Original articleClinical correlations of patterns of placental pathology in preterm pre-eclampsia
References (28)
- et al.
Serum complement values (C3 and C4) to differentiate between systemic lupus activity and preeclampsia
American Journal of Medicine
(1986) - et al.
Humoral immunity in normal and complicated pregnancy
European Journal of Obstetrics Gynecology and Reproductive Biology
(1985) - et al.
Acute atherosis in preeclampsia: maternal determinants and fetal outcome in the presence of the lesion
American Journal of Obstetrics and Gynecology
(1987) - et al.
Immune complexes in preeclampsia and normal pregnancy
American Journal of Obstetrics and Gynecology
(1985) - et al.
Clinical and pathological aspects of recurrent placental villitis
Human Pathology
(1985) - et al.
The placental bed biopsy: review from three European centers
American Journal of Obstetrics and Gynecology
(1986) - et al.
Intrauterine growth retardation in infants of less than 32 weeks gestational age: Associated placental pathology
American Journal of Obstetrics and Gynecology
(1995) - et al.
Placental pathology of preterm preeclampsia
American Journal of Obstetrics and Gynecology
(1995) - et al.
Placental haemorrhagic endovasculitis: Risk factors and impact on pregnancy outcome
International Journal of Gynecology and Obstetrics
(1984) - et al.
The use of dilute Russell viper venom time for the diagnosis of lupus anticoagulants
Blood
(1986)
The human placental villitides: a review of chronic intrauterine infection
Current Topics in Pathology
Antigenic relationships between placenta and kidney in humans
American Journal of Obstetrics and Gynecology
On the pathogenesis of placental infarcts in preeclampsia
Journal of Obstetrics and Gynaecology of the Commonwealth
Fetal growth retardation and the arteries of the placental bed
British Journal of Obstetrics and Gynecology
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Latent class analysis of placental histopathology: a novel approach to classifying early and late preterm births
2022, American Journal of Obstetrics and GynecologyCitation Excerpt :Various approaches have previously classified PTBs by patterns of histopathologic features. Previous approaches have been based on anticipated groupings of histopathology (eg, inflammatory or vascular impairment) using correlative measures, factor analysis, and predefined groups based on expert opinion.12–15 These methods may presuppose placental pathology groups, miss key histopathologic features and/or lack strong associations with clinical outcomes.
Pregnancy outcomes in correlation with placental histopathology in subsequent pregnancies complicated by preeclampsia
2019, Pregnancy HypertensionCitation Excerpt :Impaired early placentation and dysfunctional trophoblast development leading to defective placental angiogenesis has been one of the primary mechanisms suggested [7,8]. Defective placentation resulting in maternal vascular malperfusion (MVM) and fetal vascular malperfusion (FVM) lesions is more profound as the clinical course of the disease is more severe [9,10]. We recently published that MVM and FVM lesions are independently associated with increased risk for recurrence of preeclampsia [11].
The role of placental malperfusion in the pathogenesis of preeclampsia in dichorionic twin and singleton pregnancies
2018, PlacentaCitation Excerpt :Our main findings are as follows: (1) HDP in dichorionic-twin pregnancies is significantly less likely to be associated with placental MVM pathology and, to a lesser degree, with fetal vascular malperfusion pathology when compared to HDP in singletons; (2) This difference in the rate and severity of MVM pathology was observed in women with either PE or GHTN and remained significant in the subpopulations of women with early onset HDP and in HDP pregnancies complicated by SGA; and (3) These histopathological differences may contribute to the lower rate of prematurity and of SGA observed in the current study in twin pregnancies with HDP compared with singleton pregnancies with HDP. In singleton pregnancies, the pathogenesis of HDP is most commonly attributed to abnormal placentation which subsequently results in chronic uteroplacental hypoperfusion [10–18,27,33,41–43]. In twin gestations, the increased risk for HDP has thus far been attributed to either relative placental hypoperfusion (similar to what is observed in singleton, although the cause for placental hypoperfusion is the increased placenta mass rather than abnormal placentation) or to enhanced abnormal production of antiangiogenic proteins simply due to the greater amount of trophoblast tissue in twin pregnancies [24,25].
Pregnancy and the Kidney
2017, Textbook of Nephro-Endocrinology