Dynamics of human chorionic gonadotropin, prolactin, and growth hormone in serum and amniotic fluid throughout normal human pregnancy

doi:10.1016/0002-9378(85)90665-9

American Journal of Obstetrics and Gynecology

Volume 151, Issue 7, 1 April 1985, Pages 878-884

https://doi.org/10.1016/0002-9378(85)90665-9 Get rights and content

Abstract

This study was performed to establish the dynamics of human chorionic gonadotropin, prolactin, and growth hormone throughout pregnancy in serum and amniotic fluid. Two hundred fifty healthy women at 8 to 42 weeks' gestation were studied. The highest serum human chorionic gonadotropin level was measured between weeks 8 to 12 (53,715 ± 3574 mlU/ml, mean ± SEM), with a decline to a mean plateau of 11,806 ± 1250 mlU/ml from week 18. Amniotic fluid human chorionic gonadotropin had a similar pattern with a mean of 68,100 ± 8422 mlU/ml at weeks 8 to 10, declining from week 18 to a plateau of 2005 ± 260 mlU/ml. Human chorionic gonadotropin showed a significant correlation (r = 0.85, p < 0.001) between levels of both compartments demonstrating an even distribution. Prolactin levels showed a dichotomy of patterns and levels. Serum prolactin showed a continuous rise from 45.3 ± 14 ng/ml at week 8 to 224 ± 20 ng/ml at week 36. In contrast, amniotic fluid prolactin remained low until week 14 (33.1 ± 0.8 ng/ml), followed by a sharp and significant (p < 0.001) increase to a plateau of 3750 ± 200 ng/ml between weeks 18 to 26, declining to a second plateau of 500 ± 50 ng/ml at week 36. Serum growth hormone increased from a mean of 3.5 ± 1.4 ng/ml seen at weeks 8 to 10 to a mean of 14 ± 2.0 ng/ml at weeks 28 to 30, followed by a plateau of similar levels. The pattern of growth hormone secretion in amniotic fluid demonstrated a sharp increase during the 14–16 interval with a maximum mean level of 15.5 ± 1.5 ng/ml and a slow steady decline thereafter. In conclusion, the similar pattern are concentration of human chorionic gonadotropin throughout pregnancy in both maternal and amniotic fluid are probably the result of direct human chorionic gonadotropin diffusion from the placenta. The dissimilar pattern and concentration of prolactin are the result of two different sources of prolactin secretion during pregnancy. Serum prolactin originates from the pituitary and amniotic fluid prolactin from the decidua. Since the pattern of growth hormone secretion resembles that of prolactin, it is possible that growth hormone, like prolactin, is secreted by the same sources.

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The interaction between endometrial stromal cells and decidual macrophages influence the conversion of each other. During decidualization, uterine endometrium, decidua and placenta were suggested to produce a wide range of cytokines attracting leukocytes to the decidualized tissue, such as CSF-1, vascular endothelial growth factor (VEGF), monocyte chemoattractant protein-1 (Abrahams et al., 2005), prolactin (PRL) (Kletzky et al., 1985; Golander et al., 1978), insulin growth factor binding protein-1 (IGFBP-1) (Rutanen et al., 1986; Liu et al., 1995), cell adhesion molecules like intercellular adhesion molecule-1 (ICAM-1) (Liu et al., 1995), and various chemokines (Mei et al., 2019; Quinn et al., 2016; Du et al., 2014). CSF-1 not only promoted the survival and proliferation of tissue macrophages but also recruited peripheral monocytes into tissue (Pixley and Stanley, 2004; Tagliani et al., 2011) and macrophages with higher expression of CXCR6 or CCR2 were preferentially recruited to the uterus (Vento-Tormo et al., 2018).
A successful pregnancy requires that the maternal immune system recognizes and tolerates the semi-allogeneic fetus without compromising the capability of protecting both mother and fetus from various pathogens. Decidual macrophages present unique phenotypes to play a key role in the establishment of the immunological aspects of maternal-fetal interaction. Dysfunction of decidual macrophages gives rise to pregnancy complications such as preeclampsia, recurrent spontaneous miscarriage, preterm labor and fetal growth restriction. Here, we reviewed the latest knowledge on the origin, differentiation, unique phenotype and function of macrophages in normal pregnancy and in pregnancy complications. We mainly focused on the significant roles of decidual macrophages in the process of extravillous trophoblast invasion, spiral arterial remodeling, decidual stromal cells cultivation and immune tolerance maintenance in normal pregnancy, and their pathological roles in pregnancy-related complications, offering more integrated information in maternal-fetal immunity.
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Prolactin measured in the amniotic fluid (placental lactogen) remains low until week 14 (around 30 ng/ml), before sharply increasing to around 3500–4000 ng/ml between weeks 18–26. These levels further decline to plateau at around 500 ng/ml at week 36 of gestation (Kletzky et al., 1985). Similarly, in non-human primates, levels of placental lactogen dramatically increase throughout pregnancy and reach a peak shortly before parturition (Belanger et al., 1971).
Mammalian pregnancy and lactation is accompanied by a period of infertility that takes place in the midst of a sustained increase in food intake. Indeed, successful reproduction in females is dependent on co-ordination of the distinct systems that regulate reproduction and metabolism. Rather than arising from different mechanisms during pregnancy and lactation, we propose that elevations in lactogenic hormones (predominant among these being prolactin and the placental lactogens), are ideally placed to influence both of these systems at the appropriate time. We review the literature examining the impacts of lactogens on fertility and energy homeostasis in the virgin state, during pregnancy and lactation and potential long-term impacts of reproductive experience. Taken together, the literature indicates that duration and pattern of lactogen exposure is a vital factor in the ability of these hormones to alter reproduction and food intake. Transient increases in prolactin, as typically seen in healthy virgin females and males, are unable to exert lasting impacts. Importantly, both suppression of fertility and increased food intake are only observed following exposure to chronically-elevated levels of lactogens. Physiologically, the only time this pattern of lactogenic secretion is maintained in the healthy female is during pregnancy and lactation, when co-ordination between these regulatory systems emerges.
This article is part of the special issue on ‘Neuropeptides’.
Endocrine Diseases of Pregnancy
2019, Yen & Jaffe's Reproductive Endocrinology: Physiology, Pathophysiology, and Clinical Management: Eighth Edition
Physiological and endocrine adaptations occur in the mother in response to the demands of pregnancy. These demands include support of the fetus (volume support, nutritional and oxygen supply, and clearance of fetal waste), protection of the fetus (from starvation, drugs, toxins), preparation of the uterus for labor, and protection of the mother from potential cardiovascular injury at delivery. The presence of a preexisting endocrine disorder is likely to affect the ability of the mother to adapt to the demands of pregnancy and, as a result, may influence fetal growth and development. Drugs used to treat such disorders may also affect perinatal outcome. The most common preexisting endocrine disorders that can complicate pregnancy are diabetes mellitus, thyroid dysfunction, and obesity. Less common preexisting maternal endocrine disorders include pituitary tumors, diabetes insipidus, and hyperparathyroidism.
The physiological and endocrine adaptations that characterize pregnancy can also lead to the development of pregnancy-specific diseases in previously healthy women, the most common of which are gestational diabetes and disorders of the endocrine and sympathetic nervous systems associated with preeclampsia and preterm labor. This chapter is designed to review in detail the underlying pathophysiology of these pregnancy-specific diseases, as well as the effects of pregnancy on preexisting endocrine disorders. A better understanding of these conditions will improve the ability of clinicians to optimize maternal and perinatal outcome in such pregnancies.
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2017, Journal of Reproductive Immunology
Citation Excerpt :
Consistent with our hypothesis, high levels of amniotic PRL are required to maintain pro- and anti-inflammatory cytokines in equilibrium. Our results demonstrate that co-stimulation with 4000-ng/mL PRL, which is present in amniotic fluid during the second trimester (Kletzky et al., 1985) was the only strategy capable of inhibiting LPS-induced TNF-α secretion. However, this effect was reverted when the membranes were co-incubated with a JAK2/STAT5 pathway inhibitor, indicating that this inhibition is PRL dependent (Thomas et al., 2015).
During pregnancy, prolactin (PRL) is a neuro-immuno-cytokine that contributes actively to the crosstalk between the immune and endocrine systems and, thus, to the creation of an immune-privileged milieu. This work aims to analyze the capacity of PRL to modulate the synthesis and secretion of pro-inflammatory markers associated with labor. Studies were conducted using human fetal membranes at term mounted in a model of two independent chambers. The choriodecidual region was stimulated with 500-ng/mL lipopolysaccharide (LPS), and the amnion and choriodecidual region were co-simulated with different concentrations of PRL that can arise during pregnancy: 250, 500, 1000, and 4000 ng/mL. Following these co-treatments, the tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-10 levels were measured in both compartments. As expected, treatment with LPS induced all cytokines to increase. Co-stimulation with the highest tested concentration of PRL induced significant decreases in TNF-α in the choriodecidual region and IL-1β in both regions of the fetal membranes. PRL did not modified the IL-6 and IL-10 secretion profile. These findings, coupled with clinical evidence, suggest that the high level of PRL in the amniotic cavity is involved the mechanism by which the fetal-placental unit regulates the equilibrium between pro- and anti-inflammatory modulators.
Embryo quality: the missing link between pregnancy sickness and pregnancy outcome
2017, Evolution and Human Behavior
Pregnancy sickness is widespread yet its etiology is poorly understood. It is almost certainly endocrine in origin and most likely a product of placental hormones, with human chorionic gonadotropin being the strongest candidate. It has long been known that greater levels of nausea and vomiting during pregnancy are associated with a lower incidence of spontaneous abortion, yet the causal mechanisms remain unclear. One current popular explanation is that nausea and vomiting during pregnancy is fetoprotective, inducing aversions to foods, especially meat, dairy and seafoods, which may carry toxins, pathogens or mutagens. However, most spontaneous abortions arise from genetic or epigenetic defects that are present at or near conception. Moreover, measurements of human chorionic gonadotropin (hCG) at the time of implantation, particularly its hyperglycosylated isoform, accurately predict subsequent spontaneous abortion. Thus the developmental fate of most embryos is fixed before the onset of the symptoms of pregnancy sickness. An alternative explanation for the link between pregnancy sickness and spontaneous abortion is the embryo quality hypothesis: high quality embryos are both more likely to produce the biochemical antecedents of pregnancy sickness and avoid spontaneous abortion. Recent work has shown that the link between pregnancy sickness and spontaneous abortion grows stronger with maternal age, dramatically so in mothers 35 or older. This reflects the parallel rise in the incidence of autosomal aneuploidies with maternal age. The link between pregnancy sickness and spontaneous abortion exists not because nausea and vomiting during pregnancy is fetoprotective, but because nausea and vomiting is an index of a high quality embryo. Pregnancy sickness is not adaptive per se, but the result of an antagonistic pleiotropy over thyroid function, where embryos use hCG to modulate maternal thyroid hormone production during gestation. Embryos benefit from the thyroid hormone production that is key to neurodevelopment, but produce maternal nausea and vomiting as a by-product. Pregnancy sickness, however, may still serve to protect embryo quality but by a different mechanism that posited under the MEPH. Embryo quality is protected by calibrating the dietary intake of a micronutrient – iodine – critical to neuromotor development. For most humans over most of our evolutionary history, iodine has been in short supply, and iodine deficiency is still the most common source of cognitive impairment across the globe. Thus it is of interest that the food aversions most commonly associated with pregnancy sickness, to meat, dairy and seafoods, are also the chief dietary sources of iodine. There is a further intriguing property about iodine: both too little and too much during early pregnancy are damaging to embryo brain development. Given that pregnancy sickness is closely linked to iodine intake and thyroid function (hypothyroidism is associated with lower levels of nausea and vomiting, hyperthyroidism with more), an obvious interpretation emerges. The previously described link between diet and pregnancy sickness – pregnancy sickness is less likely when plants and particularly corn/maize are the sole food staples – arises not because plant food staples are safe, as previously suggested, but because these foods are iodine poor and may, in addition, be goitrogenic. Pregnancy sickness, which reduces the dietary intake of iodine, is clearly maladaptive under conditions of iodine deficiency and hypothyroidism. Conversely, higher levels of pregnancy sickness induced by hyperthyroidism may protect embryos from the inimical effects of excessive dietary iodine during early gestation by reducing the intake of iodine rich foods.
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2017, Drug Metabolism in Diseases
This chapter provides an overview of the physiologic and pharmacokinetic changes that influence drug disposition during pregnancy. The dynamic regulation of hepatic phases I and II metabolic enzymes as well as transporters in pregnant animals and women is reviewed. Attention is also placed upon the role of individual hormones, such as estradiol and progesterone, as well as nuclear receptors in the adaptive changes in enzyme and transporter levels that occur during pregnancy. A comprehensive case study explores the coordinated regulation of metabolic enzymes, transporters, and nuclear receptors that control bile acid homeostasis in pregnant rodents. Understanding how pregnancy alters endobiotic and xenobiotic disposition is critical to ensure optimal management of diseases.

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^☆: Presented by invitation at the Third Annual Meeting of the American Gynecological and Obstetrical Society, Hot Springs, Virginia, September 5–8, 1984.

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Dynamics of human chorionic gonadotropin, prolactin, and growth hormone in serum and amniotic fluid throughout normal human pregnancy☆

Abstract

Am J Obstet Gynecol

Am J Obstet Gynecol

Life Sci

Am J Obstet Gynecol

Am J Obstet Gynecol

Am J Obstet Gynecol

Rec Prog Horm Res

Life Sci

Am J Obstet Gynecol

Hypothalamic monoamines in human fetuses

Neuroendocrinology

Studies on human sexual development. III. Fetal pituitary and serum, and amniotic fluid concentration of LH, CG, and FSH

J Clin Endocrinol Metab

The presence of lactogen receptors in human chorion laeve

J Clin Endocrinol Metab