Correlation of placental thickness with birth weight in singleton pregnancies

Background: The placenta provides the physiologic link between a pregnant woman and the fetus. During pregnancy, the normal placenta increases its thickness at a rate of approximately 1 millimeter per week. The thickness is considered normal throughout the 2nd and 3rd trimester if between 2 and 4 cm. There is a need to identify the fetus failing to reach its growth potential because an early detection of intrauterine growth retardation will be beneficial to obstetric and neonatal care.Methods: After applying inclusion and exclusion criteria, 251 antenatal women from 24-39 weeks gestation were included in the study. After informed written consent, relevant history, examination, abdominal ultrasound was performed noting fetal biometry and placental thickness. The participants were followed until delivery and birth weight noted. Statistical analysis of birth weight (< and >2500 gm) with placental thickness was done.Results: Mean age of the study was 25.88±4.34 years. The mean placental thickness in group A was 3.33±0.92 cm and in group B was 3.38±0.68 cm. Placental thickness showed a positive correlation with fetal weight (r=0.013), however it was not statistically significant. Uncomplicated pregnancy group had mean placental thickness of 3.40±0.70 cm. The difference of mean for placental thickness was statistically significant with respect to medical disorders (p=0.042).Conclusions: Placental thickness does increase with increasing birth weight of the fetus and hence, subnormal or more than normal placental thickness is helpful in signalling important maternal conditions that may be detrimental to the fetus.

Maternal B cell signaling orchestrates fetal development in mice

B cell participation in early embryo/fetal development and the underlying molecular pathways have not been explored. To understand whether maternal B cell absence or impaired signaling interferes with placental and fetal growth, we paired CD19-deficient (CD19−/-) mice, females with B cell-specific MyD88 (BMyD88−/-) or IL-10 (BIL-10−/-) deficiency as well as WT and MyD88−/- controls on C57Bl/6 background with BALB/c males. Pregnancies were followed by ultrasound and Doppler measurements. Implantation number was reduced in BMyD88−/- and MyD88−/- mice. Loss of MyD88 or B cell-specific deletion of MyD88 or IL-10 resulted in decreased implantation areas at gestation days (gd)5, 8 and 10, accompanied by reduced placental thickness, diameter and areas at gd10. Uterine artery resistance was enhanced in BIL-10−/- dams at gd10. Challenge with 0.4mg LPS/kg BW at gd16 revealed that BMyD88−/-, BIL-10−/- and CD19−/- mothers delivered preterm while controls maintained their pregnancy. B cell specific MyD88 and IL-10 expression is essential for appropriate in utero development. IL-10+B cells are involved in uterine blood flow regulation during pregnancy. Finally, B cell-specific CD19, MyD88 and IL-10 expression influences susceptibility towards preterm birth.

The Choline Metabolite TMAO Inhibits NETosis and Promotes Placental Development in GDM of Humans and Mice

Choline metabolite Trimethylamine N-oxide (TMAO) has been recognized as a risk factor of gestational diabetes mellitus (GDM), but its exact role in GDM has not been reported. In this study, we focused on the placenta development to reveal the role of TMAO in GDM. We found the TMAO levels in peripheral and cord plasma were increased in women with GDM, and TMAO levels were positively correlated with newborn weight and placental thickness. Neutrophil extracellular traps (NETs) in the peripheral and cord plasma and the myeloperoxidase expression in the placenta of women with GDM also increased. NETs could inhibit the proliferation, migration, invasion and angiogenesis of HTR-8/Svneo cells. However, TMAO could not only inhibit the formation of NETs, but also enhance the biological function of HTR-8/Svneo cells. By inducing GDM models in NETs deficient PAD4^-/- and wild-type mice, the placental weight of PAD4^-/- mice increased significantly. TMAO feeding also inhibited the formation of NETs and further increased the weight of the placenta and fetuses, and this increase did not affect the placental structure. Our data indicated that higher TMAO levels and the formation of abnormal NETs were associated with GDM. TMAO could not only promote the development of the placenta and fetuses, but also inhibit the formation of NETs.

The Choline Metabolite TMAO Inhibits NETosis and Promotes Placental Development in GDM of Humans and Mice

Choline metabolite Trimethylamine N-oxide (TMAO) has been recognized as a risk factor of gestational diabetes mellitus (GDM), but its exact role in GDM has not been reported. In this study, we focused on the placenta development to reveal the role of TMAO in GDM. We found the TMAO levels in peripheral and cord plasma were increased in women with GDM, and TMAO levels were positively correlated with newborn weight and placental thickness. Neutrophil extracellular traps (NETs) in the peripheral and cord plasma and the myeloperoxidase expression in the placenta of women with GDM also increased. NETs could inhibit the proliferation, migration, invasion and angiogenesis of HTR-8/Svneo cells. However, TMAO could not only inhibit the formation of NETs, but also enhance the biological function of HTR-8/Svneo cells. By inducing GDM models in NETs deficient PAD4^-/- and wild-type mice, the placental weight of PAD4^-/- mice increased significantly. TMAO feeding also inhibited the formation of NETs and further increased the weight of the placenta and fetuses, and this increase did not affect the placental structure. Our data indicated that higher TMAO levels and the formation of abnormal NETs were associated with GDM. TMAO could not only promote the development of the placenta and fetuses, but also inhibit the formation of NETs.

STUDY OF MORPHOLOGY AND HISTOLOGY OF PLACENTA AND ITS CORRELATION WITH MATERNAL PARAMETERS AND BIRTH WEIGHT OF NEWBORN IN ANAEMIC MOTHERS

The aim of this study was to determine whether maternal anaemia [Hb <11gm/dl]would affect the morphology and histology of placenta and and correlate it with maternal parameters and birth weight of newborn and compare this with that of non-anaemic mothers. It was a cross-sectional comparative study carried out at the maternity ward and anatomy department of NSCB MEDICAL COLLEGE JABALPUR. Background & Method: Background & Method: The study was carried out on 100 placentae, mothers and their babies. The placenta was collected from Obstetrics and Gynaecology, Department of NSCB Medical College, Jabalpur. Out of 100 placentae 50 from anaemic and 50 from NON anaemic mothers. As soon as the placenta was delivered, the umblical cord was cut it was put into formal saline. It was kept in a tray, to the membranes were trimmed off cord was cut about 10 cm from the insertion. The blood clots adherent to maternal surface were picked up. Morphological parameters like placental weight, volume. diameter, thickness, no of cotyledons were measured .Any abnormality like calcification, accessory lobe, haematoma, etc were noted. histological slides were made and stained with H and stain and Masson’s Trichrome stain. Result: A Macroscopic study of the placenta revealed placental weight, placental volume, diameter, placental thickness were more than non anaemic group and number of cotyledons were less in study group. Mean placental weight in study group was 474gm and in control group was 425 (p<0.05). Mean placental volume in study group & control group were 393.23and352 ml respectively (p<0.05). Mean number of cotyledons were 13.24and 16 in study & control group significant[p<0.05] and mean diameter 18.30cms and17.05cms in study and control group. Mean placental thickness 2.4cms in study and 2.1 in control group respectively. There was an accessory lobe present in one patient of anaemic group. All morphometric parameters of placenta weight, volume, diameter, thickness were increased ,no of cotyledons were reduced .Histological findings were placental tissues shows intense congestion of septal capillaries.In the present study age, parity, height, weight, built, doesn’t found to be related with morphology of placenta. Maternal blood Hb found to be +vely correlated with weight, volume, diameter, thickness and –vely correlated with no of cotyledons and birth weight of baby. Conclusion: From the study it is concluded anaemia in pregnancy affects morphology and histology of placenta and it is correlated with various maternal parameters and birth weight of baby. Keywords: morphology, histology, placenta, anaemia, birth weight & mothers.

STUDY OF MORPHOLOGY AND HISTOLOGY OF PLACENTA IN HYPERSENSITIVE MOTHERS

Background: Hypertensive pregnancy may be responsible for vascular damage, enhanced systemic inflammation and insulin resistance in the placenta as oxygen and nutrient transfer is impaired and oxidative stress is generated affecting the placental growth and development. Placental growth pattern in hypertensive pregnancies shows a variable pattern owing to placental insufficiency. Method: The study was carried out on 80 sets placentae, mothers and their babies. The placentae were collected from Obstetrics & Gynecology Department of NSCB Medical College Jabalpur. Out of 80 placentae, 40 were from normal pregnant mothers and 40 from pregnancies complicated by PIH in previously normotensive women, serial number of placentae, mother and baby were same. placentae were collected soon after the normal vaginal delivery or caesarian section along with 10 cm long stump of umbilical cord. Aims and objectives: The aim of this study was to determine whether maternal PIH would affect the morphology and histology of placenta and compare this with that of normotensive mothers. It was a cross-sectional comparative study carried out at the maternity ward and anatomy department of NSCB Medical College, Jabalpur. Result: A Macroscopic study of the placenta revealed placental weight, placental volume, diameter, placental thickness and number of cotyledons were less in study group. Mean placental weight in study group was 336gm and in control group was 425 (p<0.05). Mean placental volume in study group & control group were 236and352 ml respectively (p<0.05). Mean number of cotyledons were 14.7and 16 in study & control group respectively but not significant and mean diameter15.6 cms and17.05cms in study and control group. But in the present study placental thickness was not significant (p<0.539). There was a single umbilical artery present in one patient in PIH group. All morphometric parameters of placenta weight, volume, diameter, thickness, no. of cotyledons were reduced. Histological findings were cytotrophoblastic cellular proliferation, syncitial knot formation, fibrin plaque formation. In 20 percent cases, villi were hypovascular. The hypovascular villi have abundance of syncitial knots, usually lack vasculosyncitial membrane and increased stromal collagen. Conclusion: PIH adversely affect both morphology and histology of placenta. Keywords: morphology, histology, placenta, hypersensitive & mothers.