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New advances on placental hydrops and related villous lymphatics.

Identifieur interne : 000C76 ( PubMed/Corpus ); précédent : 000C75; suivant : 000C77

New advances on placental hydrops and related villous lymphatics.

Auteurs : L. Roncati ; G. Barbolini ; T. Pusiol ; F. Piscioli ; A. Maiorana

Source :

RBID : pubmed:26333212

English descriptors

Abstract

Fetoplacental hydrops is the final stage of several pathological conditions in which the placenta and umbilical cord become edematous and the fetus develops an anasarcatic state characterized by an excessive accumulation of extravascular fluids in at least two serous cavities of the body. It is a common histological finding of stillbirth, characterized by the appearance of markedly edematous villi, suggesting an increased interstitial fluid accumulation. The recent improved knowledge of lymphangiogenesis and the availability of monoclonal antibodies selectively labeling lymphatic endothelium lead to the hypothesis that villous edema is essentially a lymphedema from defective lymphatic function following inadequate villous blood circulation. Lymphedema is a morphologic phenotype found by our research group in a 24-case series of stillbirths from different morbid conditions such as chromosomal aberrations, congenital malformations, inherited hemoglobinopathies, and prolonged perinatal severe anoxia. Unlike long-lived organs, the placenta is devoid of innervation by the autonomic nervous system; therefore, the vascular tone regulation and the peripheral perfusion are modulated by the expression of the angiotensin converting enzyme (ACE) in the vascular endothelia. This finding may suggest to the clinician to search for a more suitable therapy in case of mother's hypertension during pregnancy.

PubMed: 26333212

Links to Exploration step

pubmed:26333212

Le document en format XML

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<title xml:lang="en">New advances on placental hydrops and related villous lymphatics.</title>
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<name sortKey="Roncati, L" sort="Roncati, L" uniqKey="Roncati L" first="L" last="Roncati">L. Roncati</name>
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<name sortKey="Barbolini, G" sort="Barbolini, G" uniqKey="Barbolini G" first="G" last="Barbolini">G. Barbolini</name>
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<name sortKey="Pusiol, T" sort="Pusiol, T" uniqKey="Pusiol T" first="T" last="Pusiol">T. Pusiol</name>
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<name sortKey="Piscioli, F" sort="Piscioli, F" uniqKey="Piscioli F" first="F" last="Piscioli">F. Piscioli</name>
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<name sortKey="Maiorana, A" sort="Maiorana, A" uniqKey="Maiorana A" first="A" last="Maiorana">A. Maiorana</name>
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<div type="abstract" xml:lang="en">Fetoplacental hydrops is the final stage of several pathological conditions in which the placenta and umbilical cord become edematous and the fetus develops an anasarcatic state characterized by an excessive accumulation of extravascular fluids in at least two serous cavities of the body. It is a common histological finding of stillbirth, characterized by the appearance of markedly edematous villi, suggesting an increased interstitial fluid accumulation. The recent improved knowledge of lymphangiogenesis and the availability of monoclonal antibodies selectively labeling lymphatic endothelium lead to the hypothesis that villous edema is essentially a lymphedema from defective lymphatic function following inadequate villous blood circulation. Lymphedema is a morphologic phenotype found by our research group in a 24-case series of stillbirths from different morbid conditions such as chromosomal aberrations, congenital malformations, inherited hemoglobinopathies, and prolonged perinatal severe anoxia. Unlike long-lived organs, the placenta is devoid of innervation by the autonomic nervous system; therefore, the vascular tone regulation and the peripheral perfusion are modulated by the expression of the angiotensin converting enzyme (ACE) in the vascular endothelia. This finding may suggest to the clinician to search for a more suitable therapy in case of mother's hypertension during pregnancy.</div>
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<AbstractText>Fetoplacental hydrops is the final stage of several pathological conditions in which the placenta and umbilical cord become edematous and the fetus develops an anasarcatic state characterized by an excessive accumulation of extravascular fluids in at least two serous cavities of the body. It is a common histological finding of stillbirth, characterized by the appearance of markedly edematous villi, suggesting an increased interstitial fluid accumulation. The recent improved knowledge of lymphangiogenesis and the availability of monoclonal antibodies selectively labeling lymphatic endothelium lead to the hypothesis that villous edema is essentially a lymphedema from defective lymphatic function following inadequate villous blood circulation. Lymphedema is a morphologic phenotype found by our research group in a 24-case series of stillbirths from different morbid conditions such as chromosomal aberrations, congenital malformations, inherited hemoglobinopathies, and prolonged perinatal severe anoxia. Unlike long-lived organs, the placenta is devoid of innervation by the autonomic nervous system; therefore, the vascular tone regulation and the peripheral perfusion are modulated by the expression of the angiotensin converting enzyme (ACE) in the vascular endothelia. This finding may suggest to the clinician to search for a more suitable therapy in case of mother's hypertension during pregnancy.</AbstractText>
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