[Drug treatment of prostatic carcinoma]

The basis for the medical treatment of prostate cancer is inhibition of the influence of testosterone on the prostate. Surgical castration is in 1997 still the gold standard; it reduces the testosterone level by 90% and the level of dihydrotestosterone (the active metabolite) by 60%. In the eighties luteinising hormone releasing hormone (LH-RH) analogues were introduced to avoid the psychological burden of castration. After an initial stimulation (the flare-up) testosterone decreases to castrate level within 3 weeks. Recently (non-steroidal) anti-androgens, competitive inhibitors of dihydrotestosterone on receptor level were introduced. There are also drugs which inhibit the conversion of testosterone to dihydrotestosterone: 5 alpha-reductase inhibitors. Non-steroidal anti-androgens and 5 alpha-reductase inhibitors do not decrease the testosterone level and therefore cause less loss of libido and energy than castration. Combination of (chemical) castration and anti-androgens is called maximum androgen blockade. This treatment has limited additional value in proportion to the increase in side effects and costs. A new form of treatment is intermittent androgen blockade. With this strategy growth of hormone-insensitive cells in the prostate, which is considered the main determinant of the poor prognosis, might be delayed with reduction of side effects and costs. The role of imidazoles is still investigated; the role of cytotoxic drugs is mainly palliative.