The purpose of the study is to establish quantitative parameters of cell proliferation and apoptosis in the trophoblast of the chorionic villi in chorioamnionitis and basal deciduitis combined with iron-deficiency anemia in gravidas by means of immunohistochemical method. Materials and methods. 198 placentas were examined. The immunohistochemical procedure was performed using primary antibodies against Ki-67 and Bax antigen with imaging by a polymer system with diaminobenzidine dye. The number of Ki-67-positive nuclei of the chorionic villi trophoblast was counted, and for the Bax antigen, the optical density of the immunohistochemical staining was measured by means of microdensitometric method. Comparison of differences in mean trends was performed using the odd Student’s two-sided t-test (p≤0.05). Results and discussion. The number of Ki-67-positive trophoblast nuclei in acute chorioamnionitis with iron-deficiency anemia in gravidas was 56±3.8 ‰, and the relative units of optical density of immunohistochemical staining for protein Bax – 0.234±0.0012, in chronic – 59±3.6 ‰ and 0.2, respectively. The number of Ki-67-positive nuclei of the chorionic villi trophoblast was counted. Placentas with acute as well as chronic chorioamnionitis and basal deciduitis showed even higher averages (p <0.001). In acute basal deciduitis in anemia, the number of Ki-67-positive trophoblast nuclei was 56±3.2 ‰, the average optical density of immunohistochemical staining for protein Bax – 0.236±0.0016, in chronic – 57±3.7 and 0.249±0.0015, respectively. It should be noted that in chronic chorioamnionitis and basal deciduitis, these rates were higher than in acute. With the same regularity the average indicators of optical density of immunohistochemical staining on protein Bax in a trophoblast of chorionic villi at comorbid iron-deficiency anemia concerning an inflammation without anemia increase. We have shown that proliferative activity in iron-deficiency anemia varies with gestational age and placental prematurity, but iron-deficiency anemia in gravidas and chorionic tree maturation both individually and in combination lead to the intensification of these processes. We obtained a justification for the arithmetic mean thickness and volume of the placenta relative to observations of placenta with inflammation without anemia in this comorbid pathology. Conclusion. Iron-deficiency anemia in gravidas leads to the intensification of proliferative processes and Bax-dependent apoptosis in the trophoblast of the chorionic villi of the placenta relative to the placenta from physiological pregnancy. In acute as well as in chronic chorioamnionitis and basal deciduitis, the proliferative activity and apoptotic processes in the trophoblast of the chorionic villi of the placenta increase, while comorbid iron-deficiency anemia in gravidas intensifies only the processes of Bax-dependent apoptosis
Keywords: inflammation of the placenta, trophoblast of the chorionic villi, anemia
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