Abstract

Preeclampsia is a leading cause of maternal and fetal/neonatal mortality and morbidity worldwide. Although the etiology of preeclampsia (PE) is still unclear, recent studies suggest that its major phenotypes, high blood pressure and proteinuria, are due in part to the disturbed angiogenic process. This study included the following groups: (1) women with normal pregnancies (n=150), (2) patients with PE (n=88), and (3) patients who delivered small growth for date (SGA) neonate (n=50). Maternal serum concentrations of VEGF, Angi-1, and sTie-2 were measured by a sensitive immunoassay. Non-parametric statistics were used for analysis. The median maternal serum concentration of sVEGF and sAngi-1 was lower in normal pregnant women as compared to that in PE and SGA and the differences were statistically significant (P<0.01). In contrast, there is a significant reduction in sTie-2 levels in PE and SGA groups as compared to that in normal pregnancy group (P<0.01). Serum VEGF and Angi-1 were significantly higher in the late onset PE subgroup as compared to that in the early onset PE (P<0.01), but sTie-2 was not significantly different in the 2 subgroups (P>0.05). Serum VEGF, sAngi-1, and sTie-2 were significantly higher and Tie-2 was significantly lower in the severe PE subgroup as compared to that of the milder PE subgroup (P<0.01 for all). Patients with PE and those with SGA fetuses have lower median serum concentrations of sTie-2 and higher sVEGF and sAngi-1 than women with normal pregnancies. These findings lend support to the hypothesis that circulating angiogenic proteins may have an important biologic role in PE.

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