Observations and Comments on Failure of Dexamethasone Suppression

Je, Linn; Bowdoin, Braxton; Ta, Farmer; Ck, Meador

doi:10.1056/nejm196708242770804

Cited by 46 publications

(7 citation statements)

References 17 publications

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“…1962;Silverman et al 1963;Linn et al 1967). The failure of suppression of plasma cortisol by "high dose" dexamethasone is unusual in pituitary dependent Cushing's syndrome, but such cases are well documented (Scott el al.…”

Section: Resultsmentioning

confidence: 99%

Acth and Cortisol Response to Bromocriptine, and Results of Long-Term Therapy, in Cushing's Disease

Kennedy

Sheridan

Montgomery

1978

European Journal of Endocrinology

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Plasma corticotrophin (ACTH) was lowered in 4 out of 5 patients with pituitary dependent Cushing's syndrome (one of whom was studied only after bilateral adrenalectomy) after a single oral dose of 2.5 mg bromocriptine, but plasma cortisols were unaltered in the 3 patients in whom it was measured.Three patients were observed during treatment with bromocriptine for 16 to 87 weeks. One improved symptomatically while maintained on a combination of metyrapone and bromocriptine, but plasma ACTH levels remained high even when the dose of bromocriptine was increased to 20 mg daily. Bromocriptine therapy was discontinued after 16 weeks in the second patient due to the development of mental depression. Her clinical features had not improved during this time. The third patient, who also underwent a course of pituitary irradiation, became, and remains, symptom free, with satisfactory plasma ACTH and cortisol levels for the 87 weeks he has received bromocriptine. The role of bromocriptine in the management of Cushing's disease seems limited despite the fact that plasma ACTH may fall after a test dose of the drug.Bromocriptine is a long-acting dopamine agonist (Corrodi et al. 1972). It has been shown to be effective in the suppression of puerperal lactation (Varga et al. 1972;Cooke et al. 1976), in the treatment of pathological hyperprolac-Requests for offprints to D. A. D. Montgomery at above address.

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Section: Resultsmentioning

confidence: 99%

Acth and Cortisol Response to Bromocriptine, and Results of Long-Term Therapy, in Cushing's Disease

Kennedy

Sheridan

Montgomery

1978

European Journal of Endocrinology

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“…Only a few cases of hyper¬ cortisolism with bilateral adrenocortical hyperplasia and resistance to dexamethasone have previ¬ ously been reported (Mosier et al 1960;Kirschner et al 1964;Harden & Forrest 1964;De Moor et al 1965;Katz 1966;Linn et al 1967). We therefore studied the hypothalamic-pituitary-adrenal func¬ tion in a patient resistant to the standard high dose dexamethasone test.…”

mentioning

confidence: 99%

Cyclic Cushing's syndrome combined with cortisol suppressible, dexamethasone non-suppressible ACTH secretion: a new variant of Cushing's syndrome

Schweikert

Fehm²,

Fahlbusch

et al. 1985

Acta Endocrinologica

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A 55 year old woman with an unusual form of Cushing's disease was studied. During several periods (periods lasting up to 84 days) evidence of cortisol hypersecretion with cycles occurring every 6 days was found. Suppression of plasma cortisol through orally administered dexamethasone (up to 32 mg per day) could not be achieved either during periods of cyclic cortisol hypersecretion or during apparent remission with normal cortisol secretion. Marked suppression of plasma ACTH was measured in response to an iv infusion of 50 mg cortisol over a period of 55 min whereas a similar test with 2 mg dexamethasone (iv bolus) did not suppress ACTH secretion. Transsphenoidal exploration of the sella revealed a tumour surrounding the anterior pituitary. Examination of the pituitary showed a few tiny tumour structures embedded in normal tissue which could not be removed, when the tumour was resected selectively under preservation of normal appearing tissue. Post-operatively, clinical and chemical remission (normal response to 1 mg dexamethasone) was observed for about 4 months. Thereafter, cortisol hypersecretion occurred again necessitating bilateral adrenalectomy. Our results are compatible with the assumption that normal hypothalamic-pituitary-adrenal suppressibility with cortisol, but not with dexamethasone, was caused by the loss of feedback receptors for dexamethasone in the presence of cortisol receptors in the cells which secrete ACTH or CRF.The combination of cyclic hypercortisolism with dexamethasone non-suppressible Cushing's syndrome has not been reported before and thus represents a new variant of Cushing's syndrome.

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“…The pardoxical response to dexamethasone has been described in micronodular adrenocortical dysplasia (Ruder et al, 1974), adrenal adenoma or carcinoma (Scott et al, 1962) and, most frequently, pituitary adenoma (Linn et al, 1967;French et al, 1969) without cyclic hormonogenesis. French et al (1969) suggested that this phenomenon might result from upsetting of a negative feedback effect of glucocorticoid or a paradoxical positive feedback stimulation of ACTH.…”

Section: Discussionmentioning

confidence: 99%

Cushing's Syndrome Due to Huge Nodular Adrenocortical Hyperplasia with Fluctuation of Urinary 17-OHCS Excretion.

et al. 1989

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A 51-yr-old male patient with Cushing's syndrome due to huge nodular adrenocortical hyperplasia is described. Urinary 17-OHCS was not suppressed by a high dose of (8mg) dexamethasone and showed rather a tendency to paradoxical response. There was no response to metyrapone.Plasma cortisol showed a hyperresponse to insulin-induced hypoglycemia and a rapid response to corticotropin releasing hormone-lysine vasopressin (CRH-LVP) administration without an obvious ACTH response.Plasma cortisol responded to synthetic ACTH. Urinary 17-OHCS did not show parallel changes with plasma cortisol. These results and computerized tomography data suggested huge multiple nodular adrenocortical hyperplasia, which was confirmed later by surgery. The left and right adrenal glands weighed 105 and 45g, respectively. Hyperreaction of the adrenal gland to a small change in plasma ACTH or "unknown factors" may cause not only the discrepancy between cortisol and ACTH response but also the development of autonomous nodules in the adrenal gland.

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Observations and Comments on Failure of Dexamethasone Suppression

Cited by 46 publications

References 17 publications

Acth and Cortisol Response to Bromocriptine, and Results of Long-Term Therapy, in Cushing's Disease

Acth and Cortisol Response to Bromocriptine, and Results of Long-Term Therapy, in Cushing's Disease

Cyclic Cushing's syndrome combined with cortisol suppressible, dexamethasone non-suppressible ACTH secretion: a new variant of Cushing's syndrome

Cushing's Syndrome Due to Huge Nodular Adrenocortical Hyperplasia with Fluctuation of Urinary 17-OHCS Excretion.

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