A Study of the Mechanism of the Steroid Withdrawal Syndrome. Evidence for Integrity of the Hypothalamicpituitary-Adrenal System*

Tt, Amatruda; Dr, Hollingsworth; Nd, D'esopo; Gv, Upton; Pk, Bondy

doi:10.1210/jcem-20-3-339

Cited by 72 publications

(25 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The form of SWS that we have described, characterised by anorexia, nausea, lethargy, fever, arthralgia, skin desquamation, weakness, postural hypotension, vomiting and weight loss, was recognised as early as 1960, although the exact mechanism of action is not clear, nor is its prevalence (3,4,7,8). Suppression of the HPA axis by the hypercortisolaemic state, whether endogenous or exogenous, was initially thought to be responsible, until the axis was shown to be normal in these patients, with normal baseline cortisol levels (7).…”

Section: Discussionmentioning

confidence: 97%

Steroid withdrawal syndrome after successful treatment of Cushing’s syndrome: a reminder

et al. 2005

View full text Add to dashboard Cite

Steroid withdrawal syndrome (SWS) usually refers to relapse of the disease being treated after withdrawal of glucocorticoid therapy, or the symptoms of adrenal insufficiency which occur when glucocorticoids are rapidly reduced or stopped. A less well-recognised form of SWS is that which develops when patients experience a symptom complex similar to that of adrenal insufficiency despite acceptable cortisol levels. We describe three patients who presented with this form of SWS following surgical treatment for endogenous Cushing's syndrome. All responded well to a short-term increase in the dose of glucocorticoid replacement therapy, with the median duration of the syndrome being 10 months (range 6-10 months). Trough serum cortisol levels above 100 nmol/l, with peaks between 460 and 750 nmol/l were documented in the first two patients at presentation with SWS. It is thought that the syndrome may result from development of tolerance to glucocorticoids, and mediators considered to be important in its development include interleukin-6, corticotrophin-releasing hormone, vasopressin, and central noradrenergic and dopaminergic systems. The exact underlying mechanism for SWS remains unclear. However, with increasing recommendations for use of lower doses of replacement glucocorticoids, its incidence may increase. Physicians need to be aware of this condition, which is self-limiting and easily treated by a temporary increase in the dose of glucocorticoid replacement therapy. It is possible that a slower glucocorticoid tapering regimen than that used in the standard postoperative management of patients undergoing pituitary surgery may reduce the risk of development of SWS.

show abstract

Section: Discussionmentioning

confidence: 97%

Steroid withdrawal syndrome after successful treatment of Cushing’s syndrome: a reminder

et al. 2005

View full text Add to dashboard Cite

show abstract

“…However, quite a few observations raise the possibility that in addition to their ACTH inhibiting effect, corticoids directly act on the adrenal cortex to inhibit steroid secretion (Langacher and Lurie, 1957;Birmingham and Kurlents, 1958;Fukui et al, 1961;Peron et al, 1960). Although some experiments suggest a direct effect of corticoids on the anterior pituitary (Amatruda and Hollingsworth, 1960), most studies indicate an effect at the hypothalamic or higher level (Anand and Dua, 1955).…”

Section: Discussionmentioning

confidence: 99%

Acute Effect of Morphine Administration on Secretion of Adrenal Corticosterone in Rats

1970

View full text Add to dashboard Cite

SynopsisThe purpose of this study is to determine the acute effect of morphine on ACTH secretion and to determine whether morphine has a direct action on the adrenal cortex by the adult female Wistar rat. ACTH was measured by the determination of corticosterone levels in adrenal glands, adrenal venous blood and circulatory blood. It should be emphasized that in this paper, mechanism of secretion of adrenal corticosterone by the acute effect (the early stage action) following morphine administration was described. Even in morphinization with five daily morphine (2mg/100g, B. W., i. p.) injections, the account of acute effect was determined immediately after the final injection of morphine administration. Morphine alone can not act as an inhibitor of ACTH release nor as an inhibitor of ACTH release due to histamine stress, and morphinization can not act to inhibit ACTH release or to block the effect of a histamine stress on the secretion of ACTH in the early stage action of the final morphine administration, as evidenced by corticosterone levels both in adrenal glands and in circulating blood of the intact rats. Morphine (2mg/100g,B. W., i. p.) alone caused stimulation of ACTH release as well as the final morphine injection of morphinization, and pretreatment of the rats with morphine(2mg/100g, B. W., i. p.) could not act to block the effect of a histamine (0.5 mg/ 100g, B. W., i. p.) stress on the release of ACTH in the early stage action of morphine administration. A detailed account of the effect of morphine or morphinization with four daily morphine injections on corticosterone levels both in adrenal and in adrenal venous blood of the hypophysectomized-ACTH-treated rat has been reported. Morphine (2mg/100g, B. W., i. p.) alone or with pretreatment of pentobarbital (1mg/100g, B. W., i.p.) does not directly interfere with the response of the adrenal cortex to exogenous ACTH in the early stage action of morphine administration. Morphinization with four daily morphine (2mg/100g, B. W., i. p.) injections in the early stage action following the directly act on adrenal corticoidogenesis in vivo. These results suggest in the early stage action of morphine administration that morphine acts to stimulate ACTH release at a higher level than the anterior pituitary and does not directly act on adrenal cortex, and that the acute effect of strong stimuli on the rate of ACTH release is not mediated by a decrease in the concentration of circulating adrenal corticosteroids.

show abstract

“…Thus both Addison's disease and hypopituitarism are known to be associated with increased insulin sensitivity, whereas patients with Cushing's syndrome or acromegaly are resistant to its hypoglycemic action (2,3). The observation that the intravenous injection of insulin into control subjects results in rapid elevations of plasma cortisol (4,5) and growth hormone (6)(7)(8)(9) also supports the possible physiologic importance of these hormones as insulin antagonists. Since the release of these two hormones depends on adequate hypothalamic as well as pituitary and adrenal function (5,7,10), it was apparent that a rapid test of both the hypothalamo-pituitary-adrenal axis for the secretion of cortisol and the hypothalamo-pituitary axis for the secretion of growth hormone could be developed with insulininduced hypoglycemia as a stimulus.…”

mentioning

confidence: 96%

The plasma sugar, free fatty acid, cortisol, and growth hormone response to insulin. I. In control subjects.

Greenwood¹,

Landon²,

Stamp³

1966

J. Clin. Invest.

319

113

View full text Add to dashboard Cite

A Study of the Mechanism of the Steroid Withdrawal Syndrome. Evidence for Integrity of the Hypothalamicpituitary-Adrenal System*

Cited by 72 publications

References 0 publications

Steroid withdrawal syndrome after successful treatment of Cushing’s syndrome: a reminder

Steroid withdrawal syndrome after successful treatment of Cushing’s syndrome: a reminder

Acute Effect of Morphine Administration on Secretion of Adrenal Corticosterone in Rats

The plasma sugar, free fatty acid, cortisol, and growth hormone response to insulin. I. In control subjects.

Contact Info

Product

Resources

About