title: Second- and third-trimester serum levels of placental proteins in preeclampsia and small-for-gestational age pregnancies.
abstract: BACKGROUND
  Poor placentation may perpetuate preeclampsia, but the presence of a major placental pathology has been questioned in cases of preeclampsia where the newborn has an appropriate birthweight for gestational age. On the other hand, poor placentation is also observed in the absence of preeclampsia, in pregnancies with small-for-gestational-age (SGA) fetuses. In late gestation, maternal serum levels of placental protein hormones are changed in both preeclampsia and SGA, but no longitudinal pre-onset studies are available for pregnancy-associated plasma protein A (PAPP-A), pregnancy-specific beta1-glycoprotein (SP1) or human placental lactogen (HPL).
  
  
  METHODS
  In a nested case-control study we compared maternal serum levels of PAPP-A, SP1, HPL and placenta growth factor (PLGF) at 17, 25 and 33 weeks in pregnancies developing preeclampsia without fetal growth restriction (n = 28), or characterized by a growth-retarded fetus (n = 25), with gestation-matched controls (n = 65). The proteins were quantified using microplate enzyme immunometric assays and the serum levels at 17, 25 and 33 weeks compared between the three groups by nonparametric statistical tests.
  
  
  RESULTS
  In pregnancies with subsequent preeclampsia PAPP-A, SP1, HPL and PLGF were reduced at 17 weeks of gestation whereas at 25 and 33 weeks only PLGF remained below the controls. In growth-restricted pregnancies PAPP-A, SP1 and HPL were reduced at 17 weeks, and only HPL continued to be strongly affected thereafter.
  
  
  CONCLUSIONS
  The reduced serum levels of the placental proteins PAPP-A, SP1 and HPL in the early second trimester (17 weeks) in pregnancies with subsequent preeclampsia or with fetal growth restriction involve an underlying role for the placenta in either pathology independent from the other.
authors.affiliation: University Department of Obstetrics and Gynaecology, Reproductive and Perinatal Medicine, Research Laboratory, University of Berne, Insespital KKL G3-825, Berne CH-3010, Switzerland. nick.bersinger@dkf2.unibe.ch
authors.forename: Nick A
authors.initials: NA
authors.lastname: Bersinger
authors.forename: Rønnaug A
authors.initials: RA
authors.lastname: Ødegård
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D005260:Female; D005317:Fetal Growth Retardation / Q000097:blood*; D006801:Humans; D000072483:Placenta Growth Factor; D010928:Placental Lactogen / Q000097:blood; D011225:Pre-Eclampsia / Q000097:blood*; D011247:Pregnancy; D011257:Pregnancy Proteins / Q000097:blood*; D011262:Pregnancy Trimester, Second / Q000097:blood; D011263:Pregnancy Trimester, Third / Q000097:blood; D011266:Pregnancy-Associated Plasma Protein-A / Q000378:metabolism; D011268:Pregnancy-Specific beta 1-Glycoproteins / Q000378:metabolism; D011446:Prospective Studies
chemical_list: D015415:Biomarkers; C000608036:PGF protein, human; D011257:Pregnancy Proteins; D011268:Pregnancy-Specific beta 1-Glycoproteins; D000072483:Placenta Growth Factor; D010928:Placental Lactogen; D011266:Pregnancy-Associated Plasma Protein-A