Response to Low-Dose Pulsatile Cortisol in Addison's Disease with Suspected Corticotropinoma

D. B. Carr; J. E. Fisher; M. Rosenblatt

doi:10.1055/s-2007-1012375

Hormone and Metabolic Research, Inhaltsverzeichnis

Horm Metab Res 1986; 18(8): 569-573
DOI: 10.1055/s-2007-1012375

Clinical

Response to Low-Dose Pulsatile Cortisol in Addison's Disease with Suspected Corticotropinoma

D. B. Carr, J. E. Fisher, M. Rosenblatt

Analgesic Peptide Research Unit, Departments of Anesthesia and Endocrinology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, U.S.A.

Abstract

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Summary

A 65 year old woman with long-standing Addison's disease treated with oral glucocorticoid and mineralocorticoid replacement had persistently high ACTH levels, inadequate suppression of ACTH on low-dose dexamethasone, sellar enlargement, and pigmentation, and thus resembled patients alleged to develop corticotropinomas while on oral replacement for adrenal insufficiency. Since animal studies suggested that rapid rises of corticosteroids within the physiologic range can inhibit ACTH release, we administered brief infusions of cortisol every three hours with total daily dose equal to her chronic dose. Prompt suppression of ACTH and immunoreactive beta-endorphin occurred during each cortisol dose profiled, suggesting a role for ultradian cortisol fluctuations in tonic inhibition of ACTH secretion in humans, and a possible therapeutic benefit of mimicking ultradian cortisol rhythms during replacement therapy.

Key-Words

Addison's Disease - Glucocorticoid Therapy - Rate-Sensitive Feedback - ACTH - Beta-Endorphin

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