Neonatal platelet activation in preeclampsia

Preeclampsia is associated with an increased plate let activation; however, there are few studies concerning platelet activation of the newborn. The a im of our study was to compare platelet activation in newborns of preeclamp tic mothers to newborns of healthy mothers by using whole blood flow cytome try. Blood samples were obtained from 20 newborns (10 healthy controls, 10 cases of preeclampsia/HELLP [hemolysis, elevated liver enzymes, and low pla telet count] syndrome) during cesarean section. Antibodies against the foll owing antigens were used as markers for platelet activation: CD 41, CD62P, CD 63, and platelet-bound fibrinogen. In addition to the basal platelet act ivation, the ability of platelets to undergo activation as a result of in v itro incubation with a weak agonist (adenosine diphosphate) was evaluated. A significant difference between the groups concerning basal platelet activ ation could only be seen for platelet-bound fibrinogen; the control group s howed a higher extent of platelet activation (16.6 +/- 11.3 vs. 6.1 +/- 4.9 ; P = 0.03). Incubation with adenosine diphosphate in the control group res ulted in minor increases of platelet activation, which was significant only for platelet-bound fibrinogen (16.6 +/- 11.3 vs. 42.5 +/- 22.1; p = 0.02). However, the pre eclamptic group showed significantly increased levels of platelet activation for all used markers after in vitro activation (CD 41: 115.6 +/- 18.2 vs. 163.2 +/- 29.6; p = 0.002; CD62P: 2.4 +/- 0.4 vs. 3.9 +/ - 0.3; p < 0.001; CD 63: 2.7 +/- 0.5 vs. 3.7 +/- 0.6; p = 0.002; platelet-b ound fibrinogen: 6.1 +/- 4.9 vs. 55.1 +/- 9.1; p < 0.001). Preeclampsia or HELLP syndrome is therefore associated with an increased susceptibility to neonatal platelets, even against weak activators such as adenosine diphosph ate. Whether this results from peculiarities in the fetal vascular environm ent or maternal influences is yet uncertain.