Эндокринология и метаболический синдром
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ISSN: 2161-1017
ISSN: 2161-1017
Ahmed TM Elshennawy
Gestational diabetes is the glucose intolerance of varying severity and complicates about 2-4% of pregnancies. While there is a surfeit of associative data that demonstrate the placental adaptive responses to gestational diabetes, the mechanisms at placental level remain elusive. One objective of this study was to investigate various anatomical, histological and some histochemical changes in placenta of gestational diabetes patients with re-evaluation of some mechanisms of placental adaptive responses to gestational diabetes. A second objective was to find whether the placenta adapts to diabetes and ultimately protects the fetus or whether it contributes to the adverse fetal outcome with diabetic pregnancies despite good care of these gestations. Two groups each of 30 placentas were collected at term and post Caesarian Section (CS) deliveries as one group was the control group (control) and the other group was collected from patients with gestational diabetes and were treated with zinc insulin. After morphological data assay, central and peripheral biopsies were processed for histological and histochemical assay. The diabetic placentas showed mild increase in diameter, central thickness and weight. This study confirmed that the villous portion with its corresponding intervillous space is the structural and functional unit of the placenta. Syncytial clumps among peripheral placenta were bigger than those of central placenta of the diabetic group and best examined by Hematoxylin and Eosin stain and to a lower extent by Van Gieson stain for light microscopy. The diabetic placentas showed marked increase of the chorionic villi which appeared more crowded centrally while the villous vasculature was higher peripherally. The increased young, immature and unspecialized villi among the diabetic placentas explained the enhanced fetal hypoxia with subsequent increased neonatal morbidity and mortality. These anatomical, histological and histochemical findings put diabetes in the moderate-high risk factors of vascular placental pathology. Also, placenta was not the primary cause to markedly affect the perinatal morbidity as the placenta showed a good degree of potentiality to adapt with derangements of gestational diabetes. So, the elevated rates of perinatal morbidity and mortality among diabetic deliveries were most probably due to metabolic abnormalities occurred in mother and fetus because of whatever kind of diabetes. Conclusion: Placenta itself is always perfect, innocent and helpful in managing and preventing complications via its endogenous mechanisms. It was necessary histologically to examine several preparations with different and specific measures to obtain detailed picture of the totality of the placenta structure. Lastly, the premium key in gestational diabetes is to apply scientific exogenous measures in harmony and accordance with early diagnosed and strictly controlled endogenous placental measures.