Abstract:

Preeclampsia is a hypertensive disease of pregnancy complicating 5-8% of all pregnancies. A growing body of evidence demonstrated that inflammation in microvasculature plays a major role in the pathogenesis of preeclampsia. Although circulating platelets are in rested state, when they are exposed to soluble mediators or microparticles in the inflamed vasculature as in preeclampsia, platelets are activated by engagement of the mediators on surface receptors. Upon activation, platelets degranulate some soluble and adhesion molecules. When soluble mediators released into the local microenvironment, they modulate the interactions between platelets, leukocytes and endothelial cells. Adhesion molecules expressed on the surface may initiate adherence between platelets, leukocytes and endothelial cells. Platelet-leukocyte aggregates promote the recruitment of neutrophils into the inflamed microvasculature. In addition to this, adherent platelets on endothelial cells induce production of inflammatory cytokines thus lead to amplification of inflammatory response. In this review, we mention platelet dysfunction in preeclamptic pregnancies and inflammatory role of platelets in the pathogenesis of preeclampsia.

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