Fetal Demand Research Articles

Characterization of giant neuroendocrine cells in the pregnant New Zealand white rabbit vagina demonstrated by histological, histochemical, and immunohistochemical methods.

The vagina is part of the genitalia and constitutes part of the birth canal. Sperm is deposited into vagina, and it acts in transport of sperm. Pregnancy is a complex process involving different physiological changes in the body associated with hormonal and metabolic alterations that control maternal and fetal demands. During pregnancy, neuroendocrine cells in rabbit vagina are considered part of the diffuse neuroendocrine system observed throughout the body. Giant neuroendocrine cells in rabbit vagina during pregnancy have not been observed previously. This study detected the presence of giant neuroendocrine cells in the vagina of the pregnant rabbit. The presence of these cells was demonstrated with the use of different histological techniques, including hematoxylin and eosin, PAS, combined Alcian blue-PAS, Crossmon's trichrome, and the Grimelius silver method. Giant neuroendocrine cells were observed in late-pregnancy intraepithelial sites and on the lamina propria. These cells were characterized by vacuolated basophilic cytoplasm with PAS- and PAS-AB-positive granules. Moreover, neuroendocrine cells exhibited an argyrophilic character. Immunohistochemically, neuroendocrine cells in rabbit vagina during pregnancy demonstrated positive immunoreactivity to neuron-specific enolase (NSE) with different intensities, mild immunoreactivity to the vascular endothelial growth factor (VEGF), and negative immunoreactivity to CD68. HIGHLIGHTS: Neuroendocrine cells on the vagina of the female rabbit during pregnancy are considered part of the diffuse neuroendocrine system. Giant neuroendocrine cells on the vagina of the rabbit during pregnancy have not been observed previously. Giant neuroendocrine cells were demonstrated intraepithelial and on the lamina propria. Immunohistochemically, neuroendocrine cells demonstrated positive immunoreactivity to NSE and VEGF, and negative immunoreactivity to CD68.

The ruminant placental trophoblast binucleate cell: an evolutionary breakthrough.

Viviparity and the development of a placenta are two of the major reasons for the success of the mammals in colonizing all habitats, both terrestrial and aquatic. The placenta is an apposition of fetal to maternal tissue which serves two main, but competing functions: to maximize oxygen transfer and the acquisition of nutrients from the mother, but to minimize immunological rejection by the maternal immune system. This has resulted in the evolution of four main types differing in the degree of loss of the maternal uterine epithelial (UE) barrier: epitheliochorial, synepitheliochorial, endotheliochorial, and hemochorial, all providing a successful safe balance between the needs of mother and fetus. Epitheliochorial is the least invasive, a simple apposition and microvillar interdigitation of the apices of uterine epithelium and trophoblast. It is suggested to have evolved as a response to the increase in the size of the animal to provide a sufficiently long gestation to produce a single altricial (run/swim-soon-as-born) neonate as in the Cetartiodactyla. The mother needs to have good control of the fetal demands so the UE barrier is maintained. However, in the synepitheliochorial placenta, characteristic of all ruminants, the fetus has evolved a means of increasing, or at least maintaining, demand without the need for invasion. This has been achieved by the development of the trophoblast binucleate cell which, uniquely, can fuse with a UE cell to form fetomaternal hybrid tissue. This can maintain some maternal barrier function but also deliver fetally synthesized immunomodulatory and metabolic messages to the maternal circulation. This review provides the evidence for this remarkable evolutionary step and also considers an alternative explanation for the formation of the structure of the ruminant placenta.

Histopathological features in advanced abdominal pregnancies co-infected with SARS-CoV-2 and HIV-1 infections: A case evaluation.

ObjectivesThis study aims to provide a semi-qualitative histopathological report of the dual SARS-CoV-2 and HIV infected placentae in the third trimester of Advanced Abdominal Pregnancy (AAP).Study designFour AAP placentae in the third trimester of pregnancy (two positive for HIV-1 and two positives for SARS-CoV-2) were histologically examined.ResultsThe SARS-CoV-2+ HIV+ placentae were dysmorphic in shape compared to the flattened disc-like shape noted in the SARS-CoV-2+HIV-, SARS-CoV-2-HIV+and SARS-CoV-2-HIV- placentae. Diffused syncytial knots and syncytial degeneration were observed in all placentae. Intermittent cytotrophoblast increase, perivillous and intravillous fibrin deposition, mononuclear inflammatory cells with widespread degeneration/necrosis of the syncytiotrophoblast and microcalcification were pronounced in the SARS-CoV-2+HIV+ compared to the SARS-CoV-2+HIV- placentae. Vascular pathological changes included thrombi, ectasis, mural hypertrophy and atherotic vessels.ConclusionElevated syncytial trophoblast injury, villitis, microcalcifications and mineralisation of the syncytial basement membrane in the AAP placentae may be due to SARS-CoV-2 viral transgression instead of HIV infection alone. Vascular malperfusion is suggestive of a hypoxic insult arising from a compensatory response to meet the fetal oxygen and nutrient demands of an AAP. Placentae from HIV infected women on antiretroviral treatment were characterised by vascular malperfusion.

The paradox of Prader-Willi syndrome revisited: Making sense of the phenotype.

SummaryPrader-Willi syndrome arises as a consequence of absent paternal copies of maternally imprinted genes at 15q11-13. Such gender-of-origin imprinted genes are expressed in the brain and also in mammalian placenta where paternally expressed imprinted genes drive foetal nutritional demand. We hypothesise that the PWS phenotype is the result of the genotype impacting two pathways: first, directly on brain development and secondly, on placental nutritional pathways that results in its down-regulation and relative foetal starvation. The early PWS phenotype establishes the basis for the later characteristic phenotype. Hyperphagia. and other phenotypic characteristics arise as a consequence of impaired hypothalamic development. Hypothalamic feeding pathways become set in a state indicative of starvation, with a high satiety threshold and a dysfunctional neurophysiological state due to incorrect representations of reward needs, based on inputs that indicate a false requirement for food. Our hypotheses, if confirmed, would lead to novel and effective interventions.

Effect of Punarnavadi Mandoora in the Management of Garbhini Pandu w.s.r to Iron Deficiency Anemia in Pregnancy –A Review

India is one of the countries where anaemia during pregnancy is common. Anemia in pregnancy is caused by a various factors. The most common disorder in a pregnant woman is iron deficiency anaemia. Rasa Pradoshaja vikara is a disorder that arises due to inappropriate Rasa Dhatu in the mother and constantly rising foetal demands. According to Ayurvedic classics, for decades, a variety of Lauha preparations have been used to treat anaemia. Punarnava Mandoora is an Ayurvedic preparation that has been described in various Ayurvedic texts. It's a traditional Ayurvedic treatment for a variety of ailments. It works as a diuretic, cleanses the blood, and increases blood circulation. It raises hemoglobin levels and alleviates anaemia symptoms. Punarnava Mandoora is also used for Oedema, Pliha vikara (Spleen diseases), Yakruta vikara (Liver diseases), Udara (Abdominal distention), Arsha (Hemorrhoids), and Twacha vikara (Skin diseases). This review article highlights effect of Punarnavadi mandoor in the management of Garbhini Pandu W.S.R to anemia in pregnancy

Histochemical Study of Human Placental Tissues in Gestational Diabetic Mellitus

Gestational diabetes mellitus (GDM) is a serious pregnancy complication in which a woman who has never had diabetes develops chronic hyperglycemia during her pregnancy. Normal placental function is essential for optimal fetal growth. The transport of glucose from the mother to the fetus is critical for fetal nutrient demands and can be stored as glycogen in the placenta. However, the function of this glycogen deposition is unknown: It may well be a source of fuel for a placenta itself or the storage reservoir for the later use by the fetus in times of need. While the significance of the placental glycogen remains unknown, the mounting evidence indicates that the altered glycogen metabolism and/or deposition is associated with many pregnancy complications, such as gestational diabetes, that adversely affect fetal development. The aim of this study is to assess glycogen deposition using Histochemical staining of Periodic Acid Schiff (PAS) stain. The placenta tissue collected from 50 women were enrolled in this study (25 women with no complications) and (25 women with gestational diabetes). The placentas of the two groups were compared in this study based on glycogen deposition with periodic acid-Schiff stain. The results of a histochemical investigation using PAS stain revealed a significant increase in the glycogen deposition (p≤0.001) in diabetic women's placentas within the intervillous core, around fetal vessels, and the basement membranes.

Histochemical Study of Human Placental Tissues in Gestational Diabetic Mellitus

Gestational diabetes mellitus (GDM) is a serious pregnancy complication in which a woman who has never had diabetes develops chronic hyperglycemia during her pregnancy. Normal placental function is essential for optimal fetal growth. The transport of glucose from the mother to the fetus is critical for fetal nutrient demands and can be stored as glycogen in the placenta. However, the function of this glycogen deposition is unknown: It may well be a source of fuel for a placenta itself or the storage reservoir for the later use by the fetus in times of need. While the significance of the placental glycogen remains unknown, the mounting evidence indicates that the altered glycogen metabolism and/or deposition is associated with many pregnancy complications, such as gestational diabetes, that adversely affect fetal development. The aim of this study is to assess glycogen deposition using Histochemical staining of Periodic Acid Schiff (PAS) stain. The placenta tissue collected from 50 women were enrolled in this study (25 women with no complications) and (25 women with gestational diabetes). The placentas of the two groups were compared in this study based on glycogen deposition with periodic acid-Schiff stain. The results of a histochemical investigation using PAS stain revealed a significant increase in the glycogen deposition (p≤0.001) in diabetic women's placentas within the intervillous core, around fetal vessels, and the basement membranes.

Ventricular wall stress and wall shear stress homeostasis predicts cardiac remodeling during pregnancy: A modeling study.

Pregnancy is a unique and dynamic process characterized by significant changes in the maternal cardiovascular system that are required to satisfy the increased maternal and fetal metabolic demands. Profound structural and hemodynamic adaptations occur during healthy pregnancy that allows the mother to maintain healthy hemodynamics and provide an adequate uteroplacental blood circulation to ensure physiological fetal development. Investigating these adaptations is crucial for understanding the physiology of pregnancy and may provide important insights for the management of high‐risk pregnancies. However, no previous modeling studies have investigated the maternal cardiac structural changes that occur during gestation. This study, therefore, had two aims. The first was to develop a lumped parameter model of the whole maternal circulation that is suitable for studying global hemodynamics and cardiac function at different stages of gestation. The second was to test the hypothesis that myofiber stress and wall shear stress homeostasis principles can be used to predict cardiac remodeling that occurs during normal pregnancy. Hemodynamics and cardiac variables predicted from simulations with and without controlled cardiac remodeling algorithms were compared and evaluated with reference clinical data. While both models reproduced the hemodynamic variations that arise in pregnancy, importantly, we show that the structural changes that occur with pregnancy could be predicted by assuming invariant homeostatic “target” values of myocardial wall stress and chamber wall shear stress.

Cytokine Patterns in Maternal Serum From First Trimester to Term and Beyond.

Pregnancy implies delicate immunological balance between two individuals, with constant changes and adaptions in response to maternal capacity and fetal demands. We performed cytokine profiling of 1149 longitudinal serum samples from 707 pregnant women to map immunological changes from first trimester to term and beyond. The serum levels of 22 cytokines and C-reactive protein (CRP) followed diverse but characteristic trajectories throughout pregnancy, consistent with staged immunological adaptions. Eotaxin showed a particularly robust decrease throughout pregnancy. A strong surge in cytokine levels developed when pregnancies progressed beyond term and the increase was amplified as labor approached. Maternal obesity, smoking and pregnancies with large fetuses showed sustained increase in distinct cytokines throughout pregnancy. Multiparous women had increased cytokine levels in the first trimester compared to nulliparous women with higher cytokine levels in the third trimester. Fetal sex affected first trimester cytokine levels with increased levels in pregnancies with a female fetus. These findings unravel important immunological dynamics of pregnancy, demonstrate how both maternal and fetal factors influence maternal systemic cytokines, and serve as a comprehensive reference for cytokine profiles in normal pregnancies.

Awareness of maternal stress, consequences for the offspring and the need for early interventions to increase stress resilience.

Experimental and clinical studies suggest that prenatal experiences may influence health trajectories up to adulthood and high age. According to the hypothesis of developmental origins of health and disease exposure of pregnant women to stress, nutritional challenges, infection, violence, or war may "program" risks for diseases in later life. Stress and anxieties can exist or be provoked in parents after fertility treatment, after information or diagnosis of fetal abnormalities and demand simultaneous caring concepts to support the parents. In vulnerable groups, it is therefore important to increase the stress resilience to avoid harmful consequences for the growing child. "Enriched environment" defines a key paradigm to decipher how interactions between genes and environment change the structure and function of the brain. The regulation of the fetal hippocampal neurogenesis and morphology during pregnancy is one example of this complex interaction. Animal experiments have demonstrated that an enriched environment can revert consequences of stress in the offspring during critical periods of brain plasticity. Epigenetic markers of stress or wellbeing during pregnancy might even be diagnosed by fragments of placental DNA in the maternal circulation that show characteristic methylation patterns. The development of fetal senses further illustrates how external stimulation may impact individual preferences. Here, we therefore not only discuss how maternal stress influences cognitive development and resilience, but also design possibilities of non-invasive interventions for both mothers and children summarized and evaluated in the light of their potential to improve the health of future generations.

Effect of pregnancy exercises and education on pregnancy related musculoskeletal discomforts

Aim. Women experience significant physiological and anatomical adaptations during pregnancy to meet the maternal and foetal demands. Biomechanical and hormonal factors, ligament laxity, posture and weight gain may put lot of stress on musculoskeletal system which may in turn induce various musculoskeletal symptoms in pregnancy. Most of the women believe that physical activity during pregnancy is harmful to maternal and foetal health, which results reduction in their routine physical activity. Physical inactivity during gestational period leads to various maternal discomforts and complications. The purpose of this study is to evaluate the effect of structured antenatal exercise programme and education on pregnancy related musculoskeletal discomforts. Material and Methods. Total of 186 mothers were recruited for the study. 94 Participants were selected as the study group samples and 92 were chosen as the control group .The study group received structured antenatal classes and education in addition to routine antenatal care whereas the control group received routine antenatal care and exercises. Antenatal classes were conducted as individualised therapy for the interventional group along with routine antenatal care from 20th week of gestation. The primary outcome measure was pregnancy induced musculoskeletal dysfunction scale (PMDS scale). PMDS scale was assessed at 20, 24 and 32 weeks. Results and Discussion. There was a significant difference in the values of low back pain, symphysis pubic pain, knee pain, pelvic girdle pain and edema at 32 weeks (p value p< 0.05). Exercise during pregnancy increased the β endorphin levels and decrease the perception of pain and pregnancy induced musculoskeletal symptoms. Conclusion. The antenatal exercise programme and education were found to be effective in reducing pregnancy induced musculoskeletal dysfunction. Hence we suggest the pregnancy exercise and education programme in routine antenatal care to improve maternal quality of life.

Advances in understanding the crosstalk between mother and fetus on iron utilization

A full-term pregnancy comes with significant demand for iron. Not meeting this demand has adverse effects on maternal health and on the intrauterine and postnatal development of the infant. In the infant, some of these adverse effects cannot be reversed by postnatal iron supplementation, highlighting the need to tackle iron deficiency in utero. Achieving this requires sound understanding of the pathways that govern iron transfer at the fetomaternal interface. Two pathways are emerging as key players in this context; the hepcidin/ferroportin axis pathway and the iron regulatory protein (IRPs) pathway. In late gestation, suppression of maternal hepcidin, by as yet unknown factors, is required for increasing iron availability to the growing fetus. In the placenta, the rate of iron uptake by transferrin receptor TfR1 at the apical/maternal side and of iron release by ferroportin FPN at the basal/fetal side is controlled by IRP1. In fetal hepatocytes, build up of fetal iron stores requires post-translational inhibition of FPN by the cell-autonomous action of hepcidin. In the fetal liver, FPN is also subject to additional control at the transcriptional level, possibly by the action of hypoxia-inducible factor HIF2α. The rates of apical iron uptake and basal iron release in the placenta are modulated according to iron availability in the maternal blood and the placenta's own needs. This placental modulation ensures that the amount of iron delivered to the fetal circulation is maintained within a normal range, even in the face of mild maternal iron deficiency or overload. However, when maternal iron deficiency or overload are extreme, placental modulation is not sufficient to maintain normal iron supply to the fetus, resulting in fetal iron deficiency and overload respectively. Thus, the rate of iron transfer at the fetomaternal interface is subject to several regulatory signals operating simultaneously in the maternal liver, the placenta and the fetal liver. These regulatory signals act in concert to maintain normal iron supply to the fetus within a wide range of maternal iron states, but fail to do so when maternal iron deficiency or overload are extreme. The limitations of existing experimental models must be overcome if we are to gain better understanding of the role of these regulatory signals in normal and complicated pregnancy. Ultimately, that understanding could help identify better markers of fetal iron demand and underpin novel iron replacement strategies to treat maternal and fetal iron deficiency.

Uterine Vascular Control Preconception and During Pregnancy.

Successful pregnancy and reproduction are dependent on adequate uterine blood flow, placental perfusion, and vascular responsivity to fetal demands. The ability to support pregnancy centers on systemic adaptation and endometrial preparation through decidualization, embryonic implantation, trophoblast invasion, arterial/arteriolar reactivity, and vascular remodeling. These adaptations occur through responsiveness to endocrine signaling and local uteroplacental mediators. The purpose of this article is to highlight the current knowledge associated with vascular remodeling and responsivity during uterine preparation for and during pregnancy. We focus on maternal cardiovascular systemic and uterine modifications, endometrial decidualization, implantation and invasion, uterine and spiral artery remodeling, local uterine regulatory mechanisms, placentation, and pathological consequences of vascular dysfunction during pregnancy. © 2021 American Physiological Society. Compr Physiol 11:1-23, 2021.

Relationship between Maternal and Cord Blood Iron Status in Women and their New Born Pairs

Maintaining iron homeostasis is of great importance to the growing fetus and neonates. There is no consensus as to whether the neonates iron status is determined by fetal demands or by maternal iron status. There is no conclusive data confirming the likelihood of neonates born to anemic mothers suffering from compromised iron status. Therefore the aim of our study was to evaluate the relationship of iron indices between maternal and cord blood collected from mother and infant pairs and explore the association of maternal anemia on the iron status indicators of the cord blood. This prospective study included 60 mother and newborn pairs. The study population was subdivided as anemic and non-anemic groups based on hemoglobin (Hb) levels. The maternal venous blood samples were collected 1.5 h ± 20 min before the delivery. 5 ml of cord blood was collected soon after child birth. Samples were analyzed for hemoglobin (Hb), serum ferritin and iron. Significantly lower values of Hb, Ferritin, iron (p < 0.05) was observed in neonates born to anemic mothers when compared to the indices of neonates born to non-anemic mothers. On multivariate linear regression analysis , maternal Hb showed positive linear correlation with cord Hb and ferritin (r =0.87, p<0.05). However, correlation between maternal Hb and cord iron was not significant. Maternal anemia can effect neonatal iron stores. Lowered concentration of iron status indicators in cord blood of neonates born to anemic mothers indicates that fetal iron transfer may be dependent on that of the iron stores of the mothers. However, this process may involve complex factors.

Bone resorption and dietary calcium in pregnancy-a window to future maternal bone health.

Pregnancy is characterized by increased bone turnover and reversible loss of bone mineral density (BMD) to meet fetal calcium demands. The long-term effect of bone turnover and maternal diet in pregnancy on maternal bone is not well established. We aimed to determine if an association exists between [1] bone resorption, [2] dietary calcium, and [3] serum 25-hydroxyvitamin D in pregnancy with maternal BMD 5-year postpartum. This is a prospective, longitudinal study of 107 women recruited to the ROLO low glycemic index dietary intervention trial in pregnancy and followed-up at 13, 28, and 34weeks' gestation and 5years' postpartum. At 13 and 28weeks' gestation, a biomarker of bone resorption, urine cross-linked N-telopeptide of type I collagen (uNTX), was measured. At the 5-year follow-up BMD was measured using dual-energy X-ray absorptiometry. Anthropometry, dietary intakes, and serum 25-hydroxyvitamin D were measured in pregnancy and at 5years. Multiple linear regression, controlling for confounders, was used for analysis. Mean BMD at 5years was 1.208g/cm2. In pregnancy, 24-34% reported dietary calcium intakes <800mg/day. Vitamin D deficiency (< 30nmol/L) was observed in 38-41% of women in pregnancy and in 29% of women at the 5-year follow-up. At 13 and 28weeks' gestation, uNTX levels greater than the median were associated with 0.060 and 0.050g/cm2 lower BMD 5years later, respectively. Dietary calcium <800mg/day in trimester 3 was associated with 0.072g/cm2 lower BMD 5years later. Vitamin D deficiency at 5years, but not in pregnancy, was associated with lower BMD. Higher bone resorption and low dietary calcium in pregnancy were associated with lower BMD 5years later. These findings could enable the identification of women at risk of declining of BMD in later life, but further research is needed. Adequate dietary calcium should be advised in the antenatal setting to promote lifelong maternal bone health.

328 Chorionic villi angiogenic protein expression in normal human pregnancy

Our goal was to examine the changes in chorionic villi (CV) expression of angiogenic proteins VEGF165, VEGF165b and MMP-9 throughout gestation in normal human pregnancy. Placentas were obtained from normal pregnant women who underwent elective abortion in the first and second trimesters of pregnancy, and from women who delivered at term. CV protein expressions were analyzed by ELISA using monoclonal antibodies to human VEGF165, VEGF165b and MMP-9 proteins (R&D Systems, Minneapolis, MN). Non-parametric test considered p<0.05 as significant. Our study highlights gestational age-specific alterations in all three CV proteins. VEGF165b protein peaked in the 2nd trimester while VEGF165 protein peaked in the third. MMP-9 protein progressively increased with increase in gestational age. Spearman's correlation showed that VEGF165, VEGF165b and MMP-9 proteins were significantly correlated with gestational age in days (r2=+0.236, p=0.001; r2= +0.158, p=0.028; r2=+0.475, p=0.0001, respectively). In the 3rd trimester, a significant positive correlation was seen between VEGF165 and VEGF165b (r2=+0.368, p=0.001); and a significant negative correlation was seen between VEGF165 and MMP-9 proteins (r2= -0.306, p=0.003). Of the three proteins selected, VEGF165 is the dominant angiogenic protein and its overexpression can result in tumorigenesis. VEGF165b is down-regulated in tumors. MMP-9 degrades ECM and promotes endothelial cell migration and is considered angiogenic. The 3rd trimester of human pregnancy is a unique phase when maximum angiogenesis needs to occur, yet as pregnancy approaches parturition the angiogenic process needs to be terminated. The correlation seen between the two isoforms of VEGF in the 3rd trimester suggest that when fetal demand is at its peak the two VEGF isoforms work synergistically to maximize angiogenesis. And, the ample presence of VEGF165b in the 3rd trimester and the inverse correlation seen between MMP-9 and VEGF165 could be mechanisms at place to restrict overexpression of VEGF165 and placental angiogenesis as pregnancy approaches parturition.

Global metabolomic profiling reveals hepatic biosignatures that reflect the unique metabolic needs of late-term mother and fetus.

Gestational disorders including preeclampsia, growth restriction and diabetes are characterized, in part, by altered metabolic interactions between mother and fetus. Understanding their functional relevance requires metabolic characterization under normotypic conditions. We performed untargeted metabolomics on livers of pregnant, late-term C57Bl/6J mice (N = 9 dams) and their fetuses (pooling 4 fetuses/litter), using UPLC-MS/MS. Multivariate analysis of 730 hepatic metabolites revealed that maternal and fetal metabolite profiles were highly compartmentalized, and were significantly more similar within fetuses (ρaverage = 0.81), or within dams (ρaverage = 0.79), than within each maternal-fetal dyad (ρaverage = - 0.76), suggesting that fetal hepatic metabolism is under distinct and equally tight metabolic control compared with its respective dam. The metabolite profiles were consistent with known differences in maternal-fetal metabolism. The reduced fetal glucose reflected its limited capacity for gluconeogenesis and dependence upon maternal plasma glucose pools. The fetal decreases in essential amino acids and elevations in their alpha-keto acid carnitine conjugates reflects their importance as secondary fuel sources to meet fetal energy demands. Whereas, contrasting elevations in fetal serine, glycine, aspartate, and glutamate reflects their contributions to endogenous nucleotide synthesis and fetal growth. Finally, the elevated maternal hepatic lipids and glycerol were consistent with a catabolic state that spares glucose to meet competing maternal-fetal energy demands. The metabolite profile of the late-term mouse dam and fetus is consistent with prior, non-rodent analyses utilizing plasma and urine. These data position mouse as a suitable model for mechanistic investigation into how maternal-fetal metabolism adapts (or not) to gestational stressors.

Pregnancy-Related Change in pQCT and Bone Biochemistry in a Population With a Habitually Low Calcium Intake.

In pregnancy, changes in maternal calcium (Ca) economy occur to satisfy fetal Ca demand. It is unclear whether maternal mineral reserves facilitate these requirements and no data exist from sub-Saharan Africa. The aim was to determine skeletal changes with peripheral quantitative computed tomography (pQCT) and bone biochemistry between early second and third trimesters. Pregnant rural Gambians aged 18 to 45 years (n=467) participating in a trial of antenatal nutritional supplements (ISRCTN49285450) had pQCT scans and blood collections at mean (SD) 14 (3) and 31 (1) weeks' gestation. Outcomes were pQCT: radius/tibia 4% total volumetric bone mineral density (vBMD), trabecular vBMD, total cross-sectional area (CSA), 33%/38% radius/tibia cortical vBMD, bone mineral content (BMC), total CSA; biochemistry: collagen type 1 cross-linked β-C-telopeptide (β-CTX), type 1 procollagen N-terminal (P1NP), parathyroid hormone (PTH), and 1,25(OH)2 D. Independent t tests tested whether pooled or within-group changes differed from 0. Multiple regression was performed adjusting for age. Data for change are expressed as mean (confidence interval [CI] 2.5, 97.5%). Radius trabecular vBMD, cortical vBMD, and BMC increased by 1.15 (0.55, 1.75)%, 0.41 (0.24, 0.58)%, and 0.47 (0.25, 0.69)%. Tibia total and trabecular vBMD increased by 0.34 (0.15, 0.54)% and 0.46 (0.17, 0.74)%, while tibia cortical vBMD, BMC, and cortical CSA increased by 0.35 (0.26, 0.44)%, 0.55 (0.41, 0.68)% and 0.20 (0.09, 0.31)%, respectively. CTX, PTH, and 1,25(OH)2 D increased by 23.0 (15.09, 29.29)%, 13.2 (8.44, 19.34)%, and 21.0 (17.67, 24.29)%, while P1NP decreased by 32.4 (-37.19, -28.17)%. No evidence of mobilization was observed in the peripheral skeleton. Resorption, although higher in late versus early gestation, was lower throughout pregnancy compared with non-pregnant non-lactating (NPNL) in the same community. Formation was lower in late pregnancy than in early, and below NPNL levels. This suggests a shift in the ratio of resorption to formation. Despite some evidence of change in bone metabolism, in this population, with habitually low Ca intakes, the peripheral skeleton was not mobilized as a Ca source for the fetus. © 2021 crown copyright . Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR). The article published with the permission of the Controller of HMSO and the Queen's Printer of Scotland..

Comparative sonographic evaluation of placental thickness in pregnancy-induced hypertension and normotensive pregnant women in the University of Calabar Teaching Hospital, Calabar, Nigeria

Objectives: The human placenta is the nourishing reservoir for the sustenance of the fetus and synthesizes a growth-stimulating hormone to enhance proper growth and maturation. The size or thickness of the placenta enlarges as the pregnancy progresses in age to attain a favorable state which can cope with the increasing fetal demands. Placental thickness (PT) is a reflector of fetal well-being, and it is related to fetal weight making it necessary to assess the influence of pregnancy-induced hypertension (PIH), a common pathology in pregnancy, on the placental size or thickness. The main objective of this research is to compare and evaluate the PT and fetal weight in PIH and normotensive pregnant women. Material and Methods: The study was a prospective cross-sectional case-controlled study done in the Radiology Department of the University of Calabar Teaching Hospital. During a 12 months study period, 200 singleton pregnant women (consisting of 100 pregnancy-induced hypertensives and 100 normotensive pregnant women) of between 20 and 40 weeks of gestation were enrolled in this study. The two groups were gestational age-matched. The PT was measured trans-abdominally using an ultrasound scan. Pearson’s correlation analysis was used to establish the degree of relationship between PT and other fetal anthropometric and maternal parameters. Results: PT was significantly lower in pregnancy-induced hypertensives than in the controls (28.95 ± 5.71 mm vs. 32.31 ± 5.47 mm, P = 0.000). There was a significant negative correlation between the PT and the degree of proteinuria (P = 0.011). Conversely, a significant positive correlation existed between PT and estimated gestational age (P = 0.000) and also estimated fetal weight (EFW) (P = 0.000), in both groups. This same relationship was observed between the body mass index and PT (P = 0.007) as well as the EFW (P = 0.002) in the control group. The mean EFW in pregnancy-induced hypertensives (2.23 ± 1.07 kg) was higher than in the controls (2.13 ± 1.03 kg), but the difference was not significant (P = 0.505). Conclusion: There was a reduction in the PT in PIH, which may be due to the appearance of proteinuria when the blood pressure was elevated. However, we did not observe the expected reduction in the EFW due to a reduction in PT, which usually results from proteinuria.

Changes in Oral Mucosa during Pregnancy

The main aim of this review is to understand the changes in oral mucosa during pregnancy. This review&#x0D; highlights the major oral complication during pregnancy. Changes in the gingiva and physiological&#x0D; structure of the tooth take place in addition to hormonal, immunologic, dietary and behavioural changes.&#x0D; Characteristics of pregnancy gingivitis are that it gets swollen, smooth and tends to bleed easily. Enlargement&#x0D; of gingiva may occur but it tends to resolves within few months after delivery. Due to the increase in salivary&#x0D; microorganisms, there may be a decrease in salivary pH and impairment of buffer effect. This may also lead&#x0D; to dental caries or erosion during lactation period.&#x0D; The dental management of pregnant patients requires special attention. Dentists, for example, may delay&#x0D; certain elective procedures so that they coincide with the periods of pregnancy which are devoted to&#x0D; maturation versus organogenesis. At other times, the dental care professionals need to alter their normal&#x0D; pharmacological armamentarium to address the patients’ needs versus the foetal demands. Applying the&#x0D; basics of preventive dentistry at the primary level will broaden the scope of the prenatal care. Dentists&#x0D; should encourage all the patients of the childbearing ages to seek oral health counselling and examinations&#x0D; as soon as they learn that they are pregnant