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Termination of Pregnancy with Mifepristone and Prostaglandin Suppresses Transiently Circulating Glucocorticoid Bioactivity

Department of Obstetrics and Gynecology (O.H., H.H.), Institute of Biomedicine (O.H., T.R., S.R., O.A.J.), and Department of Clinical Chemistry (O.A.J.), University of Helsinki and Helsinki University Central Hospital, FIN-00014 Helsinki, Finland

Address all correspondence and requests for reprints to: Dr. Olli A. Jänne, Biomedicum Helsinki, Institute of Biomedicine (Physiology), P.O. Box 63, Haartmaninkatu 8, University of Helsinki, FIN-00014 Helsinki, Finland. E-mail: olli.janne{at}helsinki.fi.

Mifepristone is a potent antiglucocorticoid, the administration of which results in a dose-dependent activation of the hypothalamic-pituitary-adrenal axis. However, the net effect of this compound on circulating glucocorticoid activity is not known. We have used a recombinant cell bioassay to study glucocorticoid bioactivity (GBA), measured directly from serum, in 18 women undergoing medical termination of an early pregnancy with 200 mg mifepristone, followed by 0.8 mg misoprostol, a prostaglandin. Increased serum mifepristone was accompanied by an increase in serum cortisol that was insufficient to maintain circulating GBA within the normal (pre-mifepristone) range (34.7–93.8 nM cortisol equivalents); after approximately 43, 46, and 68 h of mifepristone ingestion, the mean serum GBA levels were much lower than the mean pre-mifepristone level (P < 0.0001). At the corresponding times, 16, 13, and 12 women displayed subnormal serum GBA levels (ranges, <15.6–23, <15.6–25.6, and <15.6–32.5 nM cortisol equivalents, respectively). Altogether 11 subjects displayed subnormal serum GBA (range, <15.6–32.5 nM cortisol equivalents) continuously in the presence of high concentrations of mifepristone. Two weeks after mifepristone administration, circulating GBA had returned to normal levels in all subjects. We conclude that 200 mg mifepristone elicits a significant suppression of serum GBA, to one third of the pretreatment value, despite the compensatory increase in the serum cortisol concentration.

This work was supported by The Population Council (New York, NY), Biocentrum Helsinki, Academy of Finland, Helsinki University Central Hospital Research Funds, and a Finnish Medical Foundation clinical fellowship grant (to O.H.). The content of the this report does not necessarily reflect the policy of any of the funding sources.

O.H. and T.R. contributed equally to this work.

Abbreviations: GBA, Glucocorticoid bioactivity; GR, glucocorticoid receptor; HPA, hypothalamic-pituitary-adrenal.

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