scholarly journals Fetal Cytokine Balance, Erythropoietin and Thalassemia but Not Placental Malaria Contribute to Fetal Anemia Risk in Tanzania

2021 ◽  
Vol 12 ◽  
Author(s):  
Edward R. Kabyemela ◽  
Michal Fried ◽  
Jonathan D. Kurtis ◽  
Gwamaka Moses ◽  
J. Patrick Gorres ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Cord Blood ◽  
Placental Malaria ◽  
Fetal Anemia ◽  
Red Cell ◽  
Young Infants ◽  
Cytokine Balance ◽  
Endemic Areas ◽  
The Relationship ◽  
Maternal Iron

Fetal anemia is common in malaria-endemic areas and a risk factor for anemia as well as mortality during infancy. Placental malaria (PM) and red cell abnormalities have been proposed as possible etiologies, but the relationship between PM and fetal anemia has varied in earlier studies, and the role of red cell abnormalities has not been studied in malaria-endemic areas. In a Tanzanian birth cohort study designed to elucidate the pathogenesis of severe malaria in young infants, we performed a cross-sectional analysis of risk factors for fetal anemia. We determined PM status, newborn red cell abnormalities, and maternal and cord blood levels of iron regulatory proteins, erythropoietin (EPO), cytokines and cytokine receptors. We examined the relationship between these factors and fetal anemia. Fetal anemia was present in 46.2% of the neonates but was not related to PM. Maternal iron deficiency was common (81.6%), most frequent in multigravidae, and interacted with parity to modify risk of fetal anemia, but it was not directly related to risk. Among offspring of iron-deficient women, the odds of fetal anemia increased with fetal α+-thalassemia, as well as these patterns of cord blood cytokines: increased cord IL-6, decreased TNF-RI, and decreased sTfR. The EPO response to fetal anemia was low or absent and EPO levels were significantly decreased in newborns with the most severe anemia. This study from an area of high malaria transmission provides evidence that 1) fetal α+-thalassemia and cytokine balance, but not PM at delivery, are related to fetal anemia; 2) maternal iron deficiency increases the risk that other factors may cause fetal anemia; and 3) fetal anemia has a multifactorial etiology that may require a variety of interventions, although measures that reduce maternal iron deficiency may be generally beneficial.

Cord blood iron profile and breast milk micronutrients in maternal iron deficiency anemia

2011 ◽  
Vol 58 (2) ◽  
pp. 233-238 ◽  
Author(s):  
Rania Ali El-Farrash ◽  
Eman Abdel Rahman Ismail ◽  
Ahmed Shafik Nada
Keyword(s):  
Breast Milk ◽  
Iron Deficiency ◽  
Cord Blood ◽  
Iron Deficiency Anemia ◽  
Deficiency Anemia ◽  
Iron Profile ◽  
Maternal Iron

scholarly journals Study on relationship between maternal haemoglobin and the early neonatal outcome in term babies

2019 ◽  
Vol 6 (5) ◽  
pp. 1938
Author(s):  
R. Rama Krishna Paramahamsa ◽  
G. Kalyan Chakravarthi
Keyword(s):  
Birth Weight ◽  
Iron Deficiency ◽  
Head Circumference ◽  
Neonatal Outcome ◽  
Cross Sectional ◽  
Term Neonates ◽  
Medical College ◽  
History Of ◽  
The Relationship ◽  
Maternal Iron

Background: Iron stores of neonates born to anaemic mothers are low, iron content in breast milk in anaemic women is low and because of these factors substantial proportion of infants become anaemic by six months. Thus maternal iron deficiency and anaemia makes the offspring vulnerable for developing iron deficiency anaemia right from infancy. The current study was made attempt to evaluate and establish the relationship between maternal haemoglobin and early neonatal outcome in term babies.Method: The present cross-sectional observational study conducted in term neonates and their mothers in first stage of labour in the Department of Paediatric and Department of Obstetrics & Gynaecology, GSL Medical College and general hospital, Rajamahendravaram, from 2015 to 2017. Relevant history of mother was recorded and blood sample from the mother was collected in first stage of labour for haemoglobin estimation.Result: The mean haemoglobin in anaemic mothers was found to be 9.48±0.413 gm/dl and that in non-anaemic mothers was 11.67±0.515gm/dl. Anaemia among mothers has significant effect on birth weight of the newborn babies, on crown heel length of the newborn babies (P<0.05) and on head circumference of Newborn babies (P< 0.05). It was found that anaemia among mothers has no significant effect on APGAR score at 5 mins and on hospital stay.Conclusion: Anaemic mothers had newborn with low mean birth weight, low mean head circumference and low crown heel length compared to the those of non anaemic mothers. 

Relationship between Leptin Concentration in Cord Blood and Foetal Growth and Maternal Anthropometry of GDM Mothers at Delivery

1970 ◽  
Vol 25 (1) ◽  
pp. 9-13
Author(s):  
S Jahan ◽  
TR Das ◽  
KB Biswas
Keyword(s):  
Body Mass Index ◽  
Birth Weight ◽  
Cord Blood ◽  
Body Mass ◽  
Anthropometric Measurements ◽  
Anthropometric Parameters ◽  
Serum Leptin ◽  
C Peptide ◽  
Cord Serum ◽  
The Relationship

Background and Aims: Cord blood leptin may reflect the leptinemic status of a newborn at birth more accurately than the leptin values of blood collected from other sites. The present study was undertaken to determine the relationship of cord serum leptin concentration at birth with neonatal and maternal anthropometric parameters. Materials and Methods: Blood was taken from the umbilical cord of the babies at delivery. Maternal anthropometric measurements were recorded at admission for delivery. Neonatal anthropometric measurements were recorded within 48 hours after delivery. Linear regression analysis was used to explore the relationship between cord serum leptin concentration and anthropometric parameters of the baby and the mother. Both Serum leptin and serum C-peptide levels were measured by chemiluminescence-based ELISA method. Results: The leptin concentration (ng/ml, mean±SD) in cord blood was 39.13±14.44. Cord leptin levels correlated with birth weight (r=0.673, p<0.0001), ponderal index (r=0.732, p<0.0001) but it did not correlate with maternal body mass index, gestational age (r=0.135, p=0.349) at delivery or cord serum C-peptide concentration (r=-0.049, p=0.735) or placental weight (r=0.203, p=0.157). Conclusion: There are associations between cord leptin concentration at delivery and birth weight, ponderal index (PI) of the babies but not body mass index (BMI) of the mothers. High leptin levels of the baby could represent an important feedback modulator of substrate supply and subsequently for adipose tissue status during late gestation. (J Bangladesh Coll Phys Surg 2007; 25 : 9-13)

scholarly journals Maternal iron deficiency perturbs embryonic cardiovascular development in mice

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jacinta I. Kalisch-Smith ◽  
Nikita Ved ◽  
Dorota Szumska ◽  
Jacob Munro ◽  
Michael Troup ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Environment Interaction ◽  
Cardiovascular Development ◽  
Retinoic Acid Signalling ◽  
Gene Environment Interaction ◽  
Iron Administration ◽  
Gene Environment ◽  
Cardiovascular Defects ◽  
Craniofacial Defects ◽  
Maternal Iron

AbstractCongenital heart disease (CHD) is the most common class of human birth defects, with a prevalence of 0.9% of births. However, two-thirds of cases have an unknown cause, and many of these are thought to be caused by in utero exposure to environmental teratogens. Here we identify a potential teratogen causing CHD in mice: maternal iron deficiency (ID). We show that maternal ID in mice causes severe cardiovascular defects in the offspring. These defects likely arise from increased retinoic acid signalling in ID embryos. The defects can be prevented by iron administration in early pregnancy. It has also been proposed that teratogen exposure may potentiate the effects of genetic predisposition to CHD through gene–environment interaction. Here we show that maternal ID increases the severity of heart and craniofacial defects in a mouse model of Down syndrome. It will be important to understand if the effects of maternal ID seen here in mice may have clinical implications for women.

Effect of iron deficiency on placental transfer of iron and expression of iron transport proteins in vivo and in vitro

2001 ◽  
Vol 356 (3) ◽  
pp. 883-889 ◽  
Author(s):  
Lorraine GAMBLING ◽  
Ruth DANZEISEN ◽  
Susan GAIR ◽  
Richard G. LEA ◽  
Zehane CHARANIA ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Transferrin Receptor ◽  
Iron Transport ◽  
Receptor Expression ◽  
Mrna Levels ◽  
Iron Transfer ◽  
Metal Transporter ◽  
Protein Levels ◽  
Copper Oxidase ◽  
Maternal Iron

Maternal iron deficiency during pregnancy induces anaemia in the developing fetus; however, the severity tends to be less than in the mother. The mechanism underlying this resistance has not been determined. We have measured placental expression of proteins involved in iron transfer in pregnant rats given diets with decreasing levels of iron and examined the effect of iron deficiency on iron transfer across BeWo cell layers, a model for placental iron transfer. Transferrin receptor expression was increased at both mRNA and protein levels. Similarly, expression of the iron-responsive element (IRE)-regulated form of the divalent metal transporter 1 (DMT1) was also increased. In contrast, the non-IRE regulated isoform showed no change in mRNA levels. Protein levels of DMT1 increased significantly. Iron efflux is thought to be mediated by the metal transporter protein, IREG1/ferroportin1/MTP1, and oxidation of Fe(II) to Fe(III) prior to incorporation into fetal transferrin is carried out by the placental copper oxidase. Expression of IREG1 was not altered by iron deficiency, whereas copper oxidase activity was increased. In BeWo cells made iron deficient by treatment with desferrioxamine (‘deferioxamine’), iron accumulation from iron-transferrin increased, in parallel with increased expression of the transferrin receptor. At the same time, iron efflux also increased, showing a higher flux of iron from the apical to the basolateral side. The data show that expression of placental proteins of iron transport are up-regulated in maternal iron deficiency, resulting in an increased efficiency of iron flux and a consequent minimization of the severity of fetal anaemia.

scholarly journals Maternal Iron Status in Pregnancy and Child Health Outcomes after Birth: A Systematic Review and Meta-Analysis

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2221
Author(s):  
Hugo G. Quezada-Pinedo ◽  
Florian Cassel ◽  
Liesbeth Duijts ◽  
Martina U. Muckenthaler ◽  
Max Gassmann ◽  
...  
Keyword(s):  
Systematic Review ◽  
Iron Deficiency ◽  
Child Health ◽  
Methodological Quality ◽  
Iron Status ◽  
Meta Analysis ◽  
Child Health Outcomes ◽  
Maternal Iron ◽  
In Pregnancy

In pregnancy, iron deficiency and iron overload increase the risk for adverse pregnancy outcomes, but the effects of maternal iron status on long-term child health are poorly understood. The aim of the study was to systematically review and analyze the literature on maternal iron status in pregnancy and long-term outcomes in the offspring after birth. We report a systematic review on maternal iron status during pregnancy in relation to child health outcomes after birth, from database inception until 21 January 2021, with methodological quality rating (Newcastle-Ottawa tool) and random-effect meta-analysis. (PROSPERO, CRD42020162202). The search identified 8139 studies, of which 44 were included, describing 12,7849 mother–child pairs. Heterogeneity amongst the studies was strong. Methodological quality was predominantly moderate to high. Iron status was measured usually late in pregnancy. The majority of studies compared categories based on maternal ferritin, however, definitions of iron deficiency differed across studies. The follow-up period was predominantly limited to infancy. Fifteen studies reported outcomes on child iron status or hemoglobin, 20 on neurodevelopmental outcomes, and the remainder on a variety of other outcomes. In half of the studies, low maternal iron status or iron deficiency was associated with adverse outcomes in children. Meta-analyses showed an association of maternal ferritin with child soluble transferrin receptor concentrations, though child ferritin, transferrin saturation, or hemoglobin values showed no consistent association. Studies on maternal iron status above normal, or iron excess, suggest deleterious effects on infant growth, cognition, and childhood Type 1 diabetes. Maternal iron status in pregnancy was not consistently associated with child iron status after birth. The very heterogeneous set of studies suggests detrimental effects of iron deficiency, and possibly also of overload, on other outcomes including child neurodevelopment. Studies are needed to determine clinically meaningful definitions of iron deficiency and overload in pregnancy.

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