Document Detail


Placental 11 beta-hydroxysteroid dehydrogenase-2 and fetal cortisol/cortisone shuttle in small preterm infants.
MedLine Citation:
PMID:  12519895     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Eero Kajantie; Leo Dunkel; Ursula Turpeinen; Ulf-Håkan Stenman; Peter J Wood; Mika Nuutila; Sture Andersson
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of clinical endocrinology and metabolism     Volume:  88     ISSN:  0021-972X     ISO Abbreviation:  J. Clin. Endocrinol. Metab.     Publication Date:  2003 Jan 
Date Detail:
Created Date:  2003-01-09     Completed Date:  2003-02-11     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0375362     Medline TA:  J Clin Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  493-500     Citation Subset:  AIM; IM    
Affiliation:
Hospital for Children and Adolescents, Helsinki University Central Hospital, 00029 HUS, Helsinki, Finland. eero.kajantie@hus.fi
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MeSH Terms
Descriptor/Qualifier:
11-beta-Hydroxysteroid Dehydrogenases
Betamethasone / therapeutic use
Birth Weight*
Cortisone / metabolism*
Female
Fetus / metabolism*
Gestational Age
Glucocorticoids / therapeutic use
Humans
Hydrocortisone / metabolism*
Hydroxysteroid Dehydrogenases / metabolism*
Infant, Newborn
Infant, Premature / metabolism*
Infant, Small for Gestational Age*
Placenta / enzymology*
Pregnancy
Pregnancy Complications / drug therapy,  metabolism
Prenatal Care
Regression Analysis
Chemical
Reg. No./Substance:
0/Glucocorticoids; 378-44-9/Betamethasone; 50-23-7/Hydrocortisone; 53-06-5/Cortisone; EC 1.1.-/Hydroxysteroid Dehydrogenases; EC 1.1.1.146/11-beta-Hydroxysteroid Dehydrogenases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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