Search

Objective: To carry out a clinical and morphological analysis of 6 cases of placental mesenchymal dysplasia (PMD) that is not associated with Beckwith-Wiedemann syndrome., Material and Methods: Medical records, placental macroscopic and microscopic changes, histochemical (MSB staining) and immunohistochemical studies of placental tissue with antibodies against p57, CD34, smooth muscle actin, desmin, and Ki-67 were analyzed., Results: Vascular anomalies in the chorionic plate and stem villi, the increased size and edema of the stem villi during normal formation of the terminal branches of the villous tree, the lack of proliferation of villous trophoblast were the typical signs of PMD and were noted in all cases. Comparison of the results of ultrasonography with the morphological pattern of the disease suggested that there were ultrasound signs that were typical of PMD. The characteristics of the course and outcomes of pregnancy in PMD were given. The features of morphological changes in the presence of PMD concurrent with preeclampsia were found. Significant variability in p57 expression in PMD was shown and variants of changes given. There were no substantial features of the expression of desmin and smooth muscle actin in PMD., Conclusion: MDP has typical morphological and ultrasound signs. The significant variability in the levels of chorionic gonadotropin and alpha-fetoprotein and in the expression of p57 does not allow their use in the differential diagnosis of PMD. The high incidence of thrombotic events in the intervillous space and fetal vessels, as well as intrauterine growth restriction, intrauterine hypoxia, and an impaired neonatal adaptation period in PMD should be taken into account when determining the management tactics for female patients and newborns.

Objective: to investigate the structural and pathogenetic features of pathological placental attachment in the scar after cesarean section., Material and Methods: The investigators explored 12 uteri; 11 of which were removed with placentas at 9 to 38 weeks' gestation (one in the first trimester, three at 18-22 weeks, two at 32-35 weeks, and five at 37-38 weeks); one uterus was removed after an artificial abortion at 12 weeks' gestation in the scar, as well as the scars excised in the first trimester in non-developing (n=4) and progressive (n=2) pregnancies. For histological examination, fragments of the full-thickness uterine wall were taken from the placental bed in different areas. The sections were stained for fibrin with hematoxylin and eosin, van Gieson stain, and the Martius scarlet/blue (MSB) technique. Decidual tissue, trophoblast, vascular component, and smooth muscle tissue were identified by an immunohistochemical assay using antibodies to vimentin, pan-cytokeratin, vascular endothelium (СD31), and smooth muscle actin., Results: In most cases, placental localization in the scar after cesarean section was accompanied by abnormal placental attachment: almost always placenta accreta, less frequently in combination with its ingrowth (placenta accreta/increta). The morphological substrate of placenta increta was a change in the content and ratio of normal histological components in the uterine wall, such as the mucosa, smooth muscle tissue, and vessels (the absence or thinning of decidual tissue and the myometrium, as well as its cicatricial changes). The structural criterion for placenta increta was necrosis of the walls of the large veins in the myometrium due to the replacement of their intermediate trophoblast and fibrin and to the destruction of vessel walls, leading to prolapse of the chorionic villi into the veins., Conclusion: In most cases, placental localization in the scar after cesarean section is accompanied by abnormal placental attachment: placenta accreta, less frequently in combination with its ingrowth (placenta accreta/increta).

Objective: to compare the clinical and morphological parallels of the mother-placenta-fetus system in diffuse toxic goiter (DTG) through current morphological examinations., Subjects and Methods: Sixty-five women whose pregnancy occurred with DTG were examined using both clinical and morphological studies (light, scanning electron, and atomic-force microscopies and macro- and microelement analysis); the placenta and uterus were investigated., Results: Destructive changes and microrelief impairment, resulting from circulatory disorders (ischemia) and hemic hypoxia, were observed in the presence of DTG during pregnancy. Abnormal placental immaturity developed; the number of terminal villi decreased; sclerosis occurred. The magnitude of changes showed up to a greater extent in the myometrium, umbilical cord, and placenta of women, whose pregnancy occurred with DTG, and in patients with disease recurrence. In preeclampsia, plethora, stasis, and thrombosis were added to circulatory disorders., Conclusion: Not only the diagnosis itself of DTG, but also the type of its course and the pattern of obstetric disease, primarily preeclampsia, affect the state of structural components of the uteroplacental unit.

Objective: To investigate the clinical and morphological features of uteroplacental blood flow during pregnancy in severe gestosis., Subjects and Methods: One hundred and twenty-five patients with severe gestosis were examined. Scanning probe and electron microscopy with macro- and microelement analysis and transmission microscopy were used to study their placentas, umbilical cords, endometrium, myometrium, and maternal blood in severe gestosis., Results: It is shown that circulatory disorders in the structural components of the examined tissues and organs, as well as changes in cytoarchitectonics and red blood cell functional properties may be a component of the trigger of disseminated intravascular coagulation, followed by impaired maternal and fetal vital activity., Conclusion: The investigation of the pathomorphological features of the microcirculatory bed in the mother-placenta-fetus system in gestosis has shown that possible methods of their correction should be further sought.

The paper gives the results of a morphological study of 13 placentas from patients with rare autoimmune polyglandular syndrome and adrenal insufficiency, a disease history of 2 to 14 years, receiving corticosteroid replacement therapy. All pregnancies were full-term; labors were term surgical. The clinical and morphological associations suggest the placental alterations characteristic of diabetes mellitus, autoimmune diseases, uteroplacental and placentofetal ischemia.

One hundred and twenty-five women with incomplete pregnancy in the presence of severe gestosis were examined. The placenta of women receiving 6% hydroxyethyl starch showed a compensatory plethora of villous chorion, stabilization of wall structures in the capillaries and red blood cell membranes, which contributed to the normalization of fetal oxygen homeostasis. In the female myometrium, the capillary lumen displayed starch fibers that stabilized the capillary wall, promoting the stabilization of the shape of vessels, and better circulation as a plethora.

In maternal thyroid diseases, the placenta shows an increase in complications during pregnancy. There are signs of lesions as alterations, focal sclerosis, and fibrinoid necrosis. There is also a circulatory disorder as plethora and thrombosis. Progression in these changes correlates with the cases of miscarriage and other pathology in the obstetric history. The concurrence of obstetric and endocrine diseases increases the risk of pregnancy, labor, and delivery complications in different maternal thyroid diseases.

Uteroplacental relationships were studied in women with and without hypothyroidism, by applying electron, atomic force, and scanning electron microscopies, which enables one to gain more insight into morphometric characteristics. Moreover, not only fixed, but also native materials were used, which brings the studies to a live object and opens up new avenues for rapid diagnosis. The use of gross and trace analysis allows the biochemical parameters of the structure of uterine and placental tissues to be studied for an additional diagnosis and development of treatment options.

The authors made a clinicoanatomic analysis of fetal death in a 32-year-old diabetic gravida at 34-35 weeks gestational age. Fetal autopsy identified the characteristic signs of fetopathy: macrosomy, cardiomegaly, hepatomegaly, and brain weight reduction. Histological analysis revealed minute foci of leukomalacia with glial proliferation in the cerebral hemispheres; adipose and hyaline drop degeneration of cardiomyocytes in the heart, that of hepatocytes in the liver, the proximal renal tubular epithelial cells; hemorrhages in the respiratory portions of the lung. The pancreas displayed inflammation foci, hypertrophy and hyperplasia of the islets of Langerhans. Immunohistochemical studies identified cells with enlarged nuclei among the beta and alpha-cells. The placenta showed a large mass with pronounced changes. It has been demonstrated that steroid diabetes may lead to the development of diabetic fetopathy and placental changes, which are typical of maternal diabetes.

Iron-deficiency anemia in pregnant females negatively affects pregnancy, delivery, neonatal infants. Anemia-caused placental changes found during pregnancy are characterized by imbalance between the processes of adaptation and dysadaptation in response to the developed hypoxia in the pregnant-placenta-fetus system and placental tissue ischemia. When iron-deficiency anemia had developed before pregnancy, placental morphological changes show the signs of chronic placental insufficiency. The developed therapy for anaemia with Ferro-Folgama corrects all the elements of the pregnant-placenta-fetus system.

Impaired microcirculation with evolving sludge phenomenon and thrombosis underlie placental changes in maternal thyroid disease. Capillary blood circulatory defect is largely due to villous immaturity. Placental tissue ischemia gives rise to fibrinoid, sclerosis, and alternative processes. Dysadaptive changes are mostly observed in thyrotoxicosis and hypothyroidism. Adaptive processes evolving at the ultrastructural level are best pronounced in euthyroid goiter.

Studies of membrane receptor system in patients with insulin-dependent diabetes mellitus revealed that insulin resistance in pregnant patients with type I diabetes is caused by disordered cellular sensitivity to threshold physiological and submaximal insulin doses, whereas the maximal doses of the hormone normalize glucose consumption by the cells. High insulin doses intensify lipid peroxidation, normalize the status of membranous proteins, reduce the number of thiol groups, reduce AOA level in membranes, and, hence, reduce membranous capacity to bind active peroxide radicals. Structural and functional changes in red cell membranes are associated with reduced affinity of insulin receptors, reduction in the number of insulin-binding sites in membranes, this disordering intracellular effects of insulin.

A dynamic follow-up of 79 pregnant patients with insulin-dependent diabetes mellitus was carried out. Specific fetoplacental hormonal profiles were detected and analyzed in complex with glycemic levels, this permitting the authors obtain new prognostic criteria of fetal and newborn viability. The results helped optimize the policy of following up such patients and the developed prediction regulations allowed preventive measures aimed at improvement of the future baby health status to be carried out before clinical manifestation of fetal intrauterine suffering.

Investigation of the insulin-binding activity of insulin receptors (IR) in insulin treated pregnant women with insulin dependent diabetes mellitus with different requirement in insulin has shown that insulin-dependent diabetes in pregnant women in characterized by heterogeneity. Insulin therapy gets to normal the activity of insulin receptors in patients with diabetes mellitus with an increased affinity to IR, and causes no increase in the level of IR in patients in whom it was not raised. Insulin-binding activity in the latter may be associated with metabolic derangement caused by insulin insufficiency.