MATERIALS AND METHODS: This is a retrospective, cross-sectional study from January 1, 2015 to December 31, 2015. A total of 30 placentae comprised of 15 hypertensive and 15 normotensive cases were assessed. VEGF expression in placenta was assessed by immunohistochemistry, and the number of syncytial knots was counted.
RESULTS: Our study showed an increased syncytial knot formation in the placenta of hypertensive mothers. VEGF expression was seen in syncytiotrophoblasts of 14 of the hypertensive cases (14/15, 93.3%), while only two of the normotensive cases were positive (2/15, 13.3%). There were no statistically significant differences in VEGF expression in other placenta cells, that is, cytotrophoblasts (P = 1.0), decidual cells (0.1394), maternal endothelial cells (0.5977), and fetal endothelial cells (P = 1.0).
CONCLUSIONS: This study showed an increased number of syncytial knots is a consistent histological finding in the placenta of patient with HDP. VEGF expression was significantly increased in syncytiotrophoblasts in placenta of hypertensive group, and it could be used as a biomarker for hypertension.
MATERIALS AND METHODS: This study evaluated the inter-observer variability in diagnosis of CHM, PHM and HA according to defined histologic criteria. Ninety abortus conception specimens were reviewed. Representative haematoxylin and eosin-stained slides were assigned independently to two pathologists who were asked to make a diagnosis of CHM, PHM or HA, and provide a report of the identified diagnostic histological criteria. Kappa value was calculated for the inter-observer agreement.
RESULTS: There was a total of 36.7% disagreement between two pathologists (K = 0.403, Strength of Agreement = moderate), of which 24.4% and 12.2%, were differentiating PHM from CHM and PHM from HA, respectively. Among defined diagnostic histological criteria, the highest rate of agreement was observed in the identification of cistern formation and hydropic changes (K = 0.746 and 0.686 respectively, Strength of Agreement = substantial).
CONCLUSION: There was moderate to substantial agreement rate between two pathologists in identification of two essential histologic criteria for diagnosis of molar pregnancies i.e. "hydropic change" and "trophoblastic proliferation".
METHODS: This was a cross-sectional study consisted of 21 pregnant women with hypertension and 23 without hypertension. The gestational age ranged from 28 to 39 weeks (hypertensive) and 32 to 40 weeks (normotensive). The paraffin embedded formalin fixed placenta tissue blocks were retrieved from the pathology archives. Endocan immunohistochemistry was performed on tissue sections of full thickness and maternal surface of the placenta. The endocan expression was determined in fetal endothelial cells, maternal endothelial cells, cytotrophoblasts, syncytiotrophoblasts and decidual cells. The differences in endocan expression in placenta between hypertensive and normotensive subjects were evaluated by Pearson chi-square test and t-test were used in the statistical analysis.
RESULTS: The endocan expression was significantly higher in fetal endothelial cells (P
Methods: This cross-sectional study included 50 patients with late-onset (≥ 32 weeks gestation) PE. Maternal serum was obtained before delivery, and placentas were obtained immediately after delivery. SEMA3B and CUL1 levels were evaluated by ELISA. Results were statistically analysed by Spearman correlation test, with a P < 0.05 considered statistically significant.
Results: While elevated serum SEMA3B levels significantly correlated with increased placental SEMA3B levels in late-onset PE (R = 0.620, P = 0.000), alteration of serum CUL1 levels did not correlate with alteration of placental CUL1.
Conclusion: Alteration of circulating maternal SEMA3B, but not CUL1, levels can potentially be used to monitor PE progression during pregnancy.