Cushing's Syndrome With Multinodular Adrenal Glands*

Mosier, H. David; Flynn, Pierce J.; Will, Drake W.; Turner, Roderick D.

doi:10.1210/jcem-20-4-632

Cited by 43 publications

(11 citation statements)

References 9 publications

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“…However, against the Kirschner's hypothesis, cases of Goldblatt (Goldblatt and Snaith, 1958), Mosier (Mosier et al, 1960), DeMoor (DeMoor et al, 1965), Klevitt (Klevitt et al, 1966) and the present authors have relatively short duration of hypercorticoid state. Also, it must be stressed that no prominent nodularity is noted in congenital adrenocortical hyperplasia despite continuous stimulation to the adrenal cortex.…”

Section: Discussioncontrasting

confidence: 70%

Cushing's Syndrome due to Huge Adrenocortical Multinodular Hyperplasia

et al. 1975

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Section: Discussioncontrasting

confidence: 70%

Cushing's Syndrome due to Huge Adrenocortical Multinodular Hyperplasia

et al. 1975

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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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“…Reported cases of macronodular adrenocortical hyperplasia whose pituitary adrenocortical functions were reported (27 cases) (Mellinger & Smith, 1956;Mosier et al, 1960;Silverman et al, 1963; Tucci et al, 1965; Katz, 1966;Neville & Symington, 1967;Choi et al, 1970;Hartemann et al, 1971;Yamaoka, 1972;Burke & Beardwell, 1973;Huguenin et al, 1973;Arce et al, 1978;Josse et al, 1980;Aron et al, 1981;Furukawa et al, 1981;Yamamoto et al, 1981;Miura et al, 1984) also indicated no suppression following the administration of 8mg of dexamethasone (20/23). However, more than half of the cases (7/11) indicated responses to metyrapone, and most cases (17/22) showed a response to ACTH administration.…”

Section: Discussionmentioning

confidence: 99%

Cortisol responsiveness to insulin-induced hypoglycemia in Cushing's syndrome with huge nodular adrenocortical hyperplasia.

Hashimoto¹,

Kawada²,

Murakami³

et al. 1986

Endocrinol Japon

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A 51-yr-old male patient with a 3yr history of Cushing's syndrome is described.The baseline plasma cortisol level was elevated, while the plasma ACTH levels remained at an undetectable level. Dynamic testing of pituitaryadrenal function revealed no suppression after 8mg of dexamethasone, and there was no response to metyrapone or CRF, while plasma cortisol showed a hyperresponse to synthetic ACTH. Plasma cortisolresponded to insulininduced hypoglycemia without an obvious ACTH response. These and the computerized tomography data suggested a "huge" bilateral nodular adrenocortical hyperplasia which was later confirmed by surgery, The left and right adrenal glands weighed 55 and 76g, respectively, In vitro experiments, using the adrenal tissue, showed that there was an adrenal cortisol response to 1-39 ACTH but not to regular insulin, arginine vasopressin, angiotensin II, norepinephrine or epinephrine. These results indicate that plasma cortisol responded to a slight hypoglycemia-induced plasma ACTH change which was not detected in the ACTH radioimmunoassay or to factors other than ACTH which might be induced by hypoglycemia.

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Cushing's Syndrome With Multinodular Adrenal Glands*

Cited by 43 publications

References 9 publications

Cushing's Syndrome due to Huge Adrenocortical Multinodular Hyperplasia

Cushing's Syndrome due to Huge Adrenocortical Multinodular Hyperplasia

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

Cortisol responsiveness to insulin-induced hypoglycemia in Cushing's syndrome with huge nodular adrenocortical hyperplasia.

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