Estrogen replacement therapy: indications, contraindications, and agent selection

Article Abstract:

During menopause estrogen is no longer produced by the ovaries. Reduced estrogen causes hot flashes, mood fluctuations, and changes in the vagina, bladder and urethra. Osteoporosis, the resorption of bone which can potentially cause fractures, increases during menopause. This breakdown of bone mass, which continues for over 15 to 20 years, can be prevented with estrogen replacement therapy (ERT). White and oriental background, a family history of osteoporosis, a small frame, poor nutrition, low calcium intake, and lack of physical activity are some of the factors placing women at risk for osteoporosis. Many women are unaware of the benefits of ERT in preventing osteoporosis. Estrogen can prevent coronary heart disease and reduce the risks for heart attack and stroke. ERT delivered orally (not by vaginal administration or skin patches) can cause a reduction in low density lipoproteins and an increase in the preferred high density lipoprotein cholesterol and, consequently, prevent the development of atherosclerotic plaques in the coronary arteries. Progestins are often given in combination with estrogen to prevent the risk for endometrial cancer which is associated with estrogen therapy alone. However, the addition of progestins has been shown to decrease the cardiovascular benefits of treatment with estrogen alone. Higher doses of estrogen improve the reduced benefits related to the addition of progestins. Estrogen can be given in 0.625 mg or 1.25 mg conjugated estrogen daily plus a two week cycle or daily dose of 2.5 mg or five mg of progesterone. Some combinations may produced menstruation. Abnormal bleeding patterns must be investigated. Simultaneous administration of calcium is also recommended. Women without a uterus do not require added progestin. There are three different types of estrogens: estradiol, estrone sulfate and conjugated estrogen. ERT should not be taken by women who have had a recent heart attack or blot clot (thromboembolism), or women with breast or endometrial cancer. Nonhormonal interventions such as diet and exercise can also be used to improve the adverse effects caused by the lack of estrogen. (Consumer Summary produced by Reliance Medical Information, Inc.)

Coronary heart disease

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Estrogens in the prevention of osteoporosis in postmenopausal women

Article Abstract:

Osteoporosis is the loss of bone density caused by an increase in bone resorption. Bone tissue becomes thinned due to the development of small holes within the bone. During menopause estrogen is no longer produced by the ovaries. The lack of estrogen contributes to osteoporosis and increases the related risk for fractures. In the United States, 1.2 million fractures each year are the result of osteoporosis. Estrogen replacement therapy reduces the risk of osteoporosis in postmenopausal women. How estrogen prevents bone loss is not understood. Although estrogen reduces the rate of bone resorption, it does not restore lost bone. Several studies have explored estrogen replacement doses and durations of effectiveness. One study reported that a lower dose of estrogen when combined with calcium supplementation was effective in preventing bone loss. It has also been demonstrated that when estrogen therapy is discontinued, bone loss increases significantly. Therefore, long-term estrogen therapy is needed. When progestins are given with estrogen (to prevent the adverse effects of sole estrogen treatment on the endometrium) they do not seem to interfere with the benefits of estrogen in preserving bone density. More studies on the effects of progestins are needed. To offer the best protection against osteoporosis, estrogen replacement therapy should begin at the onset of menopause, or within three years of the last menstrual period, and continue for at least 15 years. (Consumer Summary produced by Reliance Medical Information, Inc.)

Care and treatment, Postmenopausal women

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Monitoring skeletal response to estrogen

Article Abstract:

When, during menopause, the ovaries cease to produce the hormone estrogen, some women may experience bone loss, making their bones less dense and thus more susceptible to fractures. The depleted estrogen, which prevents bone loss, can be replaced with estrogen replacement therapy (ERT). ERT completely prevents early bone loss in 80 percent of women and is more effective on long-term bone loss. Some bones are protected less than others and are more likely to develop fractures. Bone densitometry measures the density of bone and can be useful for determining whether patients are receiving and taking adequate doses of ERT. In addition, bone densitometry can determine the effects of such factors as reduced physical activity, certain drugs, and diseases of calcium absorption, which can contribute to bone loss. Many patients taking ERT who experience side effects or have concerns about its cancer-causing effects stop the therapy within five years. This non-compliance contributes to bone loss, especially in the spine, where ERT has the greatest benefit. It is suggested that bones of the spine be monitored by bone densitometry to assess changes in bone density. To effectively monitor ERT physicians should use bone densitometry in combination with blood evaluations to improve the treatment of menopausal women.

Usage, Fractures (Injuries), Fractures, Bone densitometry

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