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Identifier 000347789
Title Η αυξητική ορμόνη του πλακούντα στηγν ανίχνευση χρωμοσωματικών και συγγενών ανωμαλιών. Η προγνωστική της αξία στην ενδομήτρια υπολειπόμενη ανάπτυξη και στην γέννηση νεογνών χαμηλού βάρους
Author Παπαδοπούλου, Ελευθερία
Thesis advisor Καλμαντή, Μαρία
Reviewer Κουμαντάκης, Ευγένιος
Καρκαβίτσας, Νικόλαος
Abstract During pregnancy, the human placenta synthesizes human placental growth hormone (hPGH), differing in only 13 amino acids from pituitary growth hormone. This hormone is the product of GH-V gene, a member of the growth hormone gene-family, which is located on the long arm of the chromosome 17. hPGH is produced and secreted by the syncytiotrophoblast, and during pregnancy progressively replaces pituitary GH in maternal serum. Its concentrations increase in maternal serum throughout pregnancy from 5-7 weeks’ gestation until term. hPGH is not detectable in the fetal circulation, but it is believed to have an impact on the physiological adjustment of the maternal organism to gestation as well as on fetal growth. hPGH has pure somatotrophic activity and strongly stimulates gluconeogenesis, lipolysis, positive metabolism, and increases nutrient availability for the fetoplacental unit. hPGH appears to regulate the maternal levels of IGF-I, which is an important determinant of glucose and amino acids transport to the fetus. The presence of hPGH receptors in extravillous trophoblast suggests that the physiological role of this hormone also includes a direct influence upon placental development and function via an autocrine and/or paracrine mechanism. Thus, this hormone participates in the control mechanisms of fetal development, and correlates with fetal and neonatal weight. In this study we evaluated the relationship between maternal serum levels of hPGH with the fetal Down syndrome and the intrauterine growth retardation related to preeclampsia at gestational midtrimester. We analyzed samples of serum retrospectively from 21 women with Down syndrome pregnancies detected at gestational midtrimester. The samples were obtained at 16-23 weeks’ gestation during amniocentesis for fetal karyotyping. 62 serum samples were used as controls, which were obtained at 16-23 weeks’ gestation from women with singleton, uncomplicated pregnancies, who gave birth to healthy neonates with appropriate for gestational age birth weight. hPGH levels were measured by a solid phase immunoradiometric assay using two different epitopes. The median hPGH values in the serum of the Down syndrome-affected pregnancies were significantly higher (P<0.05) than those of the normal pregnancies at 16-23 weeks’ gestation: median (5th to 95th percentiles) value in the serum was 9.4 (1.49-39.03) ng/ml vs. 4.7 (0.53-7.88) ng/ml. It could be hypothesized that the enhanced hPGH production may be due to an attempt of the placenta to counteract the incipient fetal growth restriction, a constant finding in the majority of Down syndrome affected pregnancies. Further investigation is needed to examine if maternal serum hPGH could be used as an additional marker in prenatal screening of Down syndrome at gestational midtrimester. Το evaluate the alterations of hPGH levels in pregnancies complicated with fetal intrauterine growth retardation related to preeclampsia, we analyzed samples in pairs of serum and amniotic fluid retrospectively from 25 women who manifested these conditions in the late second or the third trimester of gestation. The samples were obtained at 16-22 weeks’ gestation during amniocentesis for fetal karyotyping. At this time, there was no clinical or sonographic evidence of preeclampsia or IUGR, respectively. 62 serum samples were used as controls, which were obtained at 16-22 weeks’ gestation from women with singleton, uncomplicated pregnancies, with normal outcome, and appropriate for gestational age neonatal birth weight. 47 amniotic fluid samples were also used as controls, which were obtained at 16-22 weeks’ gestation from the women that were included in the control group who underwent an amniocentesis. hPGH levels were measured by a solid phase immunoradiometric assay. The mean hPGH values in the serum and the amniotic fluid of the IUGR related to preeclampsia affected pregnancies were significantly higher (P<0.05) than those of the normal pregnancies at 16-22 weeks’ gestation: mean±SD in the serum was 13.16±10.52ng/ml vs. 4.39±2.23ng/ml; mean±SD in the amniotic fluid 2.49±1.6ng/ml vs. 0.82±0.67ng/ml. In the preclinical, latent stages of preeclampsia, the affected pregnancies may be accompanied by an excessive production of hPGH as a compensative reaction to fetal growth retardation by stimulating the placental growth hormone receptors. These effects may be exerted by an autocrine and paracrine route of action, since hPGH has a high affinity to surface receptors on syncytiotrophocytes. This hormone, in turn, enables the placenta to supply more nutrients to the developing fetus through stimulations of IGF-I synthesis in placental tissue and maternal hepatocytes. IGF-I possesses somatogenic, mitogenic, and metabolic activities in both the maternal and the fetal circulation, which influence fetal growth. The positive effects by the elevated hPGH levels are not, however, prolonged, and the fetus begins to display growth disturbance, usually following 22-24 weeks’ gestation. The unavoidable progress of the disease leads to placental insufficiency that probably causes decreased production of hPGH, which, in turn, contributes to further fetal growth restriction. Large-scale prospective studies should be conducted to validate our findings. The confirmation of our results would support the diagnostic potential of hPGH, as the evaluation of its levels at 16-22 weeks’ gestation could be used as a predictive or diagnostic marker for increased risk of developing IUGR associated with preeclampsia. Moreover, it would be of special interest to investigate the range of the IGF-I levels in parallel with the change of hPGH production, throughout the disease transition from a latent preclinical stage to the clinically manifested preeclampsia.
Physical description 131 σ. : πιν. ; 30 εκ.
Language Greek
Subject Down Syndrome
Placenta
Placental Hormones
Pre-Eclampsia
Πλακουντικές ορμόνες
Προεκλαμψία
Issue date 2007-07-26
Collection   School/Department--School of Medicine--Department of Medicine--Doctoral theses
  Type of Work--Doctoral theses
Permanent Link https://elocus.lib.uoc.gr//dlib/c/5/4/metadata-dlib-98f8a9a7dbe94f0866270e31d4c373eb_1247729362.tkl Bookmark and Share
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