Effect of Chronic Treatment with the Glucocorticoid Antagonist RU 486 in Man: Toxicity, Immunological, and Hormonal Aspects
Abstract
Suppression of immune function was traditionally thought to occur only with pharmacological levels of glucocorticoids. However, recent studies in rodents have suggested that glucocorticoids exert tonic antiinflammatory/immunosuppressive effects even at basal nonstress concentrations. To examine whether basal glucocorticoid secretion modulates immune function in man we employed the specific glucocorticoid receptor antagonist RU 486. If a tonic level of inhibition of the immune system by basal glucocorticoid levels was present, then a potentiation or enhancement of immune function might evolve in the absence of glucocorticoid action. To examine this hypothesis, we studied 11 healthy male normal volunteers who received RU 486 (10 mg/kg.day) or placebo vehicle, divided into 2 daily oral doses, for 7-14 days. Blood samples were collected every 2 days for measurement of plasma ACTH and cortisol concentrations along with 24-h urine samples for measurement of 17-hydroxysteroid and free cortisol excretion. Complete and differential blood counts, erythrocyte sedimentation rates, C-reactive protein, antinuclear antibodies, rheumatoid factor, and quantitative immunoglobulins were also determined at 2-day intervals. Leukocytes were obtained by leukopheresis for phenotypic characterization and functional analysis before and 7 days after the initiation of RU 486 or placebo therapy. Blockade of cortisol receptors with RU 486 was associated with marked compensatory elevations of plasma ACTH a…
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Administration of the GR antagonist RU486 elevates ACTH and cortisol in humans, implicating GR activation as a mediator of negative feedback inhibition.
“Administration of the GR antagonist, RU486, results in elevated levels of both ACTH and cortisol in humans, which implicates GR activation as a mediator of negative feedback inhibition.45”
From Early life adversity and the epigenetic programming of hypothalamic-pituitary-adrenal function (2014) · cites this paper as [45]
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- Authors
- LAUE, L., LOTZE, M. T., CHROUSOS, G. P., BARNES, K., LORIAUX, D. L., & FLEISHER, T. A.
- Affiliations
- National Institutes of Health (US)
- Venue
- The Journal of Clinical Endocrinology & Metabolism
- Publisher
- The Endocrine Society
- Published
- 1990-12
- Volume
- 71
- Issue
- 6
- Pages
- 1474-1480
- ISSN
- 0021-972X (ISSN-L)
- 1945-7197
- OpenAlex
- W2064035782
- Cited by
- 77
- References
- 0
- Citations by year
- 2020: 2 · 2019: 2 · 2014: 2 · 2013: 3 · 2012: 2
- FWCI
- 3.46
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- NIH Clinical Center
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Keywords
- RU486, mifepristone, glucocorticoid receptor antagonist, glucocorticoid-induced immunosuppression, ACTH, cortisol, adrenal insufficiency, rash, lymphocyte subsets, lymphocyte cytotoxicity, lymphocyte proliferation, immunoglobulins, antinuclear antibodies
- MeSH terms
- Adrenal Insufficiency, Adrenocorticotropic Hormone, Adult, Exanthema, Glucocorticoids, Humans, Hydrocortisone, Hydroxysteroids, Immunity, Leukocyte Count, Lymphocytes, Male, Mifepristone
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