PURPOSE: To evaluate the mechanisms involved in the etiology of the basement membrane of the amniotic epithelium (BMAE) thickening in patients with hypertensive syndromes in pregnancy (HSP). METHODS: Eighty placentas from patients presenting HSP were morphologically examined in staining through hematoxylin-eosin and periodic acid Schiff method. Placental morphological changes were classified into: diagnostic of low placental blood flow, characterized by a larger number of syncytial knots, fibrin deposits, and a larger number of vessels in terminal villi; and placentas with inflammation that presented inflammatory infiltrate in membranes or placental villi. Measurements of thickness were made with an automatic image analyzing software. RESULTS: BMAE thickness was higher in the group with HSP, particularly in cases with gestational hypertension and pre-eclampsia superimposed on chronic hypertension (PSCH). In the placentas of the HSP group, the thickness of the BMAE was higher in cases with inflammatory infiltrate. There was a positive and significant correlation between the BMAE thickness and the thickness of the amniotic epithelium. The BMAE thickening areas were associated with hyperplasia and edema of the amniotic epithelium. CONCLUSIONS: BMAE thickening in cases with HSP is more evident when there is an interaction between the severe effects of uteroplacental hypoxia, with consequent death and remodelling of the amniotic epithelium cells, as in PSCH, with local inflammatory processes that make this thickening much more evident.
PURPOSE: To evaluate the mechanisms involved in the etiology of the basement membrane of the amniotic epithelium (BMAE) thickening in patients with hypertensive syndromes in pregnancy (HSP). METHODS: Eighty placentas from patients presenting HSP were morphologically examined in staining through hematoxylin-eosin and periodic acid Schiff method. Placental morphological changes were classified into: diagnostic of low placental blood flow, characterized by a larger number of syncytial knots, fibrin deposits, and a larger number of vessels in terminal villi; and placentas with inflammation that presented inflammatory infiltrate in membranes or placental villi. Measurements of thickness were made with an automatic image analyzing software. RESULTS: BMAE thickness was higher in the group with HSP, particularly in cases with gestational hypertension and pre-eclampsia superimposed on chronic hypertension (PSCH). In the placentas of the HSP group, the thickness of the BMAE was higher in cases with inflammatory infiltrate. There was a positive and significant correlation between the BMAE thickness and the thickness of the amniotic epithelium. The BMAE thickening areas were associated with hyperplasia and edema of the amniotic epithelium. CONCLUSIONS: BMAE thickening in cases with HSP is more evident when there is an interaction between the severe effects of uteroplacental hypoxia, with consequent death and remodelling of the amniotic epithelium cells, as in PSCH, with local inflammatory processes that make this thickening much more evident.