Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The beneficial effects of combined estrogen-progestin-containing oral contraceptives (OCs) include prevention of pregnancy (less than 1 failure out of 100 regular users); the prevention of ectopic pregnancy; the reduction of preeclampsia (2.4 times lower risk compared with barrier methods); and reduction of pelvic inflammation to about one-half. The effects on menstruation include the reduction of sideropenic anemia (by lowering the incidence and duration of menstruation, OCs reduce the loss of iron to 50% or to as much as 33%); dysmenorrhea by 40% (symptoms receded in 90% of users); and premenstrual syndrome by 30%. OCs exert a favorable effect on menstrual epilepsy; reduce sports-related accidents in the premenstrual and menstrual periods; and reduce intermenstrual bleeding. The protection from cancer includes the lowering of endometrial cancer risk (every 2 years of use reduces the risk by 38%, 12 years of use by 70%, and the beneficial effects last 3-15 years); reduction of the risk of the ovarian cancer (already 3-6 months of use reduces the risk by 30%, and more than 5 years by 50% in women under 50 years of age with a longterm effect of 10 years or more, which drops sharply in women over 60 who are mostly at risk). Among other beneficial effects, they reduce benign mastopathy by 50-75%; reduce the risk of follicular ovarian cysts to 50% and the risk of corpus luteal ovarian cysts to 1/5; and they lessen bone loss which favorably affects osteoporosis. Low-dose OCs minimize the well-known risks of thrombotic and cerebrovascular accidents, myocardial infarction, hypertension, altered carbohydrate metabolism, gallbladder diseases, and liver cancer. A new OC with 30 mcg of ethinyl estradiol was tested with daily doses of 150 mcg of desogestrel. The high density lipoprotein (HDL) either increased or did not change with desogestrel: the HDL2 subfraction that protects from atherosclerosis did not change, and probably the HDL3 raised the HDL level.
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PMID:[Favorable effects of oral estrogen-progestin contraception]. 181 41

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

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

This review on the risks and benefits of oral contraceptives clarifies the risks and misperceptions, and discusses 10 potential health benefits. In the U.S. where maternal mortality is about 20.6/100,000, the risk of death from pills ranges from 1.8 for nonsmokers to 6.5 for smokers. It is likely that most of the small existing mortality risk of pill use is due to thromboembolism. Atherosclerosis, the major cause of death for U.S. women, may be reduced by the pill. It is still controversial whether pills increase risk of hepatocellular carcinoma and malignant melanoma; they protect against endometrial cancer (the 3rd greatest cancer killer) and ovarian (the 4th) cancer; they may increase risk slightly in some subgroups for breast and cervical cancer, although data are conflicting. Pills also protect against ectopic pregnancy, benign breast disease, pelvic inflammatory disease, ovarian cysts, iron deficiency anemia and possibly uterine fibroids and osteoporosis. It is no longer held that orals protect against toxic shock syndrome or rheumatoid arthritis. It is estimated that oral contraceptives avert 50,000 hospital admissions per year in the U.S.
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PMID:The health effects of oral contraceptives: misperceptions, controversies, and continuing good news. 266 76

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

Unopposed estrogens, both exogenous and endogenous, increase the risk of endometrial cancer although the magnitude of the association between estrogen replacement therapy and adenocarcinoma has been exaggerated by the epidemiologic case-control studies. Not all postmenopausal women need estrogen replacement therapy since some produce sufficient endogenous estrogens to remain asymptomatic and prevent atrophic vaginitis, osteoporosis and atherosclerosis. However, within this group may be those at risk for endometrial cancer, so they need to be identified and treated with cyclic progestogens. Sequential oral contraceptives did not protect young women from adenocarcinoma of the endometrium because of too little progestogen for too short a duration in view of the relatively high dosage of estrogen. However, combination birth control pills significantly decrease the risk for endometrial carcinoma. Endometrial hyperplasia is a precancerous lesion in some women and can be effectively reversed with 10-13 days of progestogen monthly in at least 98% of patients. The progestogen challenge test has been devised to identify postmenopausal women at greatest risk for adenocarcinoma. It should be administered to all postmenopausal women with an intact uterus. This includes asymptomatic women, patients receiving estrogen replacement therapy and women being evaluated for hormone therapy. If there is a positive response to the progestogen challenge, as manifested by withdrawal bleeding, then the progestogen should be continued for 13 days each month for as long as withdrawal bleeding results. If there is no response then the progestogen challenge test should be repeated at each annual examination. Universal use of the progestogen challenge test should prevent nearly all endometrial cancers.
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PMID:The role of hormones in the etiology and prevention of endometrial cancer. 379 26

21 women (mean age 60 years, range 48-72) were given depot medroxyprogesterone acetate (DMPA), 1,000 mg/week parenterally for 6 months, as part of the treatment for endometrial carcinoma in either clinical stage I or II. Before treatment and after 1, 3 and 6 months of treatment serum apolipoprotein AI was analyzed by electroimmunoassay. There was a significant decrease in apolipoprotein AI after the administration of DMPA, compared to the value before treatment. A low level of apolipoprotein AI is considered a risk factor for the development of atherosclerosis and cardiovascular disease. Such a risk might therefore be anticipated if the period of treatment was extended to several years.
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PMID:Changes in apolipoprotein AI after treatment with high-dose medroxyprogesterone acetate. 623 58

The effect of high dose medroxyprogesterone (MPA) on serum lipids was studied in 31 postmenopausal patients with endometrial cancer. After 3 months of MPA treatment, total cholesterol decreased by 18% (P less than 0.001), LDL cholesterol by 16% (P less than 0.01) and HDL cholesterol by 38% (P less than 0.001) from the respective pretreatment values; correspondingly, the ratio of HDL to total cholesterol decreased (P less than 0.001). Similar changes were found as early as 2 weeks after start of treatment. In the 15 controls receiving no progestin treatment, full dose intracavitary radiotherapy and gynecological surgery had no effect on these serum lipids.
Atherosclerosis 1983 Apr
PMID:Effect of high dose progestin on serum lipids. 687 Sep 84

The study included 191 patients with obesity, atherosclerosis, diabetes mellitus, endometrial cancer, breast cancer and healthy subjects of various age. Somatomedin activity was determined by incorporation of radioactive natrium sulfate in vitro into the cartilage of female rats. The results of the study showed that somatomedin activity was not changed in subjects with normal metabolic parameters and ranged from 0.47 to 0.69 U/ml. In patients with diabetes mellitus, atherosclerosis and obesity accompanied by increased blood concentration of cholesterol and triglycerides, somatomedin activity rose up to 1.36- 1.62 U/ml. In patients with breast and endometrial cancer somatomedin activity was also increased, particularly in those with hypercholesterolemia and hypertriglyceridemia (3.04 U/ml for breast cancer patients and 2.20 U/ml for endometrial cancer patients). Theoretically, this may promote proliferation of somatic cells and thus contribute to tumor processes in oncological patients whose pool of cells is extremely sensitive to mitogenic agents.
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PMID:Interrelation between lipidemia and somatomedin activity in cancer and age-associated pathology. 713 38

Depot medroxyprogesterone acetate (DMPA) is the only injectable contraceptive available in the United States. After more than 20 years of regulatory review, the Food and Drug Administration approved DMPA for contraceptive use in 1992 after the publication of reassuring data about its possible association with breast cancer. It has been used by 30 million women in more than 90 countries. The recommended dosage, 150 mg intramuscularly every 3 months, has a contraceptive efficacy exceeding 99%. After a 150 mg dose, ovulation is inhibited for at least 14 weeks. Almost all users experience menstrual changes, typically episodes of unpredictable irregular spotting and bleeding, particularly during the first year of use. With continued use, spotting and bleeding decrease, and amenorrhea becomes common. Although ovulation suppression may rarely persist for as long as 18 months after the last injection, DMPA does not permanently affect fertility. Long-term DMPA use reduces menstrual blood loss, has been associated with a decreased incidence of candidal vulvovaginitis and pelvic inflammatory disease, and dramatically lowers the risk of endometrial cancer. Prolonged DMPA use may be associated with reversible reduction in bone density, probably related to suppression of endogenous production of estrogen. The most recently published data suggest that long-term use of DMPA induces moderate changes in lipid metabolism that are unfavorable in terms of risk of atherosclerosis. DMPA should be considered a highly effective, safe, convenient, and reversible contraceptive option for appropriately selected patients.
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PMID:Long-acting injectable contraception with depot medroxyprogesterone acetate. 817 4


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