Published online Mar 28, 2014. doi: 10.3748/wjg.v20.i12.3180
Revised: December 10, 2013
Accepted: January 19, 2014
Published online: March 28, 2014
There is evidence that inflammatory bowel diseases (IBD) combine both inflammation and coagulation in their pathogenesis and clinical manifestations. Although platelets (PLT) are well known for their role in hemostasis, there are a rising number of studies supporting their considerable role as inflammatory amplifiers in chronic inflammatory conditions. IBD are associated with several alterations of PLT, including number, shape, and function, and these abnormalities are mainly attributed to the highly activated state of circulating PLT in IBD patients. When PLT activate, they increase in size, release a great variety of bio-active inflammatory and procoagulant molecules/particles, and express a variety of inflammatory receptors. These inflammatory products may represent a part of the missing link between coagulation and inflammation, and can be considered as possible IBD pathogenesis instigators. In clinical practice, thrombocytosis is associated both with disease activity and iron deficiency anemia. Controlling inflammation and iron replacement in anemic patients usually leads to a normalization of PLT count. The aim of this review is to update the role of PLT in IBD and present recent data revealing the possible therapeutic implications of anti-PLT agents in future IBD remedies.
Core tip: Many platelets (PLT) changes have been described in IBD, including morphological alterations (mean PLT volume, PLT distribution width, plateletcrit, and augmented granular content), count increase, microparticles release, over-excretion of granular content, and increased formation of PLT-PLT and PLT-leukocyte aggregates, which are all linked to PLT activation induced by inflammatory agonists. In this review article, we present the multipotent role of PLT in human biological paths and emphasize on how PLT participate in the chronic intestinal inflammation process in IBD.