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Antenatal Betamethasone Depresses Maternal and Fetal Aldosterone Levels

¹ University of Wisconsin, Madison
² University of Wisconsin, Madison, University of Michigan
³ University of Alabama at Birmingham

^* To whom correspondence should be addressed. E-mail: jmkessel{at}pediatrics.wisc.edu.

	Abstract

Antenatal glucocorticoids are used to mature lung function in fetuses at risk for preterm delivery, but they also suppress cortisol synthesis in both pregnant women and their fetuses. We recently discovered in pregnant rabbits that even though exogenous betamethasone is not a mineralocorticoid, it also suppresses production of aldosterone. Lower aldosterone levels were linked to reduced P450 side chain cleavage (P450scc) messenger RNA levels in the rabbit maternal and fetal adrenal cortex. To establish whether this occurs in humans, we assayed aldosterone levels in women and newborns treated with antenatal betamethasone for preterm labor. In mothers treated with betamethasone, maternal cortisol depression after 48 hours was accompanied by aldosterone depression. Both pregnant women and their newborns treated with betamethasone showed depressed aldosterone levels in a 1- to 3-day period after the first betamethasone dose. We conclude that suppression of aldosterone biosynthesis is a side effect of antenatal steroids that has been largely overlooked, but may be clinically relevant at a time when the newborn is learning to control plasma electrolytes and blood volume.

First published on November 7, 2008
Reproductive Sciences 2008, doi:10.1177/1933719108324140


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