Understanding decidual vasculopathy and the link to preeclampsia: A review.


Journal

Placenta
ISSN: 1532-3102
Titre abrégé: Placenta
Pays: Netherlands
ID NLM: 8006349

Informations de publication

Date de publication:
08 2020
Historique:
received: 24 04 2020
revised: 02 06 2020
accepted: 25 06 2020
entrez: 15 8 2020
pubmed: 15 8 2020
medline: 3 7 2021
Statut: ppublish

Résumé

Preeclampsia is the archetype of a spectrum of clinical disorders related to abnormal placental development or function, characterized by placental histological lesions. Among those lesions, decidual vasculopathy is a term used to describe lesions of maternal spiral arteries, which are encountered on placental examination in about half of the women with preeclampsia. The morphological features of the lesions include perivascular lymphocytic infiltration, fibrinoid necrosis and foam cell incorporation within the vessel wall. Due to the resemblance of the latter characteristic to atherosclerosis, they are alternatively termed acute atherosis. Decidual vasculopathy correlates with worse maternal and neonatal outcomes, as well as placental pathology. In this article, we review the available literature on decidual vasculopathy and address the pitfalls in histological analysis of the lesions, including the varying definitions of the lesions and sample collection methods. We also discuss the current evidence on the etiology of the lesions and propose a novel hypothesis linking the three etiological pathways to the formation of decidual vasculopathy and, ultimately, the emergence of the heterogeneous group of placental dysfunction disorders, known as the great obstetric syndromes.

Identifiants

pubmed: 32792071
pii: S0143-4004(20)30188-0
doi: 10.1016/j.placenta.2020.06.020
pii:
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

95-100

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.

Auteurs

D U Stevens (DU)

Department of Obstetrics and Gynaecology, Radboud University Medical Center, Nijmegen, the Netherlands. Electronic address: Droima.Stevens@radboudumc.nl.

J A de Nobrega Teixeira (JA)

Department of Obstetrics and Gynaecology, Maastricht University Medical Center+, Maastricht, the Netherlands; School for Oncology and Developmental Biology (GROW), Maastricht University Medical Center+, Maastricht, the Netherlands.

M E A Spaanderman (MEA)

Department of Obstetrics and Gynaecology, Radboud University Medical Center, Nijmegen, the Netherlands; Department of Obstetrics and Gynaecology, Maastricht University Medical Center+, Maastricht, the Netherlands; School for Oncology and Developmental Biology (GROW), Maastricht University Medical Center+, Maastricht, the Netherlands.

J Bulten (J)

Department of Pathology, Radboud University Medical Center, Nijmegen, the Netherlands.

J M G van Vugt (JMG)

Department of Obstetrics and Gynaecology, Radboud University Medical Center, Nijmegen, the Netherlands.

S Al-Nasiry (S)

Department of Obstetrics and Gynaecology, Maastricht University Medical Center+, Maastricht, the Netherlands; School for Oncology and Developmental Biology (GROW), Maastricht University Medical Center+, Maastricht, the Netherlands.

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