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Tamoxifen is a pure antiestrogenic trans-isomer and has differential actions at estrogen target tissues throughout the body. Tamoxifen is selectively antiestrogenic in the breast but estrogen-like in bones and endometrial cancer. [24] Tamoxifen undergo phase I metabolism in the liver by microsomal cytochrome P450 (CYP) enzymes.
Tamoxifen, sold under the brand name Nolvadex among others, is a selective estrogen receptor modulator used to prevent breast cancer in women and men. [13] It is also being studied for other types of cancer. [13] It has been used for Albright syndrome. [14] Tamoxifen is typically taken daily by mouth for five years for breast cancer. [14]
[5] [7] It has estrogenic effects in bone, the liver, and the uterus and antiestrogenic effects in the breasts. [6] [8] [9] [5] It is a triphenylethylene derivative and is closely related to tamoxifen. [10] Toremifene was introduced for medical use in 1997. [11] [12] It was the first antiestrogen to be introduced since tamoxifen in 1978. [13]
The Women's Health Initiative (WHI) is an ongoing study of over 27,000 women that began in 1991, with the most recent analyses suggesting that, when initiated within 10 years of menopause, HRT reduces all-cause mortality and risks of coronary disease, osteoporosis, and dementia; after 10 years the beneficial effects on mortality and coronary ...
Perimenopausal women on combined oral contraceptives have increased bone density, [13] and COCs can be used to decrease hot flashes. [14] Combined oral contraceptives have been shown to reduce risk of endometrial cancer, BRCA1 and BRCA2 ovarian cancer, and a modest reduction in colon cancer.
No evidence has been identified to suggest Mirena affects bone mineral density (BMD). [72] Two small studies, limited to studying BMD in the forearm, show no decrease in BMD. [73] [74] One of the studies showed at seven years of use, similar BMD at the midshaft of the ulna and at the distal radius as nonusers matched by age and BMI. [73]
Raloxifene increases bone mineral density in postmenopausal women but decreases it in premenopausal women. [14] In the MORE trial, the risk of vertebral fractures was decreased by 30%, and bone mineral density was increased in the spine (by 2.1% at 60 mg, 2.4% at 120 mg) and femoral neck (2.6% at 60 mg, 2.7% at 120 mg). [20]
Experimental evidence suggests that bone cells composed of osteocytes, osteoclasts, and osteoblasts die within 12–48 hours, and marrow fat cells die within 120 hours. [17] The death of bone does not alter its radiographic opacity nor its mineral density. Necrotic bone does not undergo resorption; therefore, it appears relatively more opaque.