Increased platelet activation and thrombo-inflammation in early and late-onset preeclampsia.

Background: Preeclampsia is a vascular complication of pregnancy with limited therapeutic options. It is associated with hypertension and an increase in angiogenic factor soluble fms-like tyrosine kinase-1 (sFlt-1)/placental growth factor. Based on its onset, preclampsia can be categorized into early-onset (E-PE) or late-onset (L-PE) preeclampsia. Thrombo-inflammation, hallmarked by maternal platelet activation and sterile inflammation, is associated with pathophysiology of preeclampsia. However, whether these mechanisms are differentially regulated in E-PE vs L-PE remains unknown. Objectives: We aim to study the role of maternal platelet activation, inflammation and endothelial dysfunction in E-PE vs L-PE. Methods: Flow-cytometry analysis of platelet activation (P-selectin and active αIIbβ3) was conducted in whole blood from pregnant women with E-PE, L-PE and gestational age-matched patients. Plasma was evaluated for interleukin (IL)-1β and soluble vascular cell adhesion molecule 1 (sVCAM-1). Results: An increase in P-selectin and active αIIbβ3 expressing platelets in both forms of preeclampsia ( Conclusions: These findings identify that thrombo-inflammation is regulated in L-PE and E-PE through likely disjunct mechanisms supporting a role of maternal factors (eg, maternal platelet activation) involved in L-PE. Further studies with a larger cohort of patients are required to fully elucidate the mechanistic relevance of these findings.