Adrenocortical function in prostatic cancer patients: effects of orchidectomy or different modes of estrogen treatment on basal steroid levels and on the response to exogenous adrenocorticotropic hormone.
Basal serum levels and ACTH-induced increments ('delta-values') of dehydroepiandrosterone (DHA) and its sulfate (DHAS), 4-androstene-3,17-dione (A-4), 17 alpha-hydroxyprogesterone (17-OHP), cortisol and testosterone and serum albumin levels were studied in patients with prostatic cancer before treatment and after orchidectomy or during estrogen treatment (intramuscular polyestradiol phosphate during the first 3 months, followed by another 3 months with additional oral ethinyl estradiol). Orchidectomy as well as single drug intramuscular or oral + intramuscular estrogens exerted a similar suppressive effect on basal levels of A-4 and 17-OHP. Orchidectomy caused a slight decrease in basal DHAS, while combined oral + intramuscular estrogens caused a pronounced decrease in basal DHAS and also in DHA. Single drug intramuscular estrogens did not affect basal DHA or DHAS levels. Increased basal cortisol levels appeared during combined oral + intramuscular estrogen therapy. delta DHA and delta A-4 values were unaffected by endocrine treatment, but delta 17-OHP and delta cortisol increased slightly after orchidectomy and during estrogen therapy. Significantly decreased albumin levels were only observed during combined oral + intramuscular estrogen treatment. Determination of estriol, which is a major metabolite of estradiol originating from polyestradiol phosphate, revealed significantly higher estriol levels during combined oral + intramuscular estrogen treatment than during single drug intramuscular estrogen therapy, indicating an increased induction of hepatic 16 alpha-hydroxylase activity. The pronounced decreases in DHAS and also in DHA during combined oral + intramuscular estrogen treatment are probably another reflexion of the liver side effects of oral estrogens.
Carlström
K
K
Department of Obstetrics, Karolinska Institutet, Huddinge University Hospital, Sweden.
Stege
R
R
D019326:17-alpha-Hydroxyprogesterone; D000284:Administration, Oral; D000302:Adrenal Cortex / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000735:Androstenedione / Q000097:blood; D003131:Combined Modality Therapy; D003687:Dehydroepiandrosterone / Q000031:analogs & derivatives / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate; D004359:Drug Therapy, Combination; D004958:Estradiol / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000627:therapeutic use; D045166:Estradiol Congeners / Q000008:administration & dosage* / Q000627:therapeutic use; D004997:Ethinyl Estradiol / Q000008:administration & dosage / Q000627:therapeutic use; D006728:Hormones / Q000097:blood*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006908:Hydroxyprogesterones / Q000097:blood; D007273:Injections, Intramuscular; D008297:Male; D009919:Orchiectomy; D011471:Prostatic Neoplasms / Q000097:blood / Q000188:drug therapy / Q000378:metabolism* / Q000601:surgery; D012709:Serum Albumin / Q000032:analysis; D039181:Steroid 16-alpha-Hydroxylase; D013739:Testosterone / Q000097:blood
D045166:Estradiol Congeners; D006728:Hormones; D006908:Hydroxyprogesterones; D012709:Serum Albumin; D013739:Testosterone; D000735:Androstenedione; D004997:Ethinyl Estradiol; D003687:Dehydroepiandrosterone; D004958:Estradiol; D019314:Dehydroepiandrosterone Sulfate; D019326:17-alpha-Hydroxyprogesterone; D000324:Adrenocorticotropic Hormone; D039181:Steroid 16-alpha-Hydroxylase; C008958:polyestradiol phosphate; D006854:Hydrocortisone