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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A continuing education examination of estrogen therapy is discussed. The most common indication of estrogen therapy is for replacement in menopausal women. Estrogens can also be used in the treatment of certain types of cancer such as prostatic cancer. A diagnosis of estrogen deficiency must be established first and then estrogen therapy must be selectively used. Psychoemotional problems must be ruled out. Perimenopausal patients may be treated somewhat differently than postmenopausal patients. 1 of the major controversies surrounding estrogen therapy, other than cancer and osteoporosis, is its implication to coronary heart disease. The evidence indicates that estrogen in some way contributes to endometrial carcinoma. Estrogen administration does not seem to show a correlation to breast cancer. Actual treatment must be individualized, and which estrogen, how much, and how long it should be used is still not clear.
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PMID:Estrogen therapy. 70 1

According to the World Health Organization, the global life expectancy at birth was 55 years in 1974, will be 63 years in 2000, and will be close to 70 years in the year 2025. By the year 2025, approximately 20% of the world's population will be more than 60 years old, and the problems associated with hormonal changes become significant with more than one third of a woman's expected life concentrated in the postmenopausal years. Much evidence suggests that the use of postmenopausal estrogen substantially reduces the morbidity and mortality of coronary heart disease, and to date, low-dose estrogen therapy is the single most effective method for prevention of osteoporosis. However, only hysterectomized women can use estrogen alone because of the risk of endometrial cancer associated with unopposed estrogen therapy. Thus, women with an intact uterus must use estrogen in combination with progestogen to avoid this risk, but the different progestogens may variously modify the beneficial effects of estrogen on lipoproteins, and, ultimately, coronary heart disease. Although hormone replacement therapy during menopause soon will be one of the major areas of preventive medicine, the effects of estrogen in combination with different progestins on coronary heart disease, blood pressure, blood coagulation, bone density, and the central nervous system have not been investigated adequately. This paper reviews the current knowledge of known or suspected effects.
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PMID:Effects of hormone replacement therapy. 135 65

Although hormone replacement therapy (HRT) has been available for almost 100 years, conflicting opinions still exist about its efficacy and safety. There is uniform agreement that vasomotor instability and vaginal atrophy are totally reversible with HRT. Effective treatment of bone loss with HRT depends on the number of years of estrogen deprivation, peak bone mass, and rapidity of bone loss. Oral, transdermal, and pellet estrogens are equality effective. Mortality from coronary heart disease decreased 20% to 40% in women on HRT, yet the mechanism has not yet been ascertained. The increased risk of endometrial cancer has been confirmed, but better diagnostic techniques for detection in the precancerous state have been developed. The relationship of breast cancer to estrogen use has not been conclusive. Meta-analysis of 13 studies results in a relative risk of 1.06, whereas a large case-control study reveals a relative risk of 0.9. However, it is clear that in the average, healthy woman, low-dose estrogen replacement for less than 10 years does not increase the risk of breast cancer. Physicians are encouraged to help patients weigh the risks and benefits of HRT.
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PMID:Hormone replacement therapy. 145 Mar 57

Tamoxifen is a nonsteroidal antiestrogen that has found successful applications for each stage of breast cancer in the treatment of selected patients. Tamoxifen was originally introduced for the treatment of advanced disease in postmenopausal women; however, the drug is now also available for the palliative treatment of premenopausal women with estrogen receptor (ER) positive disease. The proven efficacy of tamoxifen and the low incidence of side effects made the drug an ideal agent to test as an adjuvant therapy for women with node-positive breast cancer. Laboratory studies indicate that long-term treatment schedules may provide maximal benefit in preventing recurrence, and recent analysis of clinical trials demonstrates that between 2 and 5 years of adjuvant tamoxifen therapy provides a survival advantage for postmenopausal women with node-positive disease. Similarly, adjuvant studies in node-negative breast cancer have demonstrated an increase in the disease-free survival of both pre- and postmenopausal patients with ER-positive tumors. However, the extended use of tamoxifen has raised questions about the long-term safety of antiestrogen therapy. Of special concern is the impact of tamoxifen on ovarian function in premenopausal women and the potential risks to the fetus if pregnancy occurs. Fortunately, there are no reports about the teratogenicity of tamoxifen in the human, but it is important that physicians counsel women about the risk of pregnancy. Tamoxifen should not be used if a patient is pregnant. Initial concerns that the long-term administration of an antiestrogen would increase bone loss and increase the risks of coronary heart disease appear to be unwarranted. Tamoxifen has some estrogen-like activities in postmenopausal women and causes a preservation of bone in the lumbar spine and a decrease in circulating cholesterol. Indeed, a reduction in fatal myocardial infarction (MI) has been noted during 5 years of tamoxifen therapy, possibly the direct result of a prolonged reduction in circulating cholesterol. However, the estrogen-like qualities of tamoxifen that could be valuable as a hormone replacement therapy for all postmenopausal women following a diagnosis of breast cancer may also increase the risk for developing endometrial carcinoma. To date, there are only a few reports of endometrial carcinoma being diagnosed during adjuvant therapy with tamoxifen; however, any instances of uterine bleeding or spotting should be followed up with an endometrial biopsy. There are some concerns about large doses of tamoxifen promoting liver cancer in rats. These results are of particular concern if tamoxifen is to be used as a preventive in normal women.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The role of tamoxifen in the treatment and prevention of breast cancer. 158 40

Postmenopausal women may benefit from estrogen replacement. In addition to the well-established treatment indications of vasomotor symptoms, genitourinary atrophy, and osteoporosis, studies also suggest improvement in psychologic well-being and prevention of coronary heart disease. The potential cardioprotective effects of estrogen do not appear to be solely from alterations in lipid metabolism. Major risks of estrogen replacement including breast cancer continue to be a concern. Strategies of management including continuous estrogen and progestin regimens are reviewed. There exists an increasing body of evidence that successful treatment for estrogen-dependent tumors including endometrial carcinoma is not a contraindication to estrogen replacement therapy. The potential use of tamoxifen to relieve symptoms and prevent bone loss in women with breast cancer is suggested.
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PMID:Menopause: new indications and management strategies. 162 44

The evidence that estrogen protects against coronary heart disease is biologically plausible, consistent, and strong. These benefits have not been established by a randomized trial, however, so that the degree of protection against heart disease might have been overestimated because estrogen users tend to be healthier than nonusers. A randomized trial to determine whether estrogen alone or in combination with progestin protects against coronary heart disease should be given a high priority. Progestins generally attenuate the effects of estrogen on the concentrations of HDLC. It is not known whether this effect also limits the beneficial effects of estrogen on the risk of coronary heart disease. Recent studies suggest that estrogen may protect against coronary heart disease in other ways besides favorably altering serum concentrations of lipoproteins and that progestins might not have adverse effects on the risk of heart disease. Currently, theoretical concerns that progestins might be harmful seem outweighed by the evidence that they protect against endometrial cancer in women who have a uterus. For these women, some may find the side effects of progestins to be so bothersome that they prefer to take estrogen alone. This approach is reasonable so long as the patient has periodic endometrial biopsies for early detection of pre-malignant or malignant endometrial changes. Women without a uterus should take estrogen alone. Women who take long-term estrogen therapy appear to have about a 30% greater chance of developing breast cancer. On the other hand, breast cancer that develops while taking estrogen therapy might have a slightly better prognosis. Quantitative comparisons of fatal conditions suggest that the benefits of long-term therapy outweigh the risks. But these comparisons assume that all causes of deaths are equally important and do not adequately take account of other psychologic and physical effects of hormone therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluating the benefits and risks of postmenopausal hormone therapy. 175 Apr 10

The risks and benefits of specific types of postmenopausal estrogens and progestogens are explored: those affecting serum lipids, clotting elements, hepatic proteins synthesis, blood pressure, glucose tolerance, endometrial, breast and cervical cancer. Ethinyl estradiol taken orally is the only estrogen likely to cause gall bladder disease. It also induces liver protein synthesis when taken orally or vaginally. Natural estrogens do not heighten coagulation factors, and may shift towards fibrinolysis. Both ethinyl estradiol and equine estrogens may increase blood pressure, while natural estrogens may decrease it. Similarly natural estrogens induce prostacyclin synthesis, while ethinyl estradiol activates both prostacyclin and thromboxanes. Progestagens, especially so the norprogestins, disturb carbohydrate metabolism and tend to reverse the beneficial effects of estrogens on serum lipids, a 40-70% reduction in risk of mortality from coronary heart disease. A meta- analysis of 23 studies concluded that menopausal estrogens do not increase the risk of breast cancer by a measurable degree, except in high doses and in those predisposed by family history. There is an increased risk of endometrial carcinoma for those taking unopposed estrogens for more than 3-6 years. This can be attenuated by taking combined estrogen-progestins, which will eventually result in absence of bleeding, or a 12-day progestogen course every 4-6 cycles. Oral micronized progesterone decreases blood pressure. The relative androgenic effects of progestins other than the norprogesterone derivatives are less significant. As an alternative to taking a progestogen, a woman could have regular endometrial sampling or abdominal or vaginal sonograms to detect endometrial cancer.
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PMID:Risks of estrogens and progestogens. 217 Aug 23

For patients with previous endometrial cancer, ERT is not the accepted practice in the U.S. The therapeutic dictum that estrogen is contraindicated in patients with previous uterine adenocarcinoma is, however, not substantiated by clinical data. The relation of unopposed estrogen stimulation to endometrial hyperplasia and carcinoma, and the published studies relating ERT to endometrial cancer, have resulted in the clinical perception--and cautionary statements to that effect--that estrogen is contraindicated for patients with a history of endometrial carcinoma. The exact biologic effects of ERT on endometrial adenocarcinoma have not yet been studied adequately, however; the initial clinical data suggest that there is no increase in recurrence or mortality. In the meantime, the clinician is left with contradictory data as a basis for determining the proper management of symptomatic patients. The total impact of estrogen deficiency on the health of women and the ratio of benefits and risks of ERT are yet to be defined completely. The preponderance of evidence suggests that estrogen has a beneficial effect on the major cause of death in women, coronary heart disease, by increasing the high-density lipoprotein (HDL) fraction of cholesterol. It is established that estrogen prevents the demineralization of bone and delays the ravages of osteoporosis. No one has died from vaginal atrophy, bladder dysfunction, or hot flashes; the quality of life and marriage have been improved, however, by relieving these symptomatic conditions with ERT. Several studies have attempted to analyze with various statistical models the ratio of benefits to risks, and the majority of authors have concluded that the beneficial effect on cardiovascular disease alone clearly outweighs any known risk.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Estrogen-replacement therapy in patients with previous endometrial carcinoma. 240 7

Early age at natural menopause or bilateral ovariectomy substantially reduce a woman's lifetime risk of breast cancer. Reversible 'bilateral ovariectomy' can now in effect be achieved by 'high-dose' luteinising hormone releasing hormone (LHRH) agonists (LHRHAs). The harmful effects of such medical reversible bilateral ovariectomy, in particular the increased risks of coronary heart disease and osteoporosis, can in all likelihood be obviated by 'low-dose' oestrogen replacement therapy (ERT), specifically 0.625 mg of conjugated equine oestrogens (CEE) for 21 days in each 28-day treatment cycle, and such ERT use will only negate to a relatively small extent the beneficial effect of such bilateral ovariectomy on breast cancer risk. We calculate that such an LHRHA plus low-dose ERT regimen given to a premenopausal woman for 10 years will, in addition to being a most effective contraceptive, decrease her lifetime risk of breast cancer by more than 50%. We calculate that such a 10-year regimen will also decrease her risk of ovarian cancer by two-thirds. This regimen should leave endometrial cancer risk and bone metabolism unaltered, and may reduce the risk of heart disease. The addition of a 'low-dose' progestogen to the regimen for 12 days in each 28-day treatment cycle would be beneficial to the endometrium, but it will adversely affect risk factors for heart disease and it may significantly reduce the benefit of the regimen as regards breast cancer. A satisfactory compromise may be to add a low-dose progestogen for 12 days at less frequent intervals. Another possibility may be to deliver a progestogen solely to the endometrium with an intra-uterine device; the benefits of such a regimen would be a significant reduction in the incidence of breast, ovarian and endometrial cancer.
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PMID:LHRH agonists and the prevention of breast and ovarian cancer. 267 44

Unopposed estrogen stimulates mitotic activity in endometrial and breast tissue. Numerous case-control studies have evaluated the relationship between estrogen use and the risk of endometrial and breast cancers. In general, exogenous, unopposed estrogen use increases the risk of endometrial cancer by tenfold and of breast cancer by twofold after long-term use of high doses. Estrogen's positive effects on osteoporosis and coronary heart disease must be considered when evaluating the potential risks associated with its use in postmenopausal women.
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PMID:The cancer question: an overview of recent epidemiologic and retrospective data. 269 Jun 39


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