Surgical versus Medical Castration in the Management of Advanced Prostate Cancer
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  and Cabot  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.  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.
KeywordsPlacebo Toxicity Testosterone Flare Androgen
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