title: Comparative analysis of plasma 17-hydroxyprogesterone and cortisol responses to ACTH in patients with various adrenal tumors before and after unilateral adrenalectomy.
abstract: Patients with non-hyperfunctioning adrenal adenomas often have an increased plasma 17-hydroxyprogesterone response to ACTH stimulation. The effects of adrenal surgery on this abnormality have rarely been investigated. One hundred and sixty-one patients with unilateral adrenal tumors (non-hyperfunctioning adenomas, 78; cortisol-producing adenomas, 8; aldosterone-producing adenomas, 37; adrenal cysts, 12; pheochromocytomas, 26) were studied. Patients before and after adrenal surgery as well as 60 healthy subjects underwent an ACTH stimulation test using 2 mg synthetic ACTH(1-24) (Cortrosyn Depot, Organon). Basal and ACTH-stimulated plasma 17-hydroxyprogesterone and cortisol concentrations are reported. Before adrenal surgery, the basal plasma 17-hydroxyprogesterone concentrations were normal in patients with all types of tumors. However, the ACTH-stimulated plasma 17-hydroxyprogesterone levels were abnormally increased in 53% and 31% of patients with non-hyperfunctioning adenomas and aldosterone-producing adenomas, respectively. In addition, a few patients with adrenal cysts and pheochromocytomas also showed an increased ACTH-stimulated 17-hydroxyprogesterone response. After unilateral adrenalectomy, this hormonal abnormality disappeared in most, although not all patients with adrenal tumors. In patients with non-hyperfunctioning adrenal tumors, ACTH-stimulated plasma 17-hydroxyprogesterone and cortisol concentrations significantly correlated with the size of the tumors. These results firmly indicate that the tumoral mass itself may be responsible for the increased plasma 17-hydroxyprogesterone and cortisol responses after ACTH stimulation in patients with non-hyperfunctioning and hyperfunctioning adrenal adenomas.
authors.affiliation: 2nd Department of Medicine, Semmelweis University Medical School, Budapest, Hungary.
authors.forename: M
authors.initials: M
authors.lastname: Tóth
authors.forename: K
authors.initials: K
authors.lastname: Rácz
authors.forename: V
authors.initials: V
authors.lastname: Adleff
authors.forename: I
authors.initials: I
authors.lastname: Varga
authors.forename: L
authors.initials: L
authors.lastname: Fütö
authors.forename: C
authors.initials: C
authors.lastname: Jakab
authors.forename: K
authors.initials: K
authors.lastname: Karlinger
authors.forename: R
authors.initials: R
authors.lastname: Kiss
authors.forename: E
authors.initials: E
authors.lastname: Gláz
mesh_terms: D019326:17-alpha-Hydroxyprogesterone / Q000097:blood*; D000236:Adenoma / Q000473:pathology / Q000503:physiopathology / Q000601:surgery; D000293:Adolescent; D000310:Adrenal Gland Neoplasms / Q000473:pathology / Q000503:physiopathology* / Q000601:surgery*; D000315:Adrenalectomy; D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000096:biosynthesis; D003366:Cosyntropin; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010673:Pheochromocytoma / Q000473:pathology / Q000503:physiopathology / Q000601:surgery
chemical_list: D003366:Cosyntropin; D000450:Aldosterone; D019326:17-alpha-Hydroxyprogesterone; D006854:Hydrocortisone