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Serum Dehydroepiandrosterone Sulfate Concentration as an Indicator of Adrenocortical Suppression in Asthmatic Children Treated with Inhaled Steroids

Department of Pediatrics, Kuopio University Hospital, FIN-70211 Kuopio, Finland

Address all correspondence and requests for reprints to: Raimo Voutilainen, M.D., Department of Pediatrics, Kuopio University Hospital, P.O. Box 1777, FIN-70211 Kuopio, Finland. E-mail: raimo.voutilainen{at}uku.fi

Abstract

ACTH regulates adrenal androgen production, which may thus be reduced during glucocorticosteroid therapy. Dehydroepiandrosterone sulfate is the most abundant androgen secreted by the adrenals. We wished to evaluate whether serum levels of dehydroepiandrosterone sulfate can be used as an indicator of adrenal suppression during inhaled steroid treatment in children. Sixty school-aged children with newly diagnosed asthma were randomly divided into budesonide (n = 30) and fluticasone propionate (n = 30) groups. Fifteen cromone-treated children served as a control group. The budesonide dose was 800 µg/d during the first 2 months and 400 µg/d thereafter. The respective fluticasone propionate doses were 500 and 200 µg/d. Serum dehydroepiandrosterone sulfate concentrations were measured before and after 2 and 4 months of treatment.

In the budesonide group, serum dehydroepiandrosterone sulfate decreased from the baseline by a mean of 21% (95% confidence interval, 13–29%; P < 0.001) after 2 months of high dose treatment and by 16% (95% confidence interval, 8–25%; P < 0.001) after 4 months of treatment. In the fluticasone propionate group, the respective figures were 10% (95% confidence interval, 4–16%; P < 0.01) and 6% (95% confidence interval, 16% decrease–3% increase; P = NS). A low dose ACTH test indicated adrenocortical suppression at 4 months in 14 (23%) steroid-treated children. In these children, dehydroepiandrosterone sulfate decreased by a mean of 21% (95% confidence interval, 14–28%), whereas in those 46 steroid-treated children with normal ACTH test results, dehydroepiandrosterone sulfate decreased by 8% (95% confidence interval, 0–16%; P < 0.05 between these groups). In the control group, dehydroepiandrosterone sulfate levels tended to increase (by a mean of 26%), reflecting the normal physiological change at this age.

In conclusion, inhaled steroid treatment suppresses dehydroepiandrosterone sulfate production in a dose-dependent manner. Monitoring of serum dehydroepiandrosterone sulfate concentrations can be used as a practical method to follow adrenocortical function and to detect its suppression during inhaled steroid treatment in children.