Surgical versus Medical Castration in the Management of Advanced Prostate Cancer

  • M. R. G. Robinson
Conference paper
Part of the ESO Monographs book series (ESO MONOGRAPHS)


For centuries the effect of castration on sexuality and the secondary sex glands of man has been known and for the whole of this century orchidectomy has been employed as endocrine therapy for prostatic disorders. It was in 1786 that John Hunter first described scientifically the effect of castration on the prostate gland and at the end of the last century White [2] and Cabot [3] advocated, without distinguishing between benign and neoplastic disease, the removal of the testes for prostatic obstruction of the bladder neck. In 1941, Huggins et al. [4] stated that “in many instances, a malignant prostatic tumour is an overgrowth of adult prostatic epithelial cells. All known types of adult prostatic epithelial cells undergo atrophy when androgenic hormones are greatly reduced in amount. Therefore, significant improvement should occur in the clinical condition of patients with advanced prostatic carcinoma subjected to castration”. The authors observed that, following orchidectomy, patients with advanced prostatic cancer experience relief of pain associated with calcification of lytic bone metastases and a fall in pre-treatment elevated acid phosphatase levels. They also observed that the administration of exogenous testosterone caused a return of symptoms. The only disadvantages of orchidectomy are the psychological stress of the operation, minor surgical complications such as scrotal haematoma or abscess, loss of libido and impotence, hot flushes and occasional transient ankle oedema. Since 1941, because of observations of Huggins, surgical castration has been the standard endocrine treatment against which other therapies have been judged. It was not until the early 1970s that plasma testosterone levels were first measured, demonstrating that castration does remove the principal source of androgens. It was observed that orchidectomy reduced the circulating plasma testosterone by 90% to castrate levels, with the remaining androgens being derived from the adrenal cortex [5,6]. Testosterone is a pro-hormone which is converted in the prostatic cell by 5-alpha reductase to dihydrotestosterone, the active hormone. The significance of dihydrotestosterone derived from adrenal androgens is discussed in other contributions to this monograph, but in spite of its existence it has generally been accepted that in symptomatic advanced prostatic carcinoma 70–80% of patients have a subjective or objective response to castration.


Plasma Testosterone Luteinising Hormone Release Hormone Cyproterone Acetate Plasma Testosterone Level Surgical Castration 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Hunter J: Observation on Certain Parts of the Animal Oeconomy. First Edition, London 1786 p 39Google Scholar
  2. 2.
    White JW: Results of double castration in hypertrophy of the prostate. Ann Surg 1895 (22):1PubMedCrossRefGoogle Scholar
  3. 3.
    Cabot AT: A question of castration for enlarged prostate. Ann Surg 1896 (24):265PubMedCrossRefGoogle Scholar
  4. 4.
    Huggins C, Stevens RA, Hodges CB: Studies on prostatic cancer. II. The effects of castration on advanced carcinoma of the prostate gland. Arch Surg 1941 (43):209CrossRefGoogle Scholar
  5. 5.
    Robinson MRG, Thomas BS: Effect of hormonal therapy on plasma testosterone levels in prostatic carcinoma. Br Med J 1971 (5):391–394CrossRefGoogle Scholar
  6. 6.
    Shearer RJ, Hendry WF, Sommerville F, Fergusson JD: Plasma testosterone: an accurate monitor of hormone treatment in prostatic cancer. Br J Urol 1973(45):468–477CrossRefGoogle Scholar
  7. 7.
    Nesbitt RM, Baum WC: Endocrine control of prostatic carcinoma: clinical statistical survey of 1818 cases. JAMA 1950 (143):1317–1320CrossRefGoogle Scholar
  8. 8.
    Nesbitt RM, Plumb RT: Prostatic carcinoma: a follow-up of 795 patients treated prior to endocrine era and a comparison of survival rates between these patients treated by endocrine therapy. Surgery 1946 (20):263–272Google Scholar
  9. 9.
    Veterans Administration Cooperative Urological Research Group: Treatment survival of patients with cancer of the prostate. Surg Gyn Obst 1967 (124):1011–1017Google Scholar
  10. 10.
    Robinson MRG: EORTC protocol 30805: a phase III trial comparing orchidectomy versus orchidectomy and cyproterone acetate and low dose stilboestrol in the management of metastatic carcinoma of the prostate. Smith PH, Pavone-Macaluso M (eds) Management of Advanced Cancer of the Prostate and Bladder. A Liss, New York 1988 pp 101–110Google Scholar
  11. 11.
    Schally AV, Arimura A, Baba Y, Mair RMG, Matsuo H, Redding TW, Debeljuk L: Isolation of properties of the FSH and LH releasing hormone. Biochem Biophys Res Comm 1971 (43):393–399PubMedCrossRefGoogle Scholar
  12. 12.
    Wenderoth UK, Jacobi GH: Gonadotrophin-releasing hormone analogues in the palliation of carcinoma of the prostate. World J Urol 1983 (1):40CrossRefGoogle Scholar
  13. 13.
    Denis L, Kuyppens F, Mahler C, Debruyne FMJ, Weil EHJ, Lunglmayr G, Newling D, Robinson MRG, Richards B, Smith PH, Whelan P: Long-term therapy with depot LHRH analogue (Zoladex) in patients with advanced prostatic cancer. In: Murphy GP, Khoury S, Kuss R, Chatelane Ch and Denis L (eds) The Prostate Cancer. Part A: Research, Endocrine Treatment, Histopathology. A Liss, New York 1987 pp 221–228Google Scholar
  14. 14.
    Bouffioux C, Denis L, Mahler C, de Laval J: The treatment of advanced prostatic cancer with LHRH analogues: prevention of “flare-up” phenomenon. In: Murphy GP, Khoury S, Kuss R, Chatelane Ch and Denis L (eds) The Prostate Cancer. Part A: Research, Endocrine Treatment, Histopathology. A Liss, New York 1987 pp 255–260Google Scholar
  15. 15.
    Peeling WB: A comparison between surgical orchidectomy and LHRH antagonist (“Zoladex” ICI 188630). In: Murphy GP, Khoury S (eds) The Treatment of Metastatic Cancer of the Prostate. Therapeutic Progress in Urological Cancers. A Liss, New York 1989 pp 41–46Google Scholar
  16. 16.
    Labrie F, Dupont A, Belanger A, Cusan L, Lacousiere Y, Monfette G, Laberge JG, Emond JP, Fazekas ATA, Raynaud JP, Husson JM: New hormonal therapy in prostatic carcinoma: combined treatment with LHRH agonist and an anti-androgen. J Clin Invest Med 1982 (5):267–275Google Scholar
  17. 17.
    Crawford ED, Eisenberger MA, McLeod DJ, Spaulding JT, Benson R, Dorr FA, Blumenstral, Davis MA, Goodan DJ: A controlled trial of luprolide and flutamide in prostatic carcinoma. N Engl J Med 1989(321):419–424PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1991

Authors and Affiliations

  • M. R. G. Robinson
    • 1
  1. 1.Department of UrologyGeneral InfirmaryWest YorkshireUK

Personalised recommendations