Objective: To investigate proliferative, apoptotic, and antiapoptotic activity of placental trophoblast in pregnancies complicated with idiopathic intrauterine growth retardation (IUGR).
Methods: Study group included data and placentas from 52 normal singleton term pregnancies with idiopathic IUGR. Records and placentas from 69 singleton pregnancies with normal fetal growth served as a control group. IUGR was defined by birth weight less than 10th percentile of standard values. Children with congenital malformations and those born with the signs of hypoxia, laboratory or clinical signs of preeclampsia or infection, children born to anemic mothers and those born from pregnancies with an increased coagulation system activity were excluded.
Results: There was no statistically significant difference in the cytotrophoblast proliferation index value (Z = 0.24; P = 0.553), trophoblast expression of the Bcl-2 antiapoptotic factor (Z = 0.47; P = 0.634), and trophoblast apoptotic index (Z = 0.51; P = 0.613) between the idiopathic IUGR and control group.
Conclusion: The proliferative and apoptotic events in the trophoblast of placentas with idiopathic IUGR did not differ from physiologic ones. Study results suggest the IUGR syndrome to have no uniform etiology or even underlying pathophysiology that would determine the possible fetal risk and subsequent long-term consequences for fetal health and life. This imposes the need of a more precise definition and unambiguous distinction between the idiopathic and other forms of IUGR.
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http://dx.doi.org/10.3109/14767058.2010.526158 | DOI Listing |
Cureus
October 2024
Anatomy and Histology, College of Medicine, University of Duhok, Duhok, IRQ.
Background Idiopathic intrauterine growth restriction (IUGR) is a condition in which there is no discernible cause, such as problems with the mother's health, and the fetus does not grow to the expected size for its gestational age. In cases of IUGR, the placental trophoblast exhibits reduced invasiveness, leading to a less extensive invasion of uterine spiral arteries and increased resistance in the uteroplacental circulation. The consequences of these early histopathological alterations are long-lasting, resulting in compromised blood flow to the placenta and diminished transport of nutrients and oxygen from the mother to the fetus.
View Article and Find Full Text PDFJ Obstet Gynaecol Res
December 2024
Division of Perinatology, Department of Obstetrics and Gynecology, Turkish Ministry of Health Ankara City Hospital, University of Health Sciences, Ankara, Turkey.
Objectives: To evaluate the effect of idiopathic thrombocytopenic purpura (ITP) on pregnancies and the role of the delta hemoglobin indices in the evaluation of treatment effectiveness.
Methods: This case-control study was conducted with 23 ITP and 115 low-risk pregnancies. Obstetric outcomes (fetal growth retardation (FGR), preterm delivery) and neonatal outcomes (weights, APGAR scores, NICU admissions, thrombocytopenia) were recorded.
Front Endocrinol (Lausanne)
April 2024
Research Area for Innovative Therapies in Endocrinopathies, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.
Int J Mol Sci
January 2024
Department of Anatomy and Cell Biology, School of Medicine and Health Sciences, George Washington University, 2300 I Street N.W., Washington, DC 20037, USA.
We report the case of a four-year-old male patient with a complex medical history born prematurely as the result of intrauterine growth restriction due to placental insufficiency. His clinical manifestations included severe neurodevelopmental deficits, global developmental delay, Pierre-Robin sequence, and intractable epilepsy with both generalized and focal features. The proband's low levels of citrulline and lactic acidosis provoked by administration of Depakoke were evocative of a mitochondrial etiology.
View Article and Find Full Text PDFJ Mother Child
June 2023
Department of Obstetrics and Gynaecology, King George's Medical University, Lucknow.
Background: Circulating endothelial progenitor cells (EPCs) may be necessary throughout pregnancy by ensuring proper placentation and embryonic growth. The lack of standardized EPC quantification techniques has prevented conclusive proof of an increase in EPC during pregnancy.
Objectives: The purpose of this study was to determine whether EPC levels change for healthy and idiopathic fetal growth restriction (FGR) pregnancies.
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