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Physiology of Pregnancy
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The placenta acts as an endocrine organ as it produces both peptide (human chorionic gonadotrophin [HCG] and human placental lactogen [HPL]) and steroid hormones (oestrogen and progesterone). HCG is produced by the trophoblast cells 8–9 days after fertilization, and it maintains corpus luteal oestrogen and progesterone production during the first trimester to maintain pregnancy until the placenta takes over. The plasma concentration of HCG peaks at 10–12 weeks of pregnancy and then declines to term. The plasma concentration of HPL, produced by the placenta, rises throughout pregnancy and peaks near term (Figure 72.1). The actions of HPL are to mobilize free fatty acids (FFAs), antagonize the actions of insulin and retain potassium and nitrogen.
Regulation of Reproduction by Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
The maternal endocrine system undergoes significant changes during pregnancy. The profile of several important hormones in the maternal plasma during gestation is shown in Figure 10.16A. Of total plasma estrogens, the most abundant is estriol, and the least abundant is estradiol. Human placental lactogen (hPL), also called human chorionic somatomammotropin (hCS), is produced by the syncytiotrophoblast and has both growth hormone (GH)-like and PRL-like activities [86]. hCG, made by the trophoblast, maintains progesterone production by the corpus luteum during the first trimester, until the placenta takes over progesterone production by 10 weeks of gestation and its levels are then reduced. The detection of hCG in the woman’s urine is used as an early test for pregnancy.
Human Chorionic Gonadotropin Supplementation in Recurrent Pregnancy Loss
Published in Howard J.A. Carp, Recurrent Pregnancy Loss, 2020
Carlo Ticconi, Adalgisa Pietropolli, C.V. Rao
hCG is a heterodimeric glycoprotein, composed of noncovalently linked α and β subunits. The α subunit is common for TSH, FSH, hCG, and luteinizing hormone (LH) and encoded by a single gene (CGA), located to chromosome 6qq2.1–23. The β subunit of hCG is encoded by a cluster of six different non-allelic genes, CGB1, CGB2, CGB3, CGB5, CGB7, and CGB8, located on chromosome 19q13.32 [10–11]. The β subunit of hCG shares 82% homology with that of LH and binds to the same plasma membrane LH/hCG receptors, which is a seven-transmembrane G-coupled protein [12–13]. Even though LH and hCG share common receptors, there is clear evidence that some of the downstream intracellular pathways activated by them are different [10,14–15]. While LH is present in all species, hCG is only found in primates. hCG seems to have developed relatively recently in evolution, arising from LH. hCG has become responsible for multiple roles in the establishment, development, and maintenance of human pregnancy [10,15]. The major intracellular signaling pathways activated by hCG binding to the LH/hCG receptors, together with their known cellular effects, are depicted in Figure 22.1.
A stroll through the present and future of testicular germ cell tumour biomarkers
Published in Expert Review of Molecular Diagnostics, 2023
Nuno Tiago Tavares, Rui Henrique, Aditya Bagrodia, Carmen Jerónimo, João Lobo
On the other hand, HCG is a 38 kDa glycoprotein hormone that has five different isoforms and has been routinely used for a long time in pregnancy tests. TGCTs may cause serum elevations of the whole HCG or the β-unit of this hormone, β-HCG [31]. This hormone is produced by the syncytiotrophoblast cells and plays several roles in pregnancy, promoting development of the placenta and differentiation of fetal organs [32]. The half-life of β-HCG in serum ranges from 18 to 36 h, much lower than that of AFP. Like the former, its production is dependent on TGCT histologic type, being markedly elevated in the presence of trophoblastic elements, including scattered syncytiotrophoblast cells or CHC foci. For SE, this marker is elevated in about 18–31% of all patients, specifically 10–20% of clinical stage I patients and 30–50% of advanced disease [22,23,33]. For NST, it is elevated in about 53% of patients and in more than 95% CHC cases [22,23]. β-HCG may also be elevated in other types of cancers and due to heterophilic antibodies, a fact that lowers its specificity for GCTs, which is about 35–37% [25,26,34,35].
Evaluating thyroid function in pregnant women
Published in Critical Reviews in Clinical Laboratory Sciences, 2022
K. Aaron Geno, Robert D. Nerenz
During the first trimester, plasma hCG concentrations increase sharply, reaching a peak between 8 and 12 weeks’ gestation. As hCG and TSH are both members of the glycoprotein hormone family that shares a common alpha subunit and whose beta subunits demonstrate substantial homology, hCG can bind to the TSH receptor with modest affinity [145]. Some have postulated that hCG cross-reactivity with the TSH receptor can be viewed as an intentional backup plan to ensure the developing fetus receives adequate thyroid hormone during a critically important period of development in which the fetus is entirely dependent on maternal supply [145]. Stimulation of the TSH receptor by high concentrations of hCG signals the thyroid to increase production of thyroid hormone, which in turn suppresses pituitary TSH production through feedback inhibition. As a result, plasma TSH concentrations are modestly suppressed in the first trimester relative to nonpregnant women, requiring a downward adjustment of the reference interval. One recent study demonstrated that 15% of pregnant women in the first trimester generated TSH results below the lower limit of the nonpregnant reference interval, indicating that a substantial number of women would be inappropriately characterized as hyperthyroid if their TSH results were interpreted in the context of nonpregnant intervals [146]. Importantly, this downward shift is limited to the latter half of the first trimester and is typically not observed prior to week 7 [147].
Uptake of antiepileptic drugs in forskolin-induced differentiated BeWo cells: alteration of gabapentin transport
Published in Xenobiotica, 2022
Mai Koishikawa, Ayako Furugen, Nanami Ohyama, Katsuya Narumi, Shuhei Ishikawa, Masaki Kobayashi
In placental villi, nutrients, drugs, and waste products are exchanged between the mother and the foetus. On the villous surface, mononuclear cytotrophoblast cells (CT cells) are the predominant cells present in early pregnancy, and these cells differentiate into multinuclear syncytiotrophoblast cells (ST cells) as pregnancy progresses (Tetro et al. 2018). Both morphological and biochemical changes have been observed during the differentiation of CT cells into ST cells. For example, human chorionic gonadotropin (hCG) secretion and syncytin-1 expression increase during differentiation. hCG, a hormone produced during pregnancy, promotes progesterone production from the luteum, the fusion of CT cells, and their differentiation into ST cells (Cole 2010). Syncytin-1 (HERV-W) is an endogenous retrovirus envelope protein that plays a role in the membrane fusion of CT cells (Bastida-Ruiz et al. 2016). hCG and syncytin-1 are widely employed as markers of trophoblast differentiation. It has been observed that the differentiation of CT cells into ST cells can be reproduced in vitro by isolating and culturing CT cells from the human placenta (Kliman et al. 1986). Primary human trophoblast cells have the advantage of retaining the property of normal cells. Conversely, the experimental procedure is complicated, and the obtained primary human trophoblast cells possess a low proliferation capacity. Therefore, as an alternative, the human placental choriocarcinoma cell line, BeWo cells, can be induced to differentiate into ST-like cells by stimulation with forskolin, an adenylate cyclase activator (Rothbauer et al. 2017).