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

The health risks of obesity increase with its severity and reach significance at a weight greater than 20% above optimal, by using life insurance tables, or at a body mass index greater than 27. Risks include hypertension, insulin resistance and diabetes mellitus, cardiovascular disease, hypertriglyceridemia, low high-density-lipoprotein cholesterol, and, in some studies, high total-and low-density-lipoprotein cholesterol. There is an increased mortality from endometrial cancer in women and from colorectal cancer in men. Chronic hypoxia and hypercapnia, sleep apnea, gout, and degenerative joint disease can occur with more severe obesity. The distribution of body fat is directly related to these health risks. Abdominal obesity is more dangerous than gluteal-femoral obesity because the amount of intraabdominal fat seems to determine much of the increased peril; therefore, risks of cardiovascular disease, stroke, hypertension, and diabetes increase with abdominal obesity, even independently of total fat mass.
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PMID:Health implications of obesity. 203 92

Substitution of hormones does not only serve to alleviate vasomotor and psychic imbalance but mainly to prevent osteoporosis and cardiovascular disease. Essential prerequisites are good tolerance, minimal risk, compliance and low cost. Natural estrogens, in contrast to ethinyl estradiol, without effect on the coagulation system when dosed appropriately are preferred. Sequential or continuous addition of progestogens lowers the incidence of endometrial cancer. Derivatives of progesterone appear to be more suited than 19-nortestosterone derivatives because they do not affect the plasma lipid profile significantly and do not jeopardize the estrogen-induced increase in vasoprotective HDL. Dosing of estrogens follows clinical requirements and minimally effective activity against osteoporosis. Progestogens are dosed according to their endometrial activity. According to current experience only long term treatment is successful.
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PMID:[Principles of hormone substitution in the postmenopause period]. 203 41

Current findings and controversies between oral contraceptives (OCs) and cardiovascular disease and cancers. Specifically, venous thromboembolism, stroke, myocardial infarction, (MI), atherosclerosis, breast cancer, cervical cancer, endometrial cancer, and ovarian cancer are reviewed. The concentration in the literature is on higher dose estrogen (at least 50 mg) studies which suggest that there is with current users, particularly older women who smoke, a risk of myocardial infarction, venous thrombosis, and subarachnoid hemorrhage. Of the 11 case control studies and 4 cohort studies it appears that venous thrombosis increases in risk with an increase in estrogen content and remains constant for duration of use. However, definitive studies have not been completed on 50 mg doses of ethinyl estradiol (EE) and mestranol (ME). The actual individual risk may be small, 1/1000 current users/year. Thrombotic and hemorrhagic stroke in the 1970s had a risk of 37/100,000 users per year, mostly among smokers 35 years and older with predisposing medical conditions. It is suggested that although there were mixed findings between current and past users in the 1970s low dose current or past users are not substantially at risk. The pre-mid 1970 risk of MI was 7 and 67 cases/100,000 current users ged 30-39 respectively per year. The risk group is similar to stroke. Thrombosis seems to be responsible for the increased risk, rather than atherosclerosis. More data are needed on low preparations; however limited findings suggest little if any risk. There is no available data on the risk for coronary artery atherosclerosis due to OC use, even though 50% of all women die from atherosclerosis-related processes regardless of OC use. Non human primate studies, however, suggest that there may be a reduced risk, perhaps due to the presence of estrogen receptors in arterial endothelium and smooth muscles. Data clearly indicate that the overall risk of breast cancer pre and post 1950 is the same, but age may be a factor with younger OC users at risk; parity protects. The association for lifetime risk, however, cannot be determined since most use occurred in the 1960s. For cervical cancer, 8 found no increased risk and 9 did, and the suggestion is the 5 years use is related to increased risk. Biases related to sexual behavior confound control and analysis of data. The most common cancer in developing countries is cervical, which warrants greater Pap smear screening to reduce this preventable cancer. Protection from cancer of the endometrium occurs for 15 years following 12 months of OC use at a 40% reduced risk. A protected effect is also found for epithelial ovarian cancer, with a 40% risk reduction. It is concluded that health benefits of OCs far exceed the health risks.
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PMID:Long-term health risks and benefits of oral contraceptive use. 209 41

Removal of both ovaries in the premenopausal patient is performed infrequently, but when it is, attention must be paid to hormone replacement. The benefits of hormone replacement include protection from osteoporosis, elimination of vasomotor symptoms, improvement in general well-being, and some decrease in the risk of cardiovascular disease. Some evidence suggests that the addition of androgen therapy to estrogen replacement in the premenopausal woman can also be beneficial. Administration of hormonal therapy to certain premenopausal patients who have had a bilateral oophorectomy is controversial. These include patients who are disease-free after surgery for endometrial carcinoma and patients who are post-therapy for breast carcinoma. The most common question is whether a progestin should be given to the patient receiving estrogen therapy after a hysterectomy. Prevention of endometrial carcinoma is unnecessary in this patient, but the effects of the progestin on the breast and the cardiovascular system should be considered.
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PMID:Hormonal therapy in the patient with surgical menopause. 217 90

Tamoxifen (ICI46,474) is a competitive inhibitor of estrogen action which has found ubiquitous application in the treatment of breast cancer. The drug is the front line endocrine therapy for breast cancer and is the proven treatment of choice for the adjuvant therapy of postmenopausal women with node-positive disease. Tamoxifen is available for the treatment of premenopausal patients with advanced disease, and is being evaluated in clinical trials as an adjuvant therapy for premenopausal patients with either node-positive or node-negative disease. Laboratory studies demonstrate that tamoxifen is a tumoristatic agent and long-term treatment strategies (chemosuppression) should be considered to apply the antiestrogen to its maximal therapeutic advantage. Optimal therapy with tamoxifen may also be achieved by treatment strategies to lower circulating estrogen levels in the premenopausal patient. Tamoxifen is a well tolerated drug, and long-term therapy does not appear to induce metabolic tolerance. Concerns about premature osteoporosis or cardiovascular disease appear to be unfounded because tamoxifen has an appropriate level of target site-directed estrogenic activity. Isolated reports about the growth or appearance of endometrial carcinoma during long-term adjuvant tamoxifen therapy must be balanced against the risks of withholding treatment to patients with a fatal disease.
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PMID:Long-term adjuvant tamoxifen therapy for breast cancer. 219 41

The usefulness of surveillance in relating chronic disease trends to recent changes in risk exposures is often questioned on the grounds that these trends respond slowly, reflecting long periods between aetiological exposures and clinical onset of disease. We challenge this preconception on the basis of a review of several important risk factors and diseases: alcohol and liver cirrhosis; tobacco and stroke, cardiovascular disease, and lung cancer; and oestrogens and endometrial cancer. Data from cohort, cross-sectional, and modelling studies demonstrate that the time between removal of exposures and the onset of decline in morbidity or mortality is not defined by the time between initial exposure and disease occurrence. Rather, the pattern of lifetime exposures (with recent exposures often having a dominant effect), the dynamics of the disease process, and the segment of the population with reduced exposures determine how soon the decline begins.
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PMID:Public health surveillance of non-infectious chronic diseases: the potential to detect rapid changes in disease burden. 226 57

Physicians who prescribe hormone replacement therapy for menopausal women should explain the purpose, risks, and side effects of the treatment. This enhances compliance and discourages patients from discontinuing therapy because of fears of cancer or misconceptions about hormone replacement therapy. The physician should explain that the risk of endometrial cancer is virtually eliminated (reduced to that of a normal woman or a woman not receiving therapy) by the addition of progestogen to estrogen regimens, and that when this cancer does occur, it is usually diagnosed and treated early. Recent studies have not conclusively shown a significant effect of progestogen on lipid profiles relevant to cardiovascular disease. Hormone replacement therapy does not appear to be associated with an increased risk of breast cancer. Nuisance side effects (such as edema and breast tenderness) can be better tolerated if the physician prepares the patient, offers a solution, and helps to put the problem in perspective. Other measures, such as providing written information and avoiding unnecessary biopsies, also enhance compliance.
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PMID:Enhancing patient compliance with hormone replacement therapy at menopause. 231 97

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

Estrogen replacement therapy (ERT) for postmenopausal women greatly reduces the risk of osteoporotic fractures, but carries an increased risk of endometrial cancer. This risk can be reduced by the addition of progestin, which does not interfere with the osteoporotic benefit of estrogen. Although long-term use data are few, there is presently little evidence for an increase or decrease in breast cancer risk associated with estrogen by itself (unopposed estrogen), or estrogen plus progestin. In contrast, a large body of evidence suggests that unopposed estrogen significantly reduces the risk of cardiovascular disease; there is no evidence that this benefit will persist when a progestin is added. The preferred method of estrogen replacement therapy, to prevent osteoporosis in a postmenopausal woman with an intact uterus, should be chosen with these different risks and benefits in mind.
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PMID:The risks and benefits of long-term estrogen replacement therapy. 251 3

Estrogen therapy for postmenopausal women has received adverse publicity since the mid-1970s because several reports linked estrogens with an increased risk of endometrial cancer. Other studies indicated that the risk of endometrial malignancy is reduced when a progestogen is added to the estrogen replacement. Not all postmenopausal women need estrogen replacement. Because some continue to produce significant amounts of endogenous estrogens, many need progestogen replacement to reduce the risk for endometrial hyperplasia and adenocarcinoma. It has been well demonstrated that estrogen replacement therapy does not increase the risk for breast cancer. However, added progestogen may actually reduce the risk for this malignancy in some women. Where estrogen therapy retards the development of and helps to prevent osteoporosis, added progestogen may restore bone which has been lost by promoting new bone formation. The greatest benefit to accrue to postmenopausal estrogen users is prevention of cardiovascular disease. Concern has been expressed that added progestogen may negate this benefit by adverse effects on lipids. Side effects of added progestogen occur, but these may be managed by changing to another progestogen or adding a mild diuretic.
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PMID:Use of progestogens in postmenopausal women. 257 91


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