Özet:

Objectives: The placenta plays critical roles during pregnancy and is essential for fetal growth and development. Its functions are determined by the ultrastructure of the placental barrier that is an important feature to maintain the exchange surface area between the fetus and the mother. Gestational diabetes mellitus (GDM) comprises unfit conditions for embryonic and feto-placental development, and may result in placental abnormalities. The aim of this study was to detect the ultrastructural changes of the placenta in women with GDM. Methods: The placentas of 10 women with GDM without pregestational diabetics, hypertension and chronic diseases and 10 controls were studied. Six control women were delivered vaginally and the remaining cases by caesarian section at a gestational age of 36 to 39 weeks. Placental samples were measured for their thickness and prepared for light and transmission electron microscopy study. Results: Light microscopic study of the control placentas showed numerous densely packed microvilli with syncytial knots and thin-walled blood vessels and wide intervillous spaces. The placentas of GDM cases showed reduced number of microvilli with syncytial knots, thick-walled vessels, edematous spaces, areas of fibrosis and perivillous fibrinoid degeneration. Electron microscopic study of the placentas of the control women showed terminal villi with a thick layer of syncytiotrophoblasts (Sy) with a lot of regular cylindrical microvilli and a thin layer of cytotrophoblasts (Cy). There were some endoplasmic reticulum cisternae besides few mitochondria. The underlying villus core was harboring fetal capillaries lined with flat endothelial cells and thin basement membrane. There was no fibrosis or edema. In the placenta of GDM women, there was hypertrophy of Cy with atrophy of Sy with multiple vacuoles and areas for glycogen storage. The subtrophoblastic membrane was thick and the microvilli were scarce. The villous core showed congested capillaries, stromal macrophages, edematous spaces, glycogen storage areas and fibrosis. Conclusion: All the changes in placentas of gestational diabetes were attributed to associated hypoxia and oxidative stress due to decreased uteroplacental flow that was aggravated by the thick placental barrier and the presence of edema, fibrosis and glycogenstorage areas that increased the distance of transfer between the fetus and mother.

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