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| Cancer hormonotherapy |
Hormonotherapy for metastases | |
Hormonotherapy is the leading treatment for metastatic breast cancer among post-menopausal women. It offers significant increase in survival and quality of life. Most patients with positive receptors on primitive tumours will respond positively to hormonotherapy when metastases occur. Even among patients with negative receptors, an attempt at short hormonotherapy is possible (particularly for elderly patients), since certain metastatic tumours may response, despite the fact that the primitive tumour had no receptors (tumour variability).
Hormonotherapy is generally well tolerated. Treatment should begin with tamoxifen or an antiaromatase drug. The effect is produced within a few days or a few weeks. Hormonotherapy may be associated with other specific treatment modalities such as bone radiotherapy or surgery. Patients relapsing after tamoxifen may still obtain a good response with an aromatase inhibitor.
For pre-menopausal women, tamoxifen offers more or less the same efficiency as castration: the response duration (which is not, unfortunately, constant) is generally greater than one year, but can be much longer. For young patients, castration is performed at relapse. Antiaromatase drugs are not particularly efficient due to their high level of ovarian oestrogens (except after castration). The general use of chemotherapy, with its high response rate, sometimes clouds the value of hormonotherapy in terms of patient comfort.
Bone metastases are often very sensitive to hormonotherapy (pain reduction) although it may be difficult to establish the objective responses.
When metastases develop under hormonotherapy, it should be concluded that the tumour is hormonoindependent and chemotherapy should be attempted.
When metastases occur, hormonotherapy is the leading treatment.
Surgical castration is the easiest and less expensive treatment. However, psychologically, it is often very poorly tolerated. However, its effect, (particularly for painful bone metastases) can be quite spectacular with patients experiencing no pain as early as the day after surgery. Of course, the androgenic deprivation cannot correct mechanical disorders (such as medullar compression or pre-fracture syndrome for which a surgical solution may be sought).
LHRH agonists (after a short period of antiandrogen treatment) is now the preferred chemical castration method, in a more expansive and elegant manner. Treatment should be pursued without interruption, even when the tumour becomes hormono-independent, otherwise hormone-dependent clones may reoccur. The side effects of surgical and chemical castration are identical.
Oestrogens are rarely prescribed (in correlation with their cardiovascular toxicity). They can, however, be useful if an acute metastasis occurs (with associated local treatment if necessary).
Many trials are underway in order to precisely define the role of antiandrogens which, to date, would appear to be slightly less efficient than castration. They may, however, be of value when cancer cells apparently become hormonoindependent.
It has not been clearly demonstrated that total androgen blockade (castration in association with antiandrogen) is more effective than castration alone. Similarly, trials have been carried out involving intermittent castration in an attempt to resensitise hormono-independent clones. These trials are not particularly conclusive.
Generally, the duration of hormonodependency of metastatic prostate cancer is a longer than one year. However, undifferentiated cancers can be totally resistant from their onset, whereas other cancers may be sensitive for many years.
Progesterone is prescribed for metastatic cancer, which concerns approximately 20% of patients. The response rate with progesterone is around 30%, a few patients benefiting from very long remission. It is inefficient as an adjuvant treatment.
The treatment is generally well tolerated (despite risk of embolism).
Radioactive iodine treatment allows metastasis-specific interstitial radiotherapy (or brachytherapy).
It has been clearly demonstrated that, in order to reduce cancer progression, constant diminution of thyreotrope hormone (TSH) activity is required.
Constant thyroxine treatment is therefore prescribed, with the exception of the iodine brachytherapy period. This irradiation (around 100 mCi of Iodine 131) can be repeated although the tumour gradually becomes dedifferentiated and Iodine is no longer active on the tumour. Radio-induced fibrosis may become toxic (eg. lung metastases and risk of pulmonary insufficiency).
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