Steroid Replacement in Addison's Disease and in Subjects Adrenalectomized for Cushing's Disease: Comparison of Various Glucocorticoids*

Khalid, B. A. K.; Burke, C. W.; Hurley, David M.; Funder, John W.; Stockigt, Jan R.

doi:10.1210/jcem-55-3-551

Cited by 41 publications

(18 citation statements)

References 32 publications

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“…Khalid et al . reported that neither hydrocortisone (20 mg in the morning and 10 mg in the evening) nor cortisone acetate gave adequate inhibition of ACTH secretion at 8 a.m. and that ACTH with dexamethasone treatment was better sustained throughout the 24 hr period (Khalid et al, 1982). These data support our observation that the plasma ACTH level (7-9 a.m.) remained high.…”

Section: Discussionsupporting

confidence: 86%

A case of tuberculous epididymitis associated with Addison's disease.

et al. 1984

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A 68-year-old man was admitted to the hospital because of loss of appetite, easy fatigability, and skin pigmentation.Physical examination revealed that the bilateral epididymides were enlarged and hard without tenderness.At 7 a.m., the basal cortisol level in the plasma was 22.4 ng/ml and ACTH 318 pg/ml. The clinical diagnosis was Addison's disease. Biopsy of the right epididymis revealed evidence of active tuberculosis. Hydrocortisone (18 mg/ day) and anti-tuberculous drugs were administered, and the patient became well and regained his appetite in a week.In this case, laparotomy was not performed, but all clinical findings and the course indicated that adrenal tuberculosis was the most likely cause of Addison's disease.CT scanning of the adrenal region demonstrated large, bilateral, homogenous, low density, and non-enhancing mass. This is the first report dealing with CT findings of Addison's disease with tuberculous epididymitis.

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Section: Discussionsupporting

confidence: 86%

A case of tuberculous epididymitis associated with Addison's disease.

et al. 1984

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“…From a study on steroid replacement in patients with endogenously elevated ACTH concen tration, the radioreceptor activity in plasma was compared to the ACTH-suppressive ef fect of the three glucocorticoids. It was found that dexamethasone treatment resulted in a more effective ACTH suppression, in spite of a lower glucocorticoid potency as measured by a radioreceptor glucocorticoid activity [8]. In normal human subjects, a single oral dose of hydrocortisone, prednisolone and dexa methasone was found to suppress a nonstimulatcd morning adrenal activity, as mea sured by plasma corticosterone concentration in a relation of 1 for hydrocortisone.…”

Section: Discussionmentioning

confidence: 96%

“…Under pathophysiological conditions, a sup pression of ACTH release can be an undesira ble side effect when glucocorticoids are re quired in pharmacological doses. Alternative ly, in conditions of endogenous ACTH excess, such as in Addison's disease, in Cushing's dis ease postadrcnalcctomy, and especially in the syndrome of congenital adrenal hyperplasia, a suppression of ACTH secretion is one of the aims of the treatment [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of the ACTH Adrenal Response to Stress by Treatment with Hydrocortisone, Prednisolone and Dexamethasone in the Rat

Baumann¹,

Girard²,

Christen³

et al. 1985

Horm Res

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16- and 4-week-old intact and adrenalectomized rats have been treated with different doses of the three glucocorticoids hydrocortisone, prednisolone and dexamethasone by gavage. The delayed feedback effect on plasma ACTH and corticosterone response to an ether stress have been assessed. Almost complete suppression of corticosterone response 20 min after an ether stress and an ACTH suppression to 20% of control values 5 min after an ether stress were observed with 25 µg of dexamethasone, 10 mg of prednisolone and 20 mg of hydrocortisone. Although the percent inhibition of corticosterone and ACTH response to stress was comparable, a striking dissociation of the ACTH and corticosterone release was observed in terms of absolute concentrations. A mean ACTH concentration of 462 ng/l after 25 µg of dexamethasone was measured together with a barely measurable corticosterone concentration of 3 µg%. Similarly, after 10 mg of prednisolone, the mean ACTH concentration was 404 ng/l, whilst the mean corticosterone concentration was 3 µg%. This dissociation demonstrates that the corticosterone concentration on its own does not necessarily reflect the ACTH release. At 4 weeks of age, the ACTH response to stress is more difficult to suppress than in adult animals. This is more obvious after adrenalectomy, where the excessive ACTH secretion was less inhibited by all glucocorticoids used. The time between the last steroid gavage and stress must be considered. In 4-week-old animals the ACTH response 16 h after 12.5 µg of dexamethasone was inhibited by 22%, whereas 4 h after the same dexamethasone dose the inhibition was 85%. It is concluded that under the experimental conditions used, in rats degree and duration of feedback inhibition depend on the total steroid dose applied and on the regimen of drug administration. A dissociation between corticosterone and ACTH release is obvious. A weight-related potency ratio of feedback inhibition was 1:2:400-800 for hydrocortisone to prednisolone to dexamethasone.

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“…Comparison of the two steroids in the same subjects has given conflicting results with cortisol levels achieved after oral cortisone acetate being variously reported as lower (Jenkins & Samson, 1967;Kehlet et al, 1976;Khalid et al, 1982), higher (Barbato & Landau, 1977) or no different (Fariss et al, 1978) to those seen after oral cortisol. The present study confirms that mean cortisol levels are lower after oral cortisone acetate than after cortisol, with the mean bioavailability of cortisone being 80% that of cortisol.…”

Section: Discussionmentioning

confidence: 99%

Plasma cortisol delivery from oral cortisol and cortisone acetate: relative bioavailability.

Heazelwood¹,

Galligan²,

Cannell³

et al. 1984

Brit J Clinical Pharma

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1 Plasma cortisol levels were measured before and for 6 h after the intravenous injection of 50 mg cortisol as sodium succinate and oral administration of 50 mg cortisol and 50 mg cortisone acetate in 10 subjects with primary or secondary adrenal failure and in two normal volunteers. 2 Peak cortisol levels of 1518 + 190 nmol l-l (mean + s.e. mean) and 739 + 74 nmol 1-1 were found 1.46 + 0.25 and 1.79 + 0.16 h after oral cortisol and cortisone acetate respectively. The relative bioavailability of oral cortisol and cortisone acetate varied widely (cortisol 26-91%, mean 54 + 6.9%, cortisone acetate 21-95%, mean 44 + 6.5%) but despite this wide variation there was, in individual subjects, a highly significant correlation between the bioavailability of the two steroids (r = 0.870, P < 0.001). 3 This suggests that the wide interindividual variations in plasma cortisol levels seen after oral cortisone acetate are not related to variations in bioconversion of cortisone.

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Steroid Replacement in Addison's Disease and in Subjects Adrenalectomized for Cushing's Disease: Comparison of Various Glucocorticoids*

Cited by 41 publications

References 32 publications

A case of tuberculous epididymitis associated with Addison's disease.

A case of tuberculous epididymitis associated with Addison's disease.

Inhibition of the ACTH Adrenal Response to Stress by Treatment with Hydrocortisone, Prednisolone and Dexamethasone in the Rat

Plasma cortisol delivery from oral cortisol and cortisone acetate: relative bioavailability.

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