Hum. Reprod. Advance Access originally published online on May 5, 2005
Human Reproduction 2005 20(8):2334-2339; doi:10.1093/humrep/dei039
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Vasculogenesis in complete and partial hydatidiform mole pregnancies studied with CD34 immunohistochemistry
1 Department of Obstetrics and Gynaecology, Spaarne Ziekenhuis Haarlem, PO Box 1644, 2003 BR Haarlem and 2 Department of Obstetrics and Gynaecology, Academic Medical Center, University of Amsterdam, PO Box 22700, 1100 DE Amsterdam, The Netherlands
3 To whom correspondence should be addressed. Email: b.a.lisman{at}amc.uva.nl
BACKGROUND: Defective chorionic villous vascularization is present in pregnancies complicated by absent or abnormal embryonic development. The aim of this study was to investigate the embryonic and/or maternal genomic influence on vasculogenesis in diploid complete hydatidiform mole (CHM) and in triploid partial hydatidiform mole (PHM) in comparison with normal development. METHODS: Mean villous stromal area and functional vascular area, vessels with a lumen and haemangiogenetic cords, peripherally or centrally located were measured and counted in chorionic villi of 12 CHM, 12 normal pregnancies (termination of pregnancy, TOP) and 15 PHM of which nine were without an embryo (PHME) and six were with an embryo (PHM + E), using quantitative CD34 immunohistochemistry. RESULTS: TOP showed significantly more vessels per chorionic villus, centrally and peripherally located (median, range), than CHM, PHME and PHM + E (4.0, 09 versus 0.0, 011, 0.0, 018 and 1.0, 021). CHM showed significantly more centrally located cords than PHME, PHM + E and TOP (1.5, 022 versus 1.0, 015, 0.5, 08 and 1.0, 02). CONCLUSIONS: Initiation of chorionic villous vasculogenesis is independent of the maternal genome (CHM). The development of an embryo, however, is obligatory for the modulation of normal vascularization resulting in a well developed vasculosyncytial membrane.
Key words: CD34/chorionic villous/complete hydatidiform mole/partial hydatidiform mole/vasculogenesis/triploidy
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