0

The full content of Annals is available to subscribers

Subscribe/Learn More  >
Articles |

The Role of Adrenocorticoids in the Inappropriate Antidiuretic Hormone Syndrome

MARSHAL P. FICHMAN, M.D.; and JOHN E. BETHUNE, M.D., F.A.C.P.
Ann Intern Med. 1968;68(4):806-820. doi:10.7326/0003-4819-68-4-806
Text Size: A A A
SUMMARY:

Twenty patients with all of the characteristics of the inappropriate antidiuretic hormone (ADH) syndrome were observed at the Los Angeles County General Hospital in the past 2 years. The varied causes, including chest lesions, central nervous system disorders, and unclassified causes and frequency, suggest that it is certainly not a rare syndrome. Bioassay for ADH in the majority of cases tested showed increased biologic activity in serums or tumors. The defect in acute water load excretion was correctable by intravenous diphenylhydantoin in the cases not due to autonomous tumor. Glucocorticoid administration failed to correct hyponatremia in patients with the syndrome as compared with patients with hyponatremia secondary to hypopituitarism. The failure of high doses of glucocorticoids to affect the syndrome suggests that, at least in patients with inappropriate or autonomous ADH secretion, glucocorticoids do not act as inhibitors of ADH release. Mineralocorticoids in high doses may correct the hyponatremia, and an "escape" phenomenon with a resumption of increased urinary sodium may ensue. Aldosterone excretion may be normal and important in minimizing sodium losses as shown by the inhibition of aldosterone-mediated sodium retention and aggrevation of the sodium loss by aldosterone inhibitors. Creatinine clearance was generally normal, and there was no correlation between variation in glomerular filtration rate and urine sodium excretion. The presence of normal creatinine clearance and aldosterone excretion with persistent urine sodium loss, in spite of hyponatremia, suggests that the sodium diuresis is due to some "third factor" other than increased glomerular filtration or hypervolemic inhibition of aldosterone. The mechanism of sodium loss in this syndrome appears to be similar to the escape phenomenon occurring with high doses of mineralocorticoids and may be related to proximal tubular rejection of sodium secondary to an expanded intravascular volume.

Figures

Tables

References

Letters

NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Comments

Submit a Comment
Submit a Comment

Summary for Patients

Clinical Slide Sets

Terms of Use

The In the Clinic® slide sets are owned and copyrighted by the American College of Physicians (ACP). All text, graphics, trademarks, and other intellectual property incorporated into the slide sets remain the sole and exclusive property of the ACP. The slide sets may be used only by the person who downloads or purchases them and only for the purpose of presenting them during not-for-profit educational activities. Users may incorporate the entire slide set or selected individual slides into their own teaching presentations but may not alter the content of the slides in any way or remove the ACP copyright notice. Users may make print copies for use as hand-outs for the audience the user is personally addressing but may not otherwise reproduce or distribute the slides by any means or media, including but not limited to sending them as e-mail attachments, posting them on Internet or Intranet sites, publishing them in meeting proceedings, or making them available for sale or distribution in any unauthorized form, without the express written permission of the ACP. Unauthorized use of the In the Clinic slide sets will constitute copyright infringement.

Toolkit

Buy Now

to gain full access to the content and tools.

Want to Subscribe?

Learn more about subscription options

Advertisement
Related Articles
Topic Collections
PubMed Articles
Forgot your password?
Enter your username and email address. We'll send you a reminder to the email address on record.
(Required)
(Required)