Abstract:
Objective: Iron deficiency anemia (IDA) in pregnancy is challenging, inducing a systemic pathological process in women's bodies. In this context, impaired protein metabolism, decreased respiratory enzyme activity, limitation of cells' proliferative potential, oxidative stress, hypoxia, and endothelial dysfunction affect the "mother-placenta-fetal" system. However, several features of this pathogenetic cascade, including the spread of extravillous cytotrophoblasts (ECT), are yet to be investigated. This research aimed to study the immunohistochemical features and quantitative indicators of ECT spread throughout the uteroplacental bed (UPB) in IDA at 37–40-week gestation.
Conclusions: It is established that, during gestation with IDA, a deepening of CT invasion in the structure of the UPB, an increase in the lining distance of the endothelium-replacing CT in the artery walls, and consequently, a dilatation of spiral and radial arteries takes place in the uterus of pregnant women. However, the invasive ability and synthetic activity of the CT and as a result, the adequacy of the gestational transformation of UPB structures are affected by the hypoxia and depend on the degree of IDA of pregnant women.
