Impaired Placentation and Early Pregnancy Loss in Patients with MTHFR Polymorphisms and Type-1 Diabetes Mellitus

A cut‐off value for systemic immune‐inflammation index in the prediction of adverse neonatal outcomes in preterm premature rupture of the membranes

“…Adaptive changes in the maternal immune system during pregnancy and an appropriate maternofetal interaction through the maternal fetal interface are the key elements for favorable obstetric outcomes. 31,32 Appropriate regulation of the intervillous space, which is composed, of superficial decidual epithelium, endothelium of spiral veins, syncytiotrophoblasts of chorionic villi and endovascular trophoblasts covering the tips of spiral arteries is crucial for proper fetal perfusion. [32][33][34] It has been reported that destruction of cellular components of the intervillous space by various molecules/agents named "placental inflammation" leads to obstetric complications and poor neonatal outcomes.…”

“…31,32 Appropriate regulation of the intervillous space, which is composed, of superficial decidual epithelium, endothelium of spiral veins, syncytiotrophoblasts of chorionic villi and endovascular trophoblasts covering the tips of spiral arteries is crucial for proper fetal perfusion. [32][33][34] It has been reported that destruction of cellular components of the intervillous space by various molecules/agents named "placental inflammation" leads to obstetric complications and poor neonatal outcomes. Thus, clinical practice has changed from conservative management protocols to etiology-based approaches in the last decade and management of inflammation has become a new target for physicians who deal with obstetric/neonatal complications.…”

“…Thus, clinical practice has changed from conservative management protocols to etiology-based approaches in the last decade and management of inflammation has become a new target for physicians who deal with obstetric/neonatal complications. [32][33][34] In addition to prematurity, maternal inflammation was also reported to be associated with increased rates of neonatal complications like sepsis, RDS, NEC, intraventricular hemorrhage, cerebral palsy and neonatal death. [9][10][11][12] Maternal inflammation leads to a fetal inflammatory response, resulting in increased levels of cytokines and chemokines in the fetal/placental compartments.…”

The Effect of Asthma Severity on Perinatal Outcomes: A Tertiary Hospital Experience

“…Maternal hypoxemia leading to impaired fetal oxygenation/uteroplacental blood flow, polymorphisms of the beta-2 adrenergic receptors, and possible uterine muscle and vascular hyperreactivity in these patient cohorts were postulated to cause various obstetric complications [7,8,19,20]. Furthermore, excessive inflammatory processes may result in injury to the cellular components of the maternal-fetal interface or intervillous space [21]. The destruction of syncytiotrophoblasts and endovascular trophoblasts causes the release of cellular debris which contains paternal antigens with a potential of stimulating maternal innate and humoral immune systems [21].…”

Comparison of term and preterm labor procalcitonin and leukocyte cell volume, conductivity and light scatter (VCS) parameters in order to demonstrate the impact of inflammation on the triggering mechanisms of preterm uterin contractions

“…The destruction of the cellular components of intervillous space (syncytotrophoblasts, endovascular trophoblasts covering the tips of the spiral arteries, superficial epithelial cells of the decidua, endothelial cells of spiral veins etc) and the entrance of the cell degregades to maternal circulation may induce additional placental inflammatory processes and may stimulate maternal innate and humeral immune systems . PI and related pathological changes may cause various types of obstetrical complications such as miscarriage, preterm delivery, placental membrane rupture, preeclampsia, fetal growth retardation etc . Thus, determination of inflammatory markers has a great importance not to have gestational problems.…”