Human placental growth hormone (PGH), encoded by the growth hormone (GH) variant gene on chromosome 17, is expressed in the syncytiotrophoblast and extravillous cytotrophoblast layers of the human placenta. Its maternal serum levels increase throughout pregnancy, and gradually replaces the pulsatile secreted pituitary GH. PGH is also detectable in cord blood and in the amniotic fluid. This placental-origin hormone stimulates glyconeogenesis, lipolysis and anabolism in maternal organs, and influences fetal growth, placental development and maternal adaptation to pregnancy. The majority of these actions are performed indirectly by regulating maternal insulin-like growth factor-I levels, while the extravillous trophoblast involvement indicates a direct effect on placental development, as it stimulates trophoblast invasiveness and function via a potential combination of autocrine and paracrine mechanisms. The current review focuses on the role of PGH in fetal growth. In addition, the association of PGH alterations in maternal circulation and placental expression in pregnancy complications associated with abnormal fetal growth is briefly reviewed.
A prior Cesaria section (C-section) is an important risk factor that leads to endometrial damage and abnormal implantation of the placenta. Our retrospective study aims to correlate the frequency of placenta previa to previous C-sections, to determine the effect of male gender in this condition and to evaluate further the maternal outcome. Seventy-six cases with placenta previa were selected out of 5200 live births. Diagnosis was confirmed by ultrasound and in the operating theater. In the 76 women examined, we found 50 cases with a history of a previous C-section (66.0%) and 49 male offspring (65.0%) (p <0.001), with a mean birth weight of 2635 ± 740 g. Of all these patients, six (8.0%) cases developed placenta percreta, seven (9.0%) were transferred to the intensive care unit (ICU), 14 (18.0%) women needed blood transfusion and eight (11.0%) underwent hysterectomy. The results of our series show a strong correlation of placenta previa to a history of previous C-sections and a predominance of male fetuses. Early recognition and proper monitoring could minimize the possibility of a poor outcome.
Preeclampsia (PE) is a major complication of pregnancy with an incidence rate of 2-8% and is a leading cause of maternal mortality and morbidity. The various consequences of severe preeclampsia for the fetus, neonate and child include intrauterine growth retardation (IUGR), fetal hypoxia, oligohydramnios, intrauterine fetal demise, increased perinatal mortality and morbidity, neurodevelopmental disorders and even irreversible brain damage (cerebral palsy). A number of studies have demonstrated that differences in maternal serum concentrations of angiogenic factors between preeclampsia and normotensive pregnancies can be used as biomarkers, either alone or in combination with other markers, to predict the development of PE. The presence in the maternal circulation of two proteins of placental origin, placental growth factor (PlGF) and soluble fms-like tyrosine kinase 1 (sFlt-1), has been shown to be of clinical value, as the sFlt-1/PlGF ratio appears to be the optimal predictive tool for the development of PE. The measurement of their concentration in maternal serum in screening models, serves as predictive marker for the development of PE or IUGR later in gestation. However, further research is required to improve its clinical applicability and provide guidelines for its use worldwide to achieve more consistent clinical management of women with PE.
Neurofibromatosis type 1 (NF-1) is a condition which has markedly variable clinical expressions. During pregnancy the manifestations of the disorder are exacerbated, and as a result, mild to severe maternal and fetal complications may appear. A case of neurofibromatosis affected by pregnancy is presented. The mother presented with high arterial blood pressure, renal insufficiency, and visual impairment. At the same time the baby was born with growth restriction and cerebellar haemorrhage. Altogether, NF1 is associated with increased maternal and fetal morbidity in pregnancy but not with increased maternal mortality.
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