1994
DOI: 10.3233/jrs-1994-6201
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Malformation surveillance and maternal drug exposure: the MADRE project

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Cited by 51 publications
(14 citation statements)
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“…Since use of antihypertensive drugs during pregnancy has been associated with infant congenital cardiovascular defects (29), adjustments were made for this in the analysis of cardiovascular malformations, but this did not significantly change the results. An association between anomalies of cardiac septal closure (atrial or ventricular) and thyroid hormone therapy has earlier been proposed, but was based on only six cases (30). The 12 neonates with severe kidney malformations had different subtypes, a finding that speaks against a causal association.…”
Section: Discussionmentioning
confidence: 99%
“…Since use of antihypertensive drugs during pregnancy has been associated with infant congenital cardiovascular defects (29), adjustments were made for this in the analysis of cardiovascular malformations, but this did not significantly change the results. An association between anomalies of cardiac septal closure (atrial or ventricular) and thyroid hormone therapy has earlier been proposed, but was based on only six cases (30). The 12 neonates with severe kidney malformations had different subtypes, a finding that speaks against a causal association.…”
Section: Discussionmentioning
confidence: 99%
“…Because the database has no information on nonmalformed births and no comparable database can be used to validly extract nonmalformed births, all male subjects without hypospadias were considered controls, including those with chromosomal or monogenic defects and other syndromes. This method corresponds with the one used in the Malformation Drug Exposure (MADRE) project from the International Clearinghouse for Birth Defects Surveillance and Research (Robert et al, 1994).…”
Section: Methodsmentioning
confidence: 99%
“…Se ha demostrado, además, que los glicocorticoides en exceso son teratógenos en animales de experimentación y en humanos. La teratogénesis humana se manifiesta por restricción del crecimiento fetal, prematuridad, alteraciones anatómicas y funcionales de los órganos en la vida postnatal ( [39][40][41] ). Por otro lado, la placenta humana presenta la 11-beta hidroxiesteroide deshidrogenasa (11-BHSD) tipo 2, que transforma el exceso de cortisol y corticosterona materno en sus metabolitos inactivos cortisona y 11dehidrocosticosterona ( 42 ).…”
Section: Discussionunclassified