MORPHOLOGICAL AND ULTRASTRUCTURAL ALTERATIONS OF THE PLACENTA IN PREGNANT WOMEN WITH HYPERHOMOCYSTEINEMIA

INTERNATIONAL CONFERENCE PEDAGOGICAL REFORMS AND THEIR SOLUTIONS VOLUME 12, ISSUE 02, 2025 152 MORPHOLOGICAL AND ULTRASTRUCTURAL ALTERATIONS OF THE PLACENTA IN PREGNANT WOMEN WITH HYPERHOMOCYSTEINEMIA Akbarova Dildora Abduvaliyevna Andijan State Medical Institute, Uzbekistan Introduction: Hyperhomocysteinemia is a metabolic disorder associated with endothelial dysfunction and microcirculatory disturbances that can severely affect placental development. This study investigates morphological and ultrastructural changes in the placenta of women with elevated plasma homocysteine levels, aiming to identify histopathological markers of placental insufficiency and fetal hypoxia. Materials and Methods: The study included thirty-two women aged 21–39 years: sixteen with confirmed hyperhomocysteinemia and sixteen healthy pregnant women as controls. Blood samples were analyzed for homocysteine and folate levels. Placental biopsies were taken from the central and marginal zones immediately after delivery. Light microscopy (hematoxylin-eosin and van Gieson staining) and transmission electron microscopy (TEM) were used to assess villous morphology and ultrastructural organization. Morphometric evaluation included measurement of villous diameter, basement membrane thickness, and mitochondrial density in syncytiotrophoblast cells. Results: In the hyperhomocysteinemia group, the placentas exhibited marked structural and ultrastructural abnormalities. Light microscopy revealed irregular villous contours, stromal edema, and increased perivillous fibrin deposition. Vascular lumina were narrowed, and the endothelial lining appeared swollen and vacuolated. TEM analysis demonstrated significant ultrastructural changes: mitochondrial degeneration, disruption of microvilli on the syncytiotrophoblast surface, and accumulation of electron-dense deposits in the basal lamina. The basement membrane was thickened by 32% compared to the control (p < 0.01), and the number of mitochondria per µm² decreased by 27% (p < 0.05), indicating impaired cellular metabolism. Discussion: The combination of morphological and ultrastructural findings confirms that hyperhomocysteinemia leads to chronic ischemic and hypoxic alterations in placental tissue. Elevated homocysteine disrupts endothelial function and reduces nitric oxide bioavailability, leading to impaired fetoplacental circulation. The ultrastructural degeneration of mitochondria and syncytiotrophoblast microvilli reflects decreased metabolic activity and reduced transport efficiency, which can explain the frequent occurrence of intrauterine growth restriction and preeclampsia in these patients. The observed fibrinoid necrosis and vascular remodeling are consistent with reports by Alvino et al. (2008) and Raghunath et al. (2019), who described similar placental pathology in hyperhomocysteinemic pregnancies. INTERNATIONAL CONFERENCE PEDAGOGICAL REFORMS AND THEIR SOLUTIONS VOLUME 12, ISSUE 02, 2025 153 Conclusion: Hyperhomocysteinemia induces profound morphological and ultrastructural changes in the placenta, characterized by villous immaturity, mitochondrial degradation, endothelial swelling, and thickening of the basal membrane. These alterations impair placental perfusion and oxygen exchange, posing a serious risk to fetal development. Morphological and ultrastructural evaluation of placental tissue can serve as a valuable diagnostic tool for identifying pregnancies at risk and guiding early therapeutic intervention. References: 1. Steegers-Theunissen RP, Twigt J, Pestinger V, Sinclair KD. The periconceptional period, reproduction and long-term health of offspring: the importance of one-carbon metabolism. Hum Reprod Update. 2013;19(6):640–655. 2. Alvino G, Cozzi V, Radaelli T, Cetin I. Placental histology and ultrastructure in hyperhomocysteinemic pregnancies. Placenta. 2008;29(8):830–835. 3. Raghunath M, Venkatesh S, Balasubramanian K. Placental pathology and oxidative stress in pregnancies with maternal hyperhomocysteinemia. J Obstet Gynaecol Res. 2019;45(4):867– 875. 4. Di Simone N, Castellani R, D’Alessio MC, Caruso A. Homocysteine induces trophoblast cell apoptosis: a potential mechanism of placental injury in preeclampsia. Am J Pathol. 2003;162(2):537–544.