Linked Life Data

12519895

Source:http://linkedlifedata.com/resource/pubmed/id/12519895

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2003-1-9
pubmed:abstractText
Glucocorticoids rate among the most controversial topics in today's perinatology and neonatology. Many sick preterm infants exhibit signs of adrenal insufficiency, the etiology, diagnostic criteria, and optimal treatment of which are under debate. Moreover, most of these infants are exposed to pharmacological glucocorticoid doses both in utero and after birth. In face of this, surprisingly little is known about the physiological glucocorticoid exposure before early preterm birth. This exposure is highly variable and mainly regulated by the placental enzyme 11 beta-hydroxysteroid dehydrogenase-2 (11 beta-HSD2), which converts excess cortisol (F) to inactive cortisone (E). Impaired activity of this enzyme is common in intrauterine growth restriction and preeclampsia, conditions frequently associated with early preterm birth. To identify clinical determinants associated with decreased placental 11 beta-HSD2 function, we studied 107 small preterm infants [mean birth weight, 1067 g (range, 395-2453 g); gestational age, 28.2 wk (range, 22.4-32.0 wk)] by determining their placental 11 beta-HSD2 activity rate (per milligram protein) and total activity (per placenta) as well as cord vein F and E concentrations. An E/(E+ F) ratio expresses the overall balance of the F/E shuttle. There were positive correlations between relative birth weight and placental 11 beta-HSD2 activity rate (r = 0.30; P = 0.002) and total activity (r = 0.56; P < 0.0001) as well as E/(E+ F) ratio (r = 0.27; P = 0.01) and E concentration (r = 0.32; P = 0.003). Infants with increased umbilical artery resistance had lower total placental 11 beta-HSD2 activity (P = 0.02), E/(E+ F) ratio (P = 0.04), and E concentration (P = 0.0002). Gestational age was inversely associated with placental 11 beta-HSD2 activity rate (r = -0.25; P = 0.009). We conclude that, in small preterm infants, reduced placental 11 beta-HSD2 function is associated with low relative birth weight and severe fetal distress. Whether these conditions are associated with early postnatal adrenal insufficiency or long-term cardiovascular risk remains an important issue for further study.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0021-972X
pubmed:author
pubmed:issnType
Print
pubmed:volume
88
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
493-500
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12519895-11-beta-Hydroxysteroid Dehydrogenases, pubmed-meshheading:12519895-Betamethasone, pubmed-meshheading:12519895-Birth Weight, pubmed-meshheading:12519895-Cortisone, pubmed-meshheading:12519895-Female, pubmed-meshheading:12519895-Fetus, pubmed-meshheading:12519895-Gestational Age, pubmed-meshheading:12519895-Glucocorticoids, pubmed-meshheading:12519895-Humans, pubmed-meshheading:12519895-Hydrocortisone, pubmed-meshheading:12519895-Hydroxysteroid Dehydrogenases, pubmed-meshheading:12519895-Infant, Newborn, pubmed-meshheading:12519895-Infant, Premature, pubmed-meshheading:12519895-Infant, Small for Gestational Age, pubmed-meshheading:12519895-Placenta, pubmed-meshheading:12519895-Pregnancy, pubmed-meshheading:12519895-Pregnancy Complications, pubmed-meshheading:12519895-Prenatal Care, pubmed-meshheading:12519895-Regression Analysis
pubmed:year
2003
pubmed:articleTitle
Placental 11 beta-hydroxysteroid dehydrogenase-2 and fetal cortisol/cortisone shuttle in small preterm infants.
pubmed:affiliation
Hospital for Children and Adolescents, Helsinki University Central Hospital, 00029 HUS, Helsinki, Finland. eero.kajantie@hus.fi
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't