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

Objective: To determine whether betamethasone administered to women at risk of preterm delivery causes adrenal suppression. Methods: Ten women at risk of preterm delivery had three weekly low-dose (1 mu g) ACTH stimulation tests with the first one between 24 and 25 weeks' g estation. 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 secon d course of betamethasone. Serum cortisol levels were measured before (base line) and 30 minutes after ACTH administration. Results: All subjects had normal baseline and stimulated cortisol levels fo r the first ACTH stimulation test. Mean baseline serum cortisol levels decr eased with each ACTH stimulation test, from 25.4 +/- 4.8 mu g/dL (before be tamethasone) to 4.3 +/- 4.0 mu g/dL (1 week after the second course of beta methasone) (P < .001). The mean stimulated cortisol levels also decreased f rom 33.0 +/- 4.3 mu g/dL (before betamethasone) to 11.8 +/- 6.4 mu g/dL (1 week after the second course of betamethasone) (P < .001). Compared with in itial ACTH stimulation tests, laboratory evidence of adrenal suppression oc curred in four patients 1 week after the first course of betamethasone and in seven patients after the second course. No signs or symptoms of Addisoni an crisis occurred antepartum or intrapartum. Conclusion: Antenatal administration of betamethasone produced measurable a drenal suppression in women at risk of preterm delivery. The number of wome n with adrenal suppression increased each week that antenatal betamethasone was repeated.