Cushing Syndrome and Suppression of the Hypothalamic-Pituitary-Adrenal Axis After Chronic Use of Topical Glucocorticoids.

[~MaryO~]

http://www.theendocrinologist.org/pt/re/en...#33;8091!-1

 

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Cushing Syndrome and Suppression of the Hypothalamic-Pituitary-Adrenal Axis After Chronic Use of Topical Glucocorticoids.

 

Case Report

Endocrinologist. 18(3):117-120, May/June 2008.

Guadalix, Sonsoles MD; Jodar, Esbeban MD, PhD; Azriel, Sharona MD, PhD; Calatayud, Maria MD; Tejero, Ana Isabel MD

 

Abstract:

Topical and inhaled corticoids are considered to be safe even though some reports point out the risks, especially in children. We describe 2 adults in whom the chronic use of topical steroids led to Cushing syndrome. Patients treated with potent topical corticoids should be informed about the possibility of developing Cushing syndrome. Adrenal reserve should be monitored in those patients treated with glucocorticoids for long periods, regardless of the administration route.

 

© 2008 Lippincott Williams & Wilkins, Inc.

[MCF]

The problem with the author's recommendation for reserve testing is that I tested just fine for reserve at a time when my a.m. cortisol was 1.5 and I had severe symptoms of insufficiency after withdrawal of topical steroids. Here's a publication addressing the point, about how reserve testing fails to diagnose AI:

 

J Clin Endocrinol Metab 1996 Jan;81(1):285-90 Related Articles, Books, LinkOut

 

 

The potential for serious consequences from misinterpreting normal responses to the rapid adrenocorticotropin test.

 

Streeten DH, Anderson GH Jr, Bonaventura MM

 

Department of Medicine, State University of New York Health Science Center, Syracuse 13210, USA.

 

Despite unequivocal published evidence that patients with subnormal hypothalamic-pituitary-adrenal (HPA) function may respond normally to ACTH, such normal results are still considered reliable indications of unimpaired HPA function. This view was tested in four patients with clinical features suggesting corticotropin deficiency, in whom cosyntropin (0.25 mg, i.v.) raised serum cortisol above 560 nmol/L (20 micrograms/dL) at 1 h. All four patients had subnormal responses to metyrapone and excellent persistent improvement during subsequent glucocorticoid therapy. Serum cortisol concentrations 1 h after cosyntropin treatment in these patients closely resembled cortisol concentrations 1 h after uncomplicated cholecystectomy in six other patients. However, the rapid ACTH test in the patients with hypopituitarism failed to indicate whether more prolonged stimulation by ACTH or their endogenous stress would stimulate the normal continuing rise in serum cortisol, which reached 1358 +/- 170 nmol/L (+/- SE) 5 h after the incision in the cholecystectomized patients. As the three hypocorticotropic patients who were recognizably stressed had unstressed serum cortisol levels despite persistent adrenocortical reserve (shown by their ACTH responses) and recovered during glucocorticoid therapy, the ACTH test, if interpreted to indicate normal HPA function, would probably have had disastrous consequences. We conclude that a normal response to the rapid ACTH test can be dangerously misleading, particularly in incomplete ACTH deficiency states.

 

Comments:

Comment in: J Clin Endocrinol Metab 1996 Nov;81(11):4176

 

PMID: 8550765, UI: 96142001