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

Lifetime risk is a useful way to estimate and compare the risk of various conditions. Hip fractures, Colles' fractures, and coronary heart disease, and breast and endometrial cancers are important conditions in postmenopausal women that might be influenced by the use of hormone replacement therapy. We used population-based data to estimate a woman's lifetime risk of suffering a hip, Colles', or vertebral fracture and her risk of dying of coronary heart disease. A 50-year-old white woman has a 16% risk of suffering a hip fracture, a 15% risk of suffering a Colles' fracture, and a 32% risk of suffering a vertebral fracture during her remaining lifetime. These risks exceed her risk of developing breast or endometrial cancer. She has a 31% risk of dying of coronary heart disease, which is about 10 times greater than her risk of dying of hip fractures or breast cancer. These lifetime risks provide a useful description of the comparative risks of conditions that might be influenced by postmenopausal hormone therapy.
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PMID:Lifetime risks of hip, Colles', or vertebral fracture and coronary heart disease among white postmenopausal women. 281 6

Epidemiological studies of oral contraceptives pertaining to premenopausal women are briefly reviewed. Therapeutic considerations are noted. The clinical effects of aging and hormone replacement therapy are indicated in terms of metabolism, the endometrium, and bone mass. The pharmacological advantages and consequences of nonhormonal and hormonal contraception are explored. For aging women over 40, there is a need for relief of menopausal symptoms, contraception, and reduction of risks for atherosclerosis, hypertension, coronary heart disease, endometrial carcinoma, breast cancer, and osteoporosis. With the availability and use of low estrogen products, women over 40 can insure tissue support and prevent bone loss as long as the therapy is instituted within 3 years of the last menses. Over-40 women who drink and smoke should not use oral contraceptives. Sterilization does not satisfy longterm hormonal needs, and has other reported menstrual side effects. The dose and duration regimen of hormonal therapy must be carefully considered due to the effects on the endometrium., the coagulation system, the liver, lipids, and bone. Combination estrogen and progestogen is necessary, but consideration must be given to existing levels of endogenous hormones. Lipid patterns may change due to hormone replacement or as a result of aging and contribute to coronary heart disease. Hormone replacement can reverse the atherogenic pattern of increased low density lipoprotein levels and decreased high density lipoprotein levels; a chart gives the effects on lipids and coagulation from various estrogen or estrogen plus progestogen products. For the estrogen-deficient menopausal woman, high estrogen can decrease antithrombin III plasminogen and alpha-antitrypsin antigen levels. Lower dose progestogens are recommended. Studies of dose and effects on bone mass are reviewed and vaginal rings and transdermal steroid patches, triphasic formulations, and new progestational agents such as 19-nortestosterone derivatives are described. Newer low dose formulations are needed for the aging woman, as well as further research on what product best suits the variability of women aged 40-50
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PMID:Contraception for the perimenopausal patient. 330 20

In a prospective study, mortality ratios were computed in relation to overweight, cancer, and other diseases. The study included 750 000 men and women followed for 12 years. Each person was given a weight index. Death rates for overweight and underweight persons were compared with rates for persons of average weight. Men who were 40% or more overweight had a mortality ratio for cancer of 1.33; women, 1.55. This ratio was much lower than that for coronary heart disease (men, 1.95; and women, 2.07); diabetes (5.19 and 7.90), and digestive diseases (3.99 and 2.29). Overweight men had significantly higher mortality ratios for colorectal and prostate cancer; overweight women had much higher rates for cancer of the endometrium, gall bladder, and cervix; and also significantly higher rates for ovary and breast cancer.
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PMID:Overweight and cancer. 406 20

Administration of unopposed postmenopausal estrogen therapy protects against coronary heart disease (CHD) in women. This is mediated, in part, through beneficial effects on lipid and lipoprotein metabolism. Fewer data are available with regard to CHD risk reduction when a progesterone is required in addition to estrogen. Administration of continuous, rather than cyclic, estrogen-progesterone therapy may maintain the beneficial effects of estrogen and yet protect against the increase in endometrial cancer observed with estrogen therapy alone. Clinical guidelines for hormone replacement therapy await the completion of adequate controlled clinical trials.
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PMID:Postmenopausal hormone replacement therapy and cardiovascular risk reduction. A review. 751 30

We assessed the association of hormonal replacement therapy with mortality and incidence of multiple diseases in over 40,000 postmenopausal women followed for 6 years as part of the Iowa Women's Health Study. Compared with women who never used hormone replacement therapy, current users had multivariate adjusted relative risks (RR) as follows: total mortality (RR = 0.78; 95% confidence interval [CI] = 0.65, 0.94), coronary heart disease mortality (RR = 0.74; 95% CI = 0.48, 1.12), endometrial cancer incidence (RR = 4.3; 95% CI = 2.7, 6.9), breast cancer incidence (RR = 1.23; 95% CI = 0.99, 1.55), colon cancer incidence (RR = 0.72; 95% CI = 0.46, 1.12), and hip fracture incidence (RR = 0.53; 95% CI = 0.31, 0.91).
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PMID:Hormonal replacement therapy and morbidity and mortality in a prospective study of postmenopausal women. 762 11

Several lines of evidence suggest that estrogen is an important determinant of cardiovascular risk in women. Epidemiologic data document low rates of coronary heart disease (CHD) in premenopausal women, a narrowing of the gender gap in CHD mortality after menopause, and elevated risk of CHD among young women with bilateral oophorectomy not treated with estrogen. Nearly all of the more than 30 observational studies of exogenous estrogen replacement therapy have indicated a reduced risk of CHD among women receiving estrogen therapy. In a meta-analysis comparing estrogen users and nonusers, the estimated reduction of CHD among users was 44%. In angiographic studies, women taking estrogen were less likely to have coronary artery stenosis. Estrogen is known to affect a wide range of physiologic processes that may have an impact on CHD risk. Use of oral estrogen has favorable effects on serum lipid profiles; it increases high-density lipoprotein cholesterol levels by 10% to 15% and decreases low-density lipoprotein cholesterol levels by a similar magnitude. Other proposed mechanisms include inhibition of endothelial hyperplasia, reduced arterial impedance, enhanced production of prostacyclin, increased insulin sensitivity, and inhibition of oxidation of low-density lipoprotein. Nevertheless, the role of hormone replacement therapy in preventing clinical atherosclerotic events in women remains inconclusive because of the absence of randomized trial data. The benefit-to-risk ratio must be reliably assessed, because estrogen has complex actions, including postulated benefits (CHD, osteoporosis, and menopausal symptoms) and postulated risks (endometrial cancer, breast cancer, and gallstones.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postmenopausal hormone therapy and atherosclerotic disease. 797 16

The menopause is defined as cessation of menstruation, ending the fertile period. The hormonal changes are a decrease in progesterone level, followed by a marked decrease in estrogen production. Symptoms associated with these hormonal changes may advocate for hormonal replacement therapy. This review is based on the English-language literature on the effect of estrogen therapy and estrogen plus progestin therapy on postmenopausal women. The advantages of hormone replacement therapy are regulation of dysfunctional uterine bleeding, relief of hot flushes, and prevention of atrophic changes in the urogenital tract. Women at risk of osteoporosis will benefit from hormone replacement therapy. The treatment should start as soon after menopause as possible and it is possible that it should be maintained for life. The treatment may be supplemented with extra calcium intake, vitamin D, and maybe calcitonin. Physical activity should be promoted, and cigarette smoking reduced if possible. Women at risk of cardiovascular disease will also benefit from hormone replacement therapy. There is overwhelming evidence that hormone therapy will protect against both coronary heart disease and stroke, and there is no increased risk of venous thrombosis or hypertension. A disadvantage of hormone replacement therapy is an increased risk of forming gall-bladder stones and undergoing cholecystectomy. Unopposed estrogen therapy gives a higher incidence of endometrial cancer in women with an intact uterus, but the contribution of progestins for about 10 days every month excludes this risk. Breast cancer in relation to estrogen-progestogen therapy has been given much concern, and the problem is still not fully solved. If there is a risk, it is small, and only after prolonged use of estrogen (15-20 years). The decision whether or not to use hormone replacement therapy should, of course, be taken by the individual woman in question, but her decision should be based on the available scientific information. It is the opinion of the authors that the advantages of hormone replacement therapy far exceed the disadvantages. We suggest that every woman showing any signs of hormone deprivation should be treated with hormone replacement therapy. This includes women with subjective or objective vaso-motor symptoms, genito-urinary symptoms, women at risk of osteoporosis (fast bone losers), and women at risk of cardiovascular diseases.
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PMID:Postmenopausal hormone replacement therapy--clinical implications. 819 55

The incidence of coronary heart disease (CHD) rises after menopause. Hormonal replacement therapy (HRT) reduces cardiovascular morbidity and mortality. Plasma lipoproteins are modified by oral estrogen treatment: LDL are lowered while HDL and VLDL are augmented. The cardioprotective effect of oral HRT may be partially due to the reduction in the LDL/HDL ratio. Optimal changes in lipid profile are achieved with doses that usually prevent bone mass loss. Progestogens tend to blunt the increment of HDL induced by estrogens, but this depends on the type of agent and its dose. Unlike oral estrogen, HRT by the transdermal route does not always modify the lipid profile. When it does, changes are similar to those observed under the oral route in that the LDL/HDL ratio is diminished, but VLDL do not rise. Possible explanations for this discrepancy are discussed. At present there is no clear evidence that combined estrogen/progestogen treatment or transdermal estrogen alone could reduce CHD's incidence. Women with an intact uterus should receive a progestogen in addition to estrogen for prevention of endometrial carcinoma. Estrogen alone is preferable for hysterectomized women. When beneficial and adverse effects of HRT are considered simultaneously, the overall result is considered favorable, principally as a consequence of its cardioprotective properties.
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PMID:[Postmenopause, plasma lipoproteins, and hormone replacement therapy]. 820 20

In 1973, McGuire and Chamness (In: O'Malley BW and Means AR (ed) Receptors for Reproductive Hormones, Plenum Press) summarized their work on the estrogen receptor in animal and human breast tumors, and in so doing described a target for therapeutic intervention. At that time there were no clinically useful antiestrogens, but the subsequent development of tamoxifen for breast cancer therapy has revolutionized the approach to treatment. Long-term adjuvant tamoxifen adjuvant therapy (i.e., greater than one year) has proven efficacy to enhance the survival of breast cancer patients. In addition, because there is an associated 40% decrease in contralateral breast cancer during adjuvant tamoxifen therapy and tamoxifen maintains bone density and reduces fatal myocardial infarction, clinical trials to test the worth of tamoxifen as a preventive for breast cancer in high risk women have started in the United States, United Kingdom, and Italy. Initial concerns that long-term tamoxifen causes endometrial cancer have been placed in perspective and analyzed by a review of the literature. Tamoxifen only doubles the normal risk of detecting endometrial cancer (i.e., to 2 per 1,000 tamoxifen-treated women per year), and 80% of these cases are early stage, good prognosis disease. Annual gynecological examinations and education are essential to provide reassurance for patients. The success of tamoxifen has encouraged the development of new antiestrogens to exploit the estrogen receptor as a therapeutic target. Droloxifene and TAT-59 mimic the metabolite 4-hydroxytamoxifen in having a high affinity for the estrogen receptor (Jordan et al, J Endocrinol 75:305, 1977). These drugs appear to have a pharmacological profile similar to tamoxifen. In contrast, the new pure antiestrogens have a distinct mechanism of action and will be valuable either as a first line therapy for advanced breast cancer or as a second line endocrine therapy after the failure of long-term adjuvant tamoxifen therapy. Finally, a new strategy is being developed to exploit the target site specific action of antiestrogens. Raloxifene, an antiestrogen with high affinity for the estrogen receptor but only weak estrogenicity for the uterus, prevents rat mammary tumorigenesis and maintains bone density. The drug is to be evaluated as a treatment for osteoporosis, but may also prevent the development of breast and endometrial cancer in a broad group of treated subjects. The identification of the estrogen receptor as a target for therapeutic opportunities has proved to be extremely beneficial for the control of breast cancer and has the added potential to control osteoporosis and coronary heart disease in women.
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PMID:Third annual William L. McGuire Memorial Lecture. "Studies on the estrogen receptor in breast cancer"--20 years as a target for the treatment and prevention of cancer. 857 10

There has been little research concerning the health effects of whole grain intake in humans. We have synthesized 15 american and European case-control and prospective studies of whole grain intake. Most subjects were middle aged or older. The studies employed disparate dietary methods, and the foods referred to and quantities eaten are ill defined. Nevertheless there is a striking consistency in reduced risk for colorectal and gastric cancers associated with intake of whole grain, also found in isolated studies of endometrial cancer and coronary heart disease. Because reduced risk was not associated with refined grain intake, these findings do not appear to be confounded by participant confusion concerning refined vs. whole grains. The independence of these findings from reduced risk associated with fruit and vegetable intake is not established. There should be further research to establish whether whole grain intake is protective against chronic disease.
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PMID:Whole grain intake and cancer: a review of the literature. 861 41


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