title: High early uterine vascular resistance values increase the risk of adverse pregnancy outcome independently from placental VEGF and VEGFR1 reactivities.
abstract: OBJECTIVE
  From data in the literature, we hypothesized that high vascular resistance values in the uterine arteries at the end of the first trimester would increase adverse pregnancy outcomes and therefore might be accompanied by changes in VEGF/VEGFR1 immunoreactivities.
  
  
  METHODS
  In our university hospital 82 women (Study I n=62 and Study II n=20) were divided into two groups according to their uterine vascular resistance values. Uterine vascular resistance values were measured in the 10-13th weeks of gestation by color-Doppler ultrasonography. Women were divided into low and high vascular resistance groups. In the prospective follow-up study (Study I) the data of the pregnancy outcome were recorded. In cross-sectional study (Study II), VEGF and VEGFR1 immunoreactivities were measured on the tissue samples from women who underwent termination of pregnancy.
  
  
  RESULTS
  In the high vascular resistance group (PI>2.3), the probability of adverse pregnancy outcome was significantly higher (40.0% vs. 12.8%). No differences in VEGF and VEGFR1 immunoreactivities were observed between groups. In both groups, intense VEGF immunoreactivity was observed in the maternal glandular epithelium and in the decidual cells. Weak reactivity was observed in the villous trophoblast. VEGFR1 immunoreactivity was intense in all regions.
  
  
  CONCLUSIONS
  Our data suggest that high vascular resistance values in the first trimester are independent from VEGF/VEGFR1 immunoreactivities and markedly increase the probability of adverse pregnancy outcomes. This may be used for early screening of pregnant women in the first trimester.
authors.affiliation: 2nd Department of Obstetrics and Gynecology, Semmelweis University, 78a Ulloi street, Budapest H1082, Hungary. valent@noi2.sote.hu
authors.forename: Sándor
authors.initials: S
authors.lastname: Valent
authors.forename: Júlia
authors.initials: J
authors.lastname: Németh
authors.forename: Levente
authors.initials: L
authors.lastname: Sára
authors.forename: János
authors.initials: J
authors.lastname: Gidai
authors.forename: Péter
authors.initials: P
authors.lastname: Tóth
authors.forename: Zsuzsanna
authors.initials: Z
authors.lastname: Schaff
authors.forename: Ferenc
authors.initials: F
authors.lastname: Paulin
authors.forename: Attila
authors.initials: A
authors.lastname: Pajor
mesh_terms: D000328:Adult; D003430:Cross-Sectional Studies; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D010920:Placenta / Q000378:metabolism*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000209:etiology*; D011261:Pregnancy Trimester, First / Q000502:physiology; D011446:Prospective Studies; D055988:Uterine Artery / Q000502:physiology*; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000378:metabolism*; D014655:Vascular Resistance
chemical_list: C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D040281:Vascular Endothelial Growth Factor Receptor-1