ENDOCRINOLOGICAL STUDIES ON PROSTATIC CARCINOMA
1. Plasma Hormone Profiles in Patients with Prostatic Carcinoma
1981 Volume 72 Issue 8 Pages 953-966
Details
1981 Volume 72 Issue 8 Pages 953-966
Plasma testosterone (T), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEA-S, cortisol (F), luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL) levels were determined in patients with prostatic carcinoma before and during antiandrogen therapy. The relationships between clinical courses, therapeutic agents and the profiles of these hormones were examined. The results were as follows;
1) It was considered that the hormone profiles were mainly depended on the pharmacological effects of the therapeutic agents and that there were no relationships between clinical courses and the hormone profiles. However, the pretreatment values of DHEA-S were significantly lower in stage IV patients compared to stage I-III patients (p<0.001).
2) Both sythetic progestogens such as chlormadinone acetate (CMA) and synthetic estrogens such as diethylstilbestrol diphosphate (DES-diphosphate) suppressed not only T levels but also DHEA and DHEA-S levels significantly. On the other hand, the agent composed of estradiol such as estramustine phosphate (Estracyt) suppressed T levels but not DHEA and DHEA-S levels. The levels of LH and FSH were suppressed more effectively by estrogens than synthetic progestogens. The levels of F were not so affected by synthetic progestogens, while those were significantly elevated by estrogens.
3) It was considered that there were two mechanism of action to suppress the DHEA and DHEA-S levels. The first, as the ACTH-Z stimulation test in patients under CMA or DES-diphosphate administration showed, these agents might inhibit the activity of adrenal C17-C20 lyase. The second, as CMA possesses the corticosteroid-mimetic actions, there could exist another mechanism to suppress the DHEA and DHEA-S through the pituitary-adrenal axis.
4) The mild hyperprolactinemia was noticed in patients under estrogen therapy, but no relationships were noted among the levels of T, DHEA and prolactin. Therefore, it was considered that hyperprolactinemia caused by estrogens did not stimulate the adrenal androgen biosynthesis. Moreover, the elevations of T, DHEA and DHEA-S were not noticed in relapsed cases, there seemed to be no relationships between adrenal androgen levels and the reactivation of the prostatic carcinoma.
