, Raimondo De Cristofaro
Affiliations
Review

Haemostatic system in inflammatory bowel diseases: new players in gut inflammation

Franco Scaldaferri et al. World J Gastroenterol. .

Abstract

Inflammation and coagulation constantly influence each other and are constantly in balance. Emerging evidence supports this statement in acute inflammatory diseases, such as sepsis, but it also seems to be very important in chronic inflammatory settings, such as inflammatory bowel disease (IBD). Patients with Crohn's disease and ulcerative colitis have an increased risk of thromboembolic events, and several abnormalities concerning coagulation components occur in the endothelial cells of intestinal vessels, where most severe inflammatory abnormalities occur. The aims of this review are to update and classify the type of coagulation system abnormalities in IBD, and analyze the strict and delicate balance between coagulation and inflammation at the mucosal level. Recent studies on possible therapeutic applications arising from investigations on coagulation abnormalities associated with IBD pathogenesis will also be briefly presented and critically reviewed.

Keywords: Activated protein C; Coagulation; Crohn’s disease; Inflammation; Inflammatory bowel disease; Platelets; Ulcerative colitis.

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Figures

Figure 1
Figure 1
Models of protease-activated receptor-1 cleavage and activation by either activated protein C or thrombin when endothelial protein C receptor is occupied by its ligand protein C. A: The unoccupied endothelial protein C receptor (EPCR) is associated with caveolin-1 (Cav-1) within lipid rafts of endothelial cells. Upon thrombin cleavage of protease-activated receptor (PAR)-1, a pro-inflammatory signal is generated through G12/13 and Gq under these conditions; B: The occupancy of EPCR by protein C (PC) results in dissociation of EPCR from Cav-1. This process is linked with the coupling of PAR-1 to Gi. Thrombin cleavage of PAR-1 initiates an antiinflammatory response under these conditions; C: The same as (B) except that the EPCR and PAR-1 dependent protective signaling response is mediated by activated protein C (APC) (adapted from[159]).
See this image and copyright information in PMC

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