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2 Preeclampsia is considered to be an angiogenic disorder originating in very early pregnancy.3,4 Coordinated vascularization of the placenta is essential for a proper placental development, and it involves processes of maternal immune recognition and placental angiogenesis.5�C7 Impaired placental trophoblastic invasion is associated with hypoxia and a release of proinflammatory agents and subsequent endothelial damage.8,9 Although the pathophysiology of the disorder is incompletely understood, familial clustering is apparent. According to Cnattingius et al, genetic factors account this website for more than half of the incidence of preeclampsia, maternal genes contribute more than fetal genes, and a couple effect can occur because of the interaction between genes of the mother and father.10 At present three confirmed genetic susceptibility loci for preeclampsia have been described. These include PEE2 Quinapyramine on chromosome 2p25, PEE3 on chromosome 9p13,11 and PEE4, caused by a mutation in the STOX1 gene on chromosome 10q22.12 Pregnancy-associated plasma protein A (PAPPA) Placental and fetal growth is promoted by the presence in the placenta of PAPPA,13 which is a placental glycoprotein cleaving insulin-like growth factor binding protein-4 (IGFBP4) and positively regulating insulin-like growth factors (IGFs).14 Previously, altered placental activity of IGFs in very early pregnancy, mediated by PAPPA, has been shown to be associated with pregnancy loss, hypertension, preeclampsia, preterm delivery, fetal growth restriction, and fetal death.15�C18 Free human chorionic gonadotropin (fhCG��) Human chorionic MS-275 mw gonadotropin (CG) is a glycoprotein hormone produced by trophoblastic cells of the placenta beginning 10�C12 days after conception. First-trimester maintenance of the pregnancy requires the production of CG in the corpus luteum of the ovary, as the placenta takes over the production of progesterone. CG consists of a noncovalent dimer of alpha and beta subunits. The beta subunits define the endocrine function of the dimer.19 Maternal serum beta subunit is the current marker of first-trimester Down syndrome screening. Furthermore, hCG might be involved in the development of preeclampsia, since Zygmunt et al suggested that hCG promotes angiogenesis. The authors�� data indicated a novel function for hCG in uterine adaptation to early pregnancy, as well as in tumor development, underlining the importance of hCG as an unrecognized angiogenic factor.20 Alpha-fetoprotein (AFP) AFP, produced by the yolk sac and fetal liver, is a major plasma protein in the fetus.21 AFP is probably the fetal counterpart of serum albumin, based on the similarity in the physical properties of AFP and albumin and the fact that their presence is inversely related. During pregnancy, maternal serum AFP has long been recognized as a marker for congenital anomalies of the fetus, eg, congenital nephrosis and spina bifida.
