Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2001-6-11
pubmed:abstractText
In spite of active perinatal management, twin-twin transfusion syndrome (TTTS) remains a severe disease with a high risk of neonatal mortality and morbidity. TTTS initially results from an unbalanced blood flow from a donor to a recipient twin. However, its pathogenesis remains unclear, although cardiovascular disturbances and regulation of fetal volemia and diuresis seem central in this syndrome. Previously, we demonstrated that the renin-angiotensin system (RAS) was up-regulated in donor twins as a consequence of hypovolemia, and down-regulated in recipients. This was the first evidence of the implication of the RAS in TTTS. We hypothesize that the RAS plays a key role in the pathogenesis of TTTS. In the donor, RAS up-regulation aggravates oligohydramnios and may increase arterial resistance, which could contribute to placental dysfunction leading to intrauterine growth restriction. In the recipient, paradoxical RAS activation, due to transfer of effectors such as angiotensin II through placental shunts, could explain fetal vascular disturbances and cardiomyopathy. According to our hypothesis, TTTS would appear similar to the classical model of hypertension referred to as '2 kidneys-1 clip' with a donor twin, comparable to the clipped kidney, intoxicating its cotwin, comparable to the normal kidney.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
1015-3837
pubmed:author
pubmed:copyrightInfo
Copyright 2001 S. Karger AG, Basel
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
241-4
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:articleTitle
Pathogenesis of twin-twin transfusion syndrome: the renin-angiotensin system hypothesis.
pubmed:affiliation
Department of Obstetrics, Hôpital Necker-Enfants Malades, AP-HP and University Paris V, France. dominque.mahieu@nck.ap-hop-paris.fr
pubmed:publicationType
Journal Article, Review