Angiogenic dysfunction in molar pregnancy.


OBJECTIVE Molar pregnancy is associated with very early-onset preeclampsia. Since excessive circulating antiangiogenic factors may play a pathogenic role in preeclampsia, we hypothesized that molar placentas produce more antiangiogenic proteins than normal placentas. STUDY DESIGN This retrospective case-control study used a semiquantitative immunohistochemical technique to compare histologic sections of molar placentas to normal controls. Tissue slides were treated with 2 antisera: one recognized the antiangiogenic markers fms-like tyrosine kinase receptor 1 (Flt1) and its soluble form (sFlt1), while the other recognized vascular endothelial marker CD31. Stain intensity was graded from 1+ (strong focal staining) to 4+ (91-100% staining). RESULTS Molar placentas (n = 19) showed significantly more staining than controls (n = 16) for Flt/sFlt1 (P < .0001). CONCLUSION There was a significant difference in Flt1/sFlt1 immunostaining intensity when molar placentas were compared to controls. This supports a hypothesis that the phenotype of preeclampsia in molar pregnancy may result from trophoblasts overproducing at least 1 antiangiogenic protein.

DOI: 10.1016/j.ajog.2009.09.005


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@article{Kanter2010AngiogenicDI, title={Angiogenic dysfunction in molar pregnancy.}, author={David Kanter and Marshall D. Lindheimer and Eileen Y Wang and Romana G Borromeo and Elizabeth Bousfield and Sushama Karumanchi and Isaac E Stillman}, journal={American journal of obstetrics and gynecology}, year={2010}, volume={202 2}, pages={184.e1-5} }