title: Luteinizing hormone (LH)-releasing hormone agonist reduces serum adrenal androgen levels in prostate cancer patients: implications for the effect of LH on the adrenal glands.
abstract: Recently, adrenal androgens have been targeted as key hormones for the  development of castration-resistant prostate cancer therapeutics. Although  circulating adrenal androgens originate mainly from the adrenal glands, the  testes also supply about 10%. Although widely used in androgen deprivation  medical castration therapy, the effect of luteinizing hormone-releasing  hormone (LH-RH) agonist on adrenal androgens has not been fully studied. In  this study, changes in testicular and adrenal androgen levels were measured  and compared to adrenocorticotropic hormone levels. To assess the possible  role of LH in the adrenal glands, immunohistochemical studies of the LH  receptor in normal adrenal glands were performed. Forty-seven patients with  localized or locally progressive prostate cancer were treated with LH-RH  agonist with radiotherapy. Six months after initiation of treatment,  testosterone, dihydrotestosterone, and estradiol levels were decreased by  90%-95%, and dehydroepiandrosterone-sulfate, dehydroepiandrosterone, and  androstenedione levels were significantly decreased by 26%-40%. The  suppressive effect of LH-RH agonist at 12 months was maintained.  Adrenocorticotropic hormone levels showed an increasing trend at 6 months and  a significant increase at 12 months. LH receptors were positively stained in  the cortex cells of the reticular layer of the adrenal glands. The long-term  LH-RH agonist treatment reduced adrenal-originated adrenal androgens. LH  receptors in the adrenal cortex cells of the reticular layer might account for  the underlying mechanism of reduced adrenal androgens.
authors.affiliation: Department of Urology, Gunma University Graduate School of Medicine, 3-39-22 Showamachi, Meabashi 371-8511, Japan.
authors.forename: Masahiro
authors.initials: M
authors.lastname: Nishii
authors.forename: Masashi
authors.initials: M
authors.lastname: Nomura
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Sekine
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Koike
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Matsui
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Shibata
authors.forename: Kazuto
authors.initials: K
authors.lastname: Ito
authors.forename: Tetsunari
authors.initials: T
authors.lastname: Oyama
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Suzuki
mesh_terms: D000311:Adrenal Glands / Q000378:metabolism; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000368:Aged; D000728:Androgens / Q000097:blood*; D007987:Gonadotropin-Releasing Hormone / Q000819:agonists* / Q000378:metabolism; D006801:Humans; D016729:Leuprolide / Q000627:therapeutic use*; D007986:Luteinizing Hormone; D008297:Male; D008875:Middle Aged; D020360:Neoadjuvant Therapy; D064129:Prostatic Neoplasms, Castration-Resistant / Q000188:drug therapy*; D013737:Testis / Q000378:metabolism
chemical_list: D000728:Androgens; D007987:Gonadotropin-Releasing Hormone; D000324:Adrenocorticotropic Hormone; D007986:Luteinizing Hormone; D016729:Leuprolide