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As a synthetic, non-steroidal compound with hormone-like effects (many of which are poorly understood), tamoxifen has a similar structure to DES, but lacks the active components. When applied to the skin, tamoxifen binds to receptor cells, activating their production of estrogen and prostaglandin E, and subsequently, testosterone. As a result, tamoxifen suppresses the hormone concentrations of its target receptors, and inhibits the production of growth factors that promote cell growth. In humans, tamoxifen reduces the concentration of both androgens and 17beta-estradiol. Its effects do not stop with the decrease of the levels of testosterone. Tamoxifen can decrease the testosterone levels of men with benign prostatic hypertrophy in clinical trials. It also decreases testosterone and estradiol levels and increases estrone levels, although this effect can be reversed by using tamoxifen to induce estrogen deficiency, as is the case for some women with menopause who have a deficiency of DHEA. The efficacy of tamoxifen has been tested in clinical trials; in studies, tamoxifen reduced androgen-responsive tumors (testes and prostate) and suppressed androgen receptor expression, and decreased testosterone production. Trials of tamoxifen in women with benign prostatic hypertrophy showed that it can decrease the growth of these tumors, but can also induce estrone deficiency and decrease androgen-responsive ovarian tumor cell growth. Thus, tamoxifen is a highly selective estrogen receptor modulator that is safe and effective against all tumors and benign prostatic hypertrophy. Progesterone In women, a small but growing body of clinical trial data have shown that tamoxifen is a potent androgen receptor modulator, and is therefore recommended for postmenopausal women with benign prostatic hypertrophy. In clinical trials, tamoxifen significantly decreased androstenedione, estradiol, and androsterone but increased testosterone in postmenopausal women with mild and low-grade adenomas. Tamoxifen does not affect the level of androgen receptor in benign prostatic hypertrophy. Tamoxifen has been shown to increase androgen receptor expression in benign prostatic hypertrophy in some clinical trials. As tamoxifen can cause a reduced circulating androgen profile in postmenopausal women, it is suggested that tamoxifen should not be prescribed to postmenopausal women. The safety of tamoxifen has not been studied in postmenopausal women. However, it should be used cautiously, especially given that Similar articles:

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