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Angiogenic dysfunction in molar pregnancy.

David Kanter¹, Marshall D Lindheimer, Eileen Wang

¹Department of Obstetrics and Gynecology, The Pritzker School of Medicine, University of Chicago, Chicago, IL, USA.

American Journal of Obstetrics and Gynecology

|November 20, 2009

Summary

This summary is machine-generated.

Molar pregnancies show higher levels of antiangiogenic proteins, specifically fms-like tyrosine kinase receptor 1 (Flt1) and its soluble form (sFlt1). This suggests overproduction contributes to early preeclampsia in molar pregnancies.

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Area of Science:

Obstetrics and Gynecology
Maternal-Fetal Medicine
Pathology

Background:

Molar pregnancy is linked to early-onset preeclampsia.
Antiangiogenic factors are implicated in preeclampsia pathogenesis.

Purpose of the Study:

To investigate whether molar placentas overproduce antiangiogenic proteins compared to normal placentas.
To test the hypothesis that increased antiangiogenic factors contribute to preeclampsia in molar pregnancy.

Main Methods:

Retrospective case-control study comparing 19 molar placentas with 16 normal controls.
Immunohistochemical analysis using antisera for fms-like tyrosine kinase receptor 1 (Flt1)/soluble Flt1 (sFlt1) and CD31.
Stain intensity was semiquantitatively graded.

Main Results:

Molar placentas exhibited significantly higher Flt1/sFlt1 staining intensity compared to normal controls (P < .0001).

Conclusions:

A significant difference in Flt1/sFlt1 immunostaining was observed between molar and normal placentas.
Findings support the hypothesis that trophoblast overproduction of antiangiogenic proteins, like Flt1/sFlt1, contributes to the preeclampsia phenotype in molar pregnancy.