Nov 5, 1977

Secondary pituitary hyperplasia in Addison's disease

Lancet
R ClaytonF D Rosenthal

Abstract

In patients with Addison's disease, whether treated or untreated for the previous 24 hours, hydrocortisone produced only a partial suppression of their elevated adrenocorticotrophic-hormone (A.C.T.H.) levels. This is comparable to untreated myxoedema, in which administration of triiodothyronine fails to inhibit secretion of thyrotrophin (T.S.H.). In myxoedema, however, continued treatment produces normal T.S.H. levels. Inadequate A.C.T.H. suppressibility in patients with Addison's disease while on treatment may be due to the maintenance of a secondary pituitary hyperplasia by inadequate replacement therapy. This may be clinically important, especially in the genesis of Nelson's syndrome.

  • References
  • Citations9

References

  • We're still populating references for this paper, please check back later.
  • References
  • Citations9

Citations

Mentioned in this Paper

Astonin
Process of Secretion
Visual Suppression
Thyrotropin
Triiodothyronine Measurement
Pituitary-Adrenal System
Metabolic Suppression
Thyroid Stimulating Hormone Measurement
Cell Secretion
Triiodothyronine

About this Paper

Related Feeds

Addison Disease

Addison's disease, also known as primary adrenal insufficiency and hypocortisolism, is a long-term endocrine disorder in which the adrenal glands do not produce enough steroid hormones. Discover the latest research on Addison's disease here.