Extract

To the Editor:

Preeclampsia is a leading cause of maternal and fetal morbidity and mortality worldwide. It occurs in two phases: abnormal implantation of the placenta leads to impaired placental blood flow, which in turn induces the release of a critical placental substance into the maternal circulation (1). Clinical onset usually occurs in the third trimester of pregnancy, long after initiation of the underlying process.

Recently, Maynard et al. (2) compared the gene expression profile in placental tissue from women with and without preeclampsia and identified soluble Flt1 (sFlt1), a vascular endothelial growth factor receptor, as a molecule of particular pathophysiologic interest. It is now suspected that trophoblastic injury markedly enhances placental sFlt1 production, antagonizing the endothelial protective role of vascular endothelial growth factor and/or placental growth factor and eventually leading to clinical preeclampsia (2)(3). A recent study pointed out that, compared with women with a retrospective diagnosis of normal pregnancy (i.e., without hypertension), preeclamptic women had increased serum sFlt1 several weeks before the onset of clinical disease, suggesting that this protein might be used as a predictive marker for preeclampsia (4).

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