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Outcomes of prostate cancer

X-ray of pelvis showing sclerotic (ivory white) changes indicative of metastatic prostate cancer.  Treatment will be by anti-hormones.
X-ray of pelvis showing sclerotic (ivory white) changes indicative of metastatic prostate cancer. Treatment will be by anti-hormones.

If there is local (i.e. relapse in the prostate region) after surgery, usually called to attention by a rising PSA and in the face of negative restaging tests for disease further afield, then external beam therapy to the prostate ‘bed’ is successful in a minority of bringing about PSA control again, but these patients are obviously at greater risk for both further local and distant (i.e. metastatic) relapse. It is an interesting observation that of patients who develop a rise in PSA after radical surgery, we can predict those who are likely to have relapse only in the prostate 'bed'. Those patients whose PSA fails to almost disappear (<0.05) after surgery or who suffer a rise in the first six months after surgery are likely to have metastatic disease. Those who have a late and slow rise in PSA (e.g. a rise to 0.1 after 2 years and then 0.3 after 2.5 years) are likely to have disease relapse in the prostate 'bed' and it is this group that is likely to benefit from radiotherapy to the 'bed'. For patients who go down the radical prostatectomy route and whose prostate margins are histologically involved when the histologist microscopically examines the surgical specimen, then early post-operative radiotherapy to the prostate 'bed' is to be recommended. The fact that we sometimes employ radiotherapy after surgery is used by some surgeons to argue that, as surgery can be followed by radiotherapy and so surgery should always be used first. This is a spurious argument in that if one had known that the margins of the operative specimen were going to be positive, then the operation was probably the wrong thing to do in the first place (as patients having transcapsular disease at the outset are best served by neoadjuvant hormonal therapy followed by conformal external beam radiotherapy). For patients with metastatic relapse (i.e. disease that has spread to other organs) then anti-hormone therapy is indicated. 

 

This is first aimed at cutting off the production of testosterone from the testes and this is achieved by either orchidectomy (the removal of the testes, castration) or the delivery of quarterly injections of a drug (LHRH agonist) which blocks the pituitary gland’s stimulating hormone, which keeps the testes active. Either of these methods is effective at reducing the serum testosterone (male hormone) to castrate levels, the desired objective, as this hormone (testosterone) is undoubtedly the main growth factor for prostate cancer. 

 

Sometimes, an antiandrogen drug will be added as well (so-called total antiandrogen blockade). Approximately four fifths of patients will respond to this hormone therapy and may well maintain this remission for up to some years. When the patient eventually relapses, a further hormone remission (usually shorter than the first) can sometimes be achieved by the removal of one anti-androgen drug and the substitution of another or the giving of the physiological steroid hormone hydrocortisone which suppresses the adrenal glands production (the last source of male hormone once the testes have been ablated). A low dose oestrogen may be added at this time. For painful relapses in bone (the commonest site for metastatic relapse) the use of radiotherapy is useful and the use of isotope therapy (e.g. strontium-90) can be useful at arresting the progression of the metastases for a time. Chemotherapy has recently made inroads into the therapy of 'hormone refractory' prostate cancer management notably the drugs: taxotere and mitozantrone -usually not combined at the same time) have been shown to be useful in good performance status patients (i.e. patients whose condition warrants more therapy), and can achieve remissions for some months. A new generation of drugs targeting vascular growth receptors (the stimuli for the essential new growth of tumour blood vessels) are starting to make a place for themselves in the therapy of hormone resistant prostate cancer. Further information concerning the developments in therapy – updated every few months from the published literature – is given by clicking onto the Research and Development section or from Dr. P. N. Plowman at St. Bartholomew's Hospital, London (tel 44-207- 601 8351).


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