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  • Title: Placental morphometrical and histopathology changes in the different clinical presentations of hypertensive syndromes in pregnancy.
    Author: Corrêa RR, Gilio DB, Cavellani CL, Paschoini MC, Oliveira FA, Peres LC, Reis MA, Teixeira VP, Castro EC.
    Journal: Arch Gynecol Obstet; 2008 Mar; 277(3):201-6. PubMed ID: 17786461.
    Abstract:
    OBJECTIVE: Even though there are clinical studies emphasizing the diagnosis and the perinatal intercurrent diseases of the Hypertensive Syndromes in Pregnancy, few of these studies establish the clinical forms of the specific hypertensive syndromes with the associated morphological placental alterations. The lack of studies on placental morphology and the etiopathogenesis of the different clinical standards for HSP, together with the need to objectively characterize these morphological placental lesions justify this study. STUDY DESIGN: A retrospective study was carried out with 91 placentas examined throughout the period from 2000 to 2003. All placentas from patients presenting HSP in this period were included in the study. These were classified according to features well established by the literature such as laboratory and clinical criteria into: gestational hypertension (GH), chronic hypertension (CH), pre-eclampsia (PE) and pre-eclampsia superimposed on chronic hypertension (PSCH). RESULTS: The number of knots presented a positive correlation with the length of time and severity of the hypertension during gestation (Spearman correlation: 0.253; P = 0.0158). The fibrin deposit was greater in all HSP groups but the pattern of distribution changes in the most severe cases from perivillous to intravillous as in the PSCH group (P = 0.002). There was no statistically significant difference in the area of the stem vessel walls among the groups. The cases with PE and CH presented a larger number of terminal villi vessels (P < 0.001). CONCLUSION: This report suggests, that although they could be different types of hypertension or an evaluation of the same disease, the final pathway that leads to microscopic lesions in the placenta is the same, with only different intensity due to the severity of the disease.
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