@article {6020,
	title = {Maternal serum leptin concentration during the second trimester of pregnancy: Association with fetal chromosomal abnormalities},
	journal = {Prenatal Diagnosis},
	volume = {22},
	year = {2002},
	month = {2002///},
	pages = {221 - 225},
	abstract = {Recent studies suggest that leptin, the product of the obese gene, is produced by the placenta during pregnancy. The present study addressed the question whether second trimester maternal serum leptin could be altered by fetal Down syndrome or Edwards syndrome. Maternal serum leptin concentrations were measured in 18 pregnancies complicated with Down syndrome, six pregnancies complicated with Edwards syndrome and 183 uncomplicated pregnancies during the second trimester of pregnancy. The present results demonstrate that leptin concentrations in uncomplicated pregnancies slightly decrease from the 16th week of pregnancy, reaching a minimum of 18.8 ng/ml around the 20th week, and then rapidly increase to 28.2 ng/ml by the 24th week. Leptin correlation with maternal body weight decreases from r=0.695 at 16-17 week of gestation to r=0.544 at < 22 weeks of gestation. There was no significant difference between the mean MoMs of Down syndrome- (0.926) or Edwards syndrome- (0.960) affected pregnancies and normal pregnancies (1.002). A weak correlation (r=0.18, p<0.02) was observed between corrected leptin MoMs and human chorionic gonadotrophin (hCG) MoMs in normal pregnancies. It is assumed that around the 20th week of pregnancy placental leptin production is activated or at least is accelerated and it is added to the amount of leptin produced by maternal adipose tissue. Fetal Down syndrome or Edwards syndrome does not seem to alter maternal leptin concentration and therefore leptin cannot be used as a marker for these chromosomal abnormalities in the early second trimester of pregnancy. Copyright {\textcopyright} 2002 John Wiley \& Sons, Ltd.},
	keywords = {Down syndrome, Edwards syndrome, Leptin, Pregnancy, Second trimester},
	author = {Rizos, D. and Hassiakos, D. and Grigori-Kostaraki, P. and Sarandakou, A. and Botsis, D. and Salamalekis, E.}
}
