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Obstet Gynecol. 2000 Aug;96(2):287-90.

Adrenal suppression induced by betamethasone in women at risk for premature delivery.

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  • 1Ehrling Bergquist Hospital, Offutt Air Force Base, Bellevue, Nebraska, USA.



To determine whether betamethasone administered to women at risk of preterm delivery causes adrenal suppression.


Ten women at risk of preterm delivery had three weekly low-dose (1 microg) ACTH stimulation tests with the first one between 24 and 25 weeks' gestation. Immediately after the first and second ACTH stimulation tests, we gave each woman a 12-mg betamethasone dose intramuscularly and repeated it 24 hours later. The third ACTH stimulation test was 1 week after the second course of betamethasone. Serum cortisol levels were measured before (baseline) and 30 minutes after ACTH administration.


All subjects had normal baseline and stimulated cortisol levels for the first ACTH stimulation test. Mean baseline serum cortisol levels decreased with each ACTH stimulation test, from 25.4 +/- 4.8 microg/dL (before betamethasone) to 4.3 +/- 4.0 microg/dL (1 week after the second course of betamethasone) (P <.001). The mean stimulated cortisol levels also decreased from 33.0 +/- 4.3 microg/dL (before betamethasone) to 11.8 +/- 6.4 microg/dL (1 week after the second course of betamethasone) (P <.001). Compared with initial ACTH stimulation tests, laboratory evidence of adrenal suppression occurred in four patients 1 week after the first course of betamethasone and in seven patients after the second course. No signs or symptoms of Addisonian crisis occurred antepartum or intrapartum.


Antenatal administration of betamethasone produced measurable adrenal suppression in women at risk of preterm delivery. The number of women with adrenal suppression increased each week that antenatal betamethasone was repeated. (Obstet Gynecol 2000;96:287-90.)

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