Secondary pituitary hyperplasia in Addison's disease.
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.
D000224:Addison Disease / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D000284:Administration, Oral; D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D005438:Fludrocortisone / Q000008:administration & dosage / Q000627:therapeutic use; D006801:Humans; D006854:Hydrocortisone / Q000008:administration & dosage / Q000378:metabolism / Q000627:therapeutic use; D009347:Nelson Syndrome / Q000150:complications* / Q000209:etiology / Q000378:metabolism; D010911:Pituitary Neoplasms / Q000150:complications*; D010913:Pituitary-Adrenal System / Q000503:physiopathology
D000324:Adrenocorticotropic Hormone; D005438:Fludrocortisone; D006854:Hydrocortisone