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Antihormone therapy is a type of hormone therapy that suppresses selected hormones or their effects, in contrast with hormone replacement therapy, which encourages hormone activity. The suppression of certain hormones can benefit patients with certain cancers because certain hormones prompt or help the growth of a tumor . [ 1 ]
Hormone replacement therapy (HRT), also known as menopausal hormone therapy (MHT), is for women with menopausal symptoms. It is based on the idea that the treatment may prevent discomfort caused by diminished circulating estrogen and progesterone hormones, or in the case of the surgically or prematurely menopausal, that it may prolong life and may reduce incidence of dementia. [1]
For the use of hormone antagonists in cancer, see hormonal therapy (oncology) A hormone antagonist is a specific type of receptor antagonist which acts upon hormone receptors. Such pharmaceutical drugs are used in antihormone therapy.
Hormonal therapy is used for several types of cancers derived from hormonally responsive tissues, including the breast, prostate, endometrium, and adrenal cortex. Hormonal therapy may also be used in the treatment of paraneoplastic syndromes or to ameliorate certain cancer- and chemotherapy -associated symptoms , such as anorexia .
Androgen deprivation therapy (ADT), also called androgen ablation therapy or androgen suppression therapy, is an antihormone therapy whose main use is in treating prostate cancer. Prostate cancer cells usually require androgen hormones , such as testosterone , to grow.
[11] [12] [13] A 2015 systematic review and meta-analysis found that opioid therapy decreased testosterone levels in men by about 165 ng/dL (5.7 nmol/L) on average, which was a reduction in testosterone level of almost 50%. [11]
The following is a list of notable clinical studies of menopausal hormone therapy (estrogen and/or progestogen therapy) in women, ...
Like other NSAAs such as flutamide and bicalutamide, nilutamide, without concomitant GnRH analogue therapy, increases serum androgen (by two-fold in the case of testosterone), estrogen, and prolactin levels due to inhibition of AR-mediated suppression of steroidogenesis via negative feedback on the hypothalamic–pituitary–gonadal axis. [14]