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

In postmenopausal women estrogens alone are effective in reversing vasomotor symptoms and vaginal atrophy. They also prevent the bone loss associated with osteoporosis and reduce the risk of cardiovascular disease, probably through their beneficial effects on lipid metabolism. Unopposed long-term estrogen therapy, however, increases the risk of developing endometrial hyperplasia, endometrial cancer, and possibly breast cancer as well. The risk of developing endometrial cancer can be reduced by combining a progestin with the estrogen, by controlling obesity, and by rigorous clinical screening and surveillance. The effect of progestins on the risk of developing breast cancer is still controversial. Although some progestins may reverse the cardioprotective effect of estrogens, those with minimal androgenicity appear less likely to do so. Hormone replacement therapy that combines estrogen with a progestin of minimal androgenicity is thus a rational alternative to unopposed estrogen therapy. Current epidemiologic knowledge suggests that the benefits of hormone replacement therapy, with or without any progestins, strongly outweigh the risks.
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PMID:The benefits and risks of hormone replacement therapy: an epidemiologic overview. 160 89

Biomedical researchers have added cardiovascular disease (CVD) to the list of symptoms resulting from lowered estrogen levels and menopause. Thus health providers promote hormone replacement therapy (HRT) to prevent CVD. Yet most women tend to be healthy during the postmenopausal years which constitute at least 33% of their lives. The medical community has taken a natural event, menopause, and labeled it as a disease which causes other diseases. Science is basically patriarchal. Physicians use it to justify their privilege to define illness and treatment. They reduce organic processes into a narrow cause-effect relationship and ignore socioeconomic and political factors. An often ignored problem with the scientific community's view of CVD is that almost all cardiovascular intervention studies included only men as subjects except the prospective Framingham Study. Traditional risk factors of CVD in women are hypertension, cholesterol levels, cigarette smoking, diabetes, excess weight, oral contraceptives, and genetics. Various studies show a reduction in the age adjusted risk of CVD morbidity any mortality in women on estrogen replacement theory (ERT). Specifically, estrogen affects serum lipids in a positive direction. Yet the women in the studies are healthy, lean, and exercise regularly. Some studies reveal an increased risk of breast cancer and endometrial cancer in women on ERT. HRT consists of a combination of estrogen and progestin, but data do not confirm that it is as protective against CVD as ERT. HRT is postmenopausal women is an untested hormonal experiment. In 1986, the US National Institutes of Health wrote a policy to include women as subjects in research studies. It did not happen so in 1991 it established the Office of Women's Health Research. The US Congress has also taken up the issue. Nurse researchers should critique methods used by patriarchal science to study menopause. Nurses can inform postmenopausal women about their choices concerning HRt to prevent CVD.
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PMID:Cardiovascular disease in women and noncontraceptive use of hormones: a feminist analysis. 160 87

Several years ago a consensus guideline conference was organised both in the United States (1984) and in the Netherlands (1985) on case finding, prevention and treatment of osteoporosis. The most important conclusion of both conferences was that oestrogen substitution can significantly reduce the incidence of fractures in postmenopausal women. This statement has not changed in the revised guidelines on osteoporosis of 1991. As far as the effect of hormonal substitution of oestrogens with or without progestagens in relation to cardiovascular disease and breast and endometrial carcinoma is concerned, insights have hardly changed in the last 5 years. The value of other drugs in the treatment of osteoporosis, however, has become better known. Both diphosphonates and anabolic steroids have recently made a comeback.
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PMID:[Revision consensus osteoporosis]. 161 68

Epidemiologic studies of breast, ovarian, and endometrial cancer and physiologic studies of epithelial tissues from which these cancers originate indicate that medical researchers can develop interventions to reduce women's risk of these 3 cancers. They already know that use of combined oral contraceptives considerably reduced the risk of endometrial and ovarian cancer. The key etiologic factors for endometrial and breast cancer are ovarian steroid hormones. Specifically, any estrogen not checked by progestogen stimulate cell division in the epithelial tissue of the endometrium thus increasing the risk of cancer. Yet estrogen and progestogen induces significantly more cell division in the epithelial tissue of the terminal duct lobular unit (from which many breast cancers originate) than does just estrogen. Ovulation damages the ovarian surface making it the leading etiologic factor for ovarian cancer. Medical researchers at the University of Southern California (USC) have designed a prototype contraceptive regimen which should prevent all 3 cancers. They re presently testing it in a clinical trial at USC. The prototype regimen consists of administration of the gonadotropin releasing hormone agonist (GnRHA) leuprolide acetate depot on day 1 of each 28-day cycle, 0.625 mg of oral conjugated equine estrogens (CEE) on Monday-Saturday (24 days) per each 28-day cycle, and 10 mg of oral medroxyprogesterone acetate (MCA) for 13 days every 4th cycle. The GnRHA reduces the risk of all 3 cancers. CEE prevents bone mineral loss, possible increase in cardiovascular disease risk, menopausal symptoms, and urogenital atrophy. MCA reverses endometrial hyperplasia and prevents increased risk of endometrial cancer. The predicted relative reduction in lifetime breast cancer risks over 5,10, and 15 years for the prototype regimen are 31%, 53%, and 70%, respectively. For endometrial cancer, they are 18%, 33%, and 45%, respectively. For ovarian cancer, they are 41%, 67%, and 84%. This regimen should also reduce the incidence or severity of hormonally mediated benign gynecologic disorders. Further research on such a regimen is needed.
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PMID:The prevention of breast cancer through reduced ovarian steroid exposure. 162 31

The favourable effects of exogenous progestagen on the endometrium are well known, but have not been adequately quantified with respect to endometrial cancer. The benefits of progestagen need to be weighted against its possible untoward effects on the risk of breast cancer and cardiovascular disease. A population-based case-control study of endometrial cancer was undertaken to evaluate the benefits of progestagen use. 158 incident cases were identified between 1985 and 1987 among women aged 40-64 years who were residents of King County, Washington. Detailed interviews were conducted and the responses were compared with those of 182 controls selected by random telephone digit dialling. The risk of endometrial cancer among women who had used unopposed oestrogen for more than 3 years was over five times that of women who had used no hormones (relative risk [RR] 5.7, 95% confidence interval [Cl] 2.5-12.8), whereas those who had also used a progestagen for at least six months of that time had an RR of only 1.6 (95% Cl 0.6-3.9). The RR differed according to days per month that progestagen was used: 2.4 (0.6-9.3) for progestagen use of less than 10 days per month versus 1.1 (0.4-3.6) for use of 10 or more days per month. These results provide additional evidence that the use of progestagen for 10 or more days per cycle can reduce the excess risk of endometrial cancer associated with long-term postmenopausal oestrogen use.
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PMID:Progestagen supplementation of exogenous oestrogens and risk of endometrial cancer. 167 10

This article reviews published papers on endometrial carcinoma from August 1989 to July 1990. The hypothesis of two different pathogenic types of endometrial carcinoma, which are well correlated with favorable and unfavorable prognosis, has been established. The prognosis for patients under 21 years of age with well-differentiated endometrial carcinoma is excellent; for them, a conservative, fertility-preserving treatment is possible. The characteristics of carcinomas with unfavorable prognoses are also discussed. These prognostic factors are measurable in tissue from preoperative curettage. Measurement of myometrial invasion by vaginal sonography and nuclear magnetic resonance imaging is possible with a high degree of safety preoperatively as well. At least intraoperatively, an exact measurement of depth of invasion can be obtained by frozen-section diagnosis. In an optimal preoperative examination, it should be possible to select patients with a high rate of metastases for intraoperative lymphadenectomy. For adjuvant postoperative therapy, percutaneous radiotherapy is indicated in high-risk patients in whom no optimal lymphadenectomy has been done. Vaginal irradiation, however, used in all cases up until now, is known to bring about more local complaints. Adjuvant progestagen treatment in low-risk patients is dangerous because it can cause a higher rate of cardiovascular disease and does not reduce death by recurrent disease. The profit for high-risk patients seems very small. Analysis of endometrial carcinoma tissue shows a high rate of receptors for luteinizing hormone-releasing hormone and analogues. Adjuvant chemotherapy in high-risk patients until now has been without measurable effect.
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PMID:Endometrial malignancy. 187 2

The metabolic effects of sex steroids pertinent to cardiovascular risk are described. These effects are discussed for estrogen inducible proteins, coagulation and fibrinolysis, blood pressure and hypertension, carbohydrate metabolism, lipids and lipoproteins, and vessel walls and local prostaglandins. Also described is the cardioprotection from estrogens and estrogen/progesterone treatment and cardiovascular risk. Oral contraceptive (OC) and cardiovascular risk are also discussed with the following effects identified: the influence on many of the multiple risk factors involved in the development of cardiovascular diseases (i.e., lipids, carbohydrate metabolism, and hemostasis), an association between OC use and thromboembolic accidents, a state of hypercoagulability counterbalanced by increased fibrinolytic activity, venous thrombosis, a relationship with the dosage of androgenic progestogens. no atherogenic origin, no age limit for prescribed, healthy, nonsmoking women, and an increased peripheral insulin resistance. It is concluded that it is rarely inadvisable to prescribe low dose natural estrogens in postmenopausal hormone replacement therapy. Factors contraindicating such use are undiagnosed genital bleeding, an active thrombolic or cardiovascular process, carcinoma of the breast or endometrium, and acute liver failure. Estrogen replacement therapy may exert some cardioprotective effect. When progestogens are added to prevent endometrial carcinoma development, the benefits might be reduced. Low estrogen and low progesterone OC use among healthy, nonsmoking women even in middle age poses no risk of death from cardiovascular disease. Premenopausal women may even be protected from coronary atherosclerosis with estrogen-containing OCs. However, it is advisable that OCs be used with the least possible impact on lipid and carbohydrate metabolism, as well as on hemostasis. For those with some prior cardiovascular risk, there are theoretical advantages at present for use of the new, less, or nonandrogenic progestins in OCs; however, caution is urged and informed consent must be obtained until epidemiological studies support this position.
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PMID:Sex hormones and cardiovascular risk. 192 64

There is increasing awareness that the long-term consequences of ovarian failure can be prevented or reduced with appropriate hormone replacement therapy (HRT). After the menopause, there is a rapid loss of trabecular bone resulting in a one in two lifetime risk of osteoporotic fracture. HRT prevents this bone loss and decreases the incidence of fracture. A minimum of 5 years treatment is recommended for significant benefit. Epidemiological evidence is accumulating that post-menopausal oestrogen therapy reduces the risk of cardiovascular disease and stroke by between 30 and 70% even in the presence of established risk factors. Given the prevalence of cardiovascular disease, this is likely to be one of the principle benefits of HRT in the next decade. Concerns about the long-term safety of HRT have focused on endometrial and breast cancer. The increase in risk of endometrial cancer associated with oestrogen only therapy is abolished with the sequential addition of a progestogen for 10-12 days each cycle. The possible effect of HRT on breast cancer risk has to be considered against the background of a one in 12 lifetime risk of developing this disease. The epidemiological studies investigating this relationship are reviewed in this paper. There is a broad consensus that 5-6 years duration of HRT does not increase breast cancer risk. Longer durations of therapy (10-15 years) have been reported to increase this risk although not all the data are in agreement. Other factors, such as family history and benign breast disease, may also influence the risk of breast cancer. The potential benefits of HRT on mortality and morbidity are enormous. Against this is a possible small increase in breast cancer risk with long-term usage. Greater awareness of the long term consequences of the menopause and the potential benefits of HRT should be encouraged so that women can make informed decisions about their need for HRT.
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PMID:The long-term risks and benefits of hormone replacement therapy. 193 2

The benefits of estrogen replacement therapy in preventing vasomotor symptoms, osteoporosis, and cardiovascular disease are well documented. Although estrogen is said to be contraindicated in patients successfully treated for endometrial and breast cancer, there are no data to substantiate this admonition. Experience suggests that it can be used safely in patients treated previously for endometrial cancer. Although there is little or no experience with estrogen use in the woman treated previously for breast cancer, circumstantial evidence suggests that it is not contraindicated in all such cases. Informed consent, patient desires, and risk-benefit considerations must enter into the decision to use estrogen in these patients.
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PMID:Estrogen replacement therapy: is previously treated cancer a contraindication? 198 99

Using data on potential years of life lost to ages 75 and 85, the potential effect of antiestrogens and estrogens on various competing causes of death is explored. Although for antiestrogens the beneficial effect sought is a reduction in breast cancer mortality, this could be largely eliminated by a small detrimental effect on cardiovascular disease mortality. Other competing causes of death, such as endometrial, ovarian, and liver cancer, and fractured neck of femur (as an indicator of osteoporosis), are of far less import. For estrogen use at the time of the menopause, no effect on mortality is sought. However, an adverse effect on breast cancer mortality would be of far greater significance than an effect on endometrial cancer. Indeed, the present endeavor to counter an adverse effect of estrogens on endometrial cancer by adding progestogens could be counterproductive. These competing causes of mortality have to be borne in mind in designing intervention trials.
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PMID:Risk/benefit considerations of antiestrogen/estrogen therapy in healthy postmenopausal women. 200 29


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