tion prove a problem with these, formestane may be substituted in postmenopausal women (it inhibits aromatase, an enzyme involved in the convertion of androgens to oestrogens). Aminoglutethimide and trilostane, which similarly inhibit the conversion of androgens to oestrogens (and have largely replaced adrenalectomy for breast cancer), are also used for postmenopausal women; concurrent glucocorticoid replacement therapy is, however, essential.

Prostatic cancer is androgen-dependent and metastatic disease can be helped by orchidectomy, or by a gonadorelin analogue, e.g. buserelin, goserelin, leuprorelin or triptorelin. These cause a transient stimulation of luteinising hormone and thus testosterone release, before inhibition occurs; some patients may experience exacerbation of tumour effects, e.g. bone pain, spinal cord compression. Where this can be anticipated, prior orchidectomy or antiandrogen treatment, e.g. with cyproterone or flutamide, is protective.

Benign prostatic hypertrophy is also androgen-dependent and drug therapy includes use of finasteride, an inhibitor of the enzyme (5a-reductase) which activates testosterone (see p. 544).

Adrenocortical steroids are used for their action on specific cancers and also to treat some of the complications of cancer, e.g. hypercalcaemia, raised intracranial pressure. Their principal use is in cancer of the lymphoid tissues and blood. In leukaemias they may also reduce the incidence of complications such as haemolytic anaemia and thrombocytopenia. A glucocorticoid is preferred, e.g. prednisolone, as high doses are used and mineralocorticoid actions are not needed and cause fluid retention.

In general, endocrine therapy carries less serious consequences for normal tissues than do cytotoxic agents.

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