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

Cigarette smoking is an established risk factor for cancer and cardiovascular disease, and is the leading cause of avoidable disease in most industrialized countries. Less well-known are possible beneficial effects, which are briefly considered in this survey. Preliminary data suggest that there may be inverse associations of smoking with uterine fibroids and endometriosis, and protective effects on hypertensive disorders and vomiting of pregnancy are likely. Smoking has consistently been found to be inversely related to the risk of endometrial cancer, but cancers of the breast and colon seem unrelated to smoking. Inverse associations with venous thrombosis and fatality after myocardial infarction are probably not causal, but indications of benefits with regard to recurrent aphthous ulcers, ulcerative colitis, and control of body weight may well reflect a genuine benefit. Evidence is growing that cigarette smoking and nicotine may prevent or ameliorate Parkinson's disease, and could do so in Alzheimer's dementia. A variety of mechanisms for potentially beneficial effects of smoking have been proposed, but three predominate: the 'anti-estrogenic effect' of smoking; alterations in prostaglandin production; and stimulation of nicotinic cholinergic receptors in the central nervous system. Even established inverse associations cannot be used as a rationale for cigarette smoking. These data can be used, however, to clarify mechanisms of disease, and point to productive treatment or preventive options with more narrowly-acting interventions.
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PMID:Beneficial effects of nicotine and cigarette smoking: the real, the possible and the spurious. 874 97

As life expectancy increases and members of the postwar generation settle into their fifth decade of life, hormone replacement therapy--estrogen or an estrogen-progestin combination--has become a major research interest. An extensive, but often confusing and even contradictory, literature exists on the uses of hormone replacement for the treatment and prevention of a multitude of difficulties that may be associated with the perimenopausal and postmenopausal periods. These include hot flushes, vaginal changes, urinary tract changes, changes in sexuality, affective or emotional symptoms, changes in the oral mucosa and skin, loss of memory and Alzheimer's disease, bone loss and osteoporosis, and cardiovascular disease. This article reviews the literature in each of these areas. It also reviews studies relating to possible side effects of hormone therapy, including endometrial cancer, gall bladder disease, and breast cancer. The article outlines principles for practitioners to follow in assisting women to make informed and individualized decisions about this therapy. Part II of this article, which will appear in the May/June 1996 issue of the Journal of Nurse-Midwifery, will cover specific therapeutic regimens and their management, as well as alternative therapies and preventive measures.
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PMID:Perimenopausal and postmenopausal hormone replacement therapy. Part 1. An update of the literature on benefits and risks. 870 9

Oestrogen deficiency is by far the major factor contributing to the high rate of osteoporotic fractures in women. The anti-osteoporotic effect of estrogen may be explained by its property to regulate cytokine secretion and thus balance bone remodeling. In oestrogen deficiency, increased resorption and remodeling will occur leading to osteoporosis. It has been extensively shown that oestrogen replacement therapy (ERT) prevents postmenopausal bone loss and reduces fracture risk by half, provided that an appropriate dose is used. In order to optimize osteoporosis prevention, ERT should be started a early as possible in menopause and be maintained as long as possible. ERT may also be effective in elderly osteoporotic patients in preventing bone loss and, reducing fracture risk. The acceptance of ERT, however, at an older age has not been thoroughly evaluated. A reduction of cardiovascular disease and of climateric symptoms are among other benefits of ERT. So far, only few postmenopausal women are treated with ERT. ERT without progestins has been repeatedly found associated with an increased risk of developing endometrial cancer, but the cyclic addition of progestins protects from endometrial hyperplasia and carcinoma. Combined oestrogen-progestin therapy is as efficient as estrogen therapy alone, but not more so. Since progestins may oppose some of the beneficial effects of estrogens, the lowest dose with the least metabolic impact should be prescribed. Women who have had a hysterectomy, should probably be treated by estrogen replacement therapy only. Meta-analyses concerning breast cancer associated with ERT found a very moderately increased risk (RR = 1.06). Therefore ERT prescription should be discussed openly with women considering all risks and benefits. In women who have suffered from breast cancer, a bone sparing effect of tamoxifen has been shown.
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PMID:Osteoporosis prevention and treatment with sex hormone replacement therapy. 884 55

Factors that exacerbate the risk of atherosclerotic plaque formation include cigarette smoking, hypertension, hypercholesterolaemia, sedentary lifestyle, and oestrogen deficiency. The potentially important role of oestrogen deficiency in this process is evidenced by the significant increase in cardiovascular risk observed in women after menopause, and in the marked reduction in cardiovascular events observed in women who take hormone replacement therapy. Oestrogen replacement therapy, through an effect on the blood vessel wall and on serum lipids, also appears to stabilize existing atherosclerotic plaques. The combination of oestrogen and progesterone reduces risk of endometrial cancer while possibly delivering the same benefits as oestrogen alone. Other measures, such as antithrombotic therapy, exercise, and smoking cessation, also contribute to reduced risk of cardiovascular disease in older women.
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PMID:Practical aspects of preventing and managing athersclerotic disease in post-menopausal women. 886 80

We have compared the cell and tissue selective estrogenic and antiestrogenic activities of tamoxifen, raloxifene, ICI 164,384 and a permanently ionized derivative of tamoxifen--tamoxifen methiodide (TMI). This non-steroidal antiestrogen has limited ability to cross the blood brain barrier and is therefore less likely to cause the central nervous system disturbances caused by tamoxifen. We have used the stimulation of the specific activity of the "estrogen induced protein", creatine kinase BB, as a response marker in bone, cartilage, uterine and adipose cells and in rat skeletal tissues, uterus and mesometrial adipose tissue. In vitro, TMI, tamoxifen and raloxifene mimicked the agonistic action of 17beta-estradiol in ROS 17/2.8 rat osteogenic osteosarcoma, female calvaria, and SaOS2 human osteoblast cells. In Ishikawa endometrial cancer cells, tamoxifen showed reduced agonistic effects and raloxifene showed no stimulation. However, as antagonists, tamoxifen and raloxifene were equally effective in Ishikawa or SaOS2 cells. In immature rats, all four of the antiestrogens inhibited estrogen action in diaphysis, epiphysis, uterus and mesometrial adipose tissue; when administered alone, tamoxifen stimulated creatine kinase (CK) specific activity in all these tissues. Raloxifene and TMI, however, stimulated only the skeletal tissues and had no stimulatory effect in the uterus or mesometrial fat, and the pure antiestrogen ICI 164,384 showed no stimulatory effect in any of the tissues. The simultaneous injection of estrogen, plus an antiestrogen which acted as an agonist, resulted in lower CK activity than after injection of either agent alone. These differential effects, in vivo and in vitro, may point the way to a wider therapeutic choice of an appropriate antiestrogen which, although antagonizing E2 action in mammary cancer, can still protect against osteoporosis and cardiovascular disease and not stimulate the uterus with its attendant undesirable changes, or interfere with the beneficial action of E2 in the brain.
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PMID:Tissue selective action of tamoxifen methiodide, raloxifene and tamoxifen on creatine kinase B activity in vitro and in vivo. 901 Mar 44

Although reduction of cardiovascular risk by estrogen substitution in the menopause has not been proven by a prospective randomized study the results of the present epidemiologic studies with the most various methodological approaches leave hardly any doubt about such a protective effect. Furthermore the published data show that women with cardiovascular risk factors or with a preexisting cardiovascular disease benefit more from estrogen substitution than healthy women. Addition of gestagen in non hysterectomized women for the reduction of increased risk for endometrial cancer seems to impair the benefit for cardiovascular risk only minimally if at all.
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PMID:[Secondary prevention in coronary diseases. Viewpoint of the gynecological endocrinologist]. 906 32

Long-term treatment with tamoxifen has produced few side effects, which are generally mild. Of the serious ones, all of them except eye toxicity seem to be related to the molecule's intrinsic mildly estrogen-like action, such as, for example, endometrial carcinoma. This property is also responsible for some favorable clinical effects including a lower risk of osteoporosis and cardiovascular disease. Whether tamoxifen causes neoplastic growth in patients who develop resistance to this drug is still controversial. Further prospective clinical studies are therefore needed to investigate such problems and also to evaluate less frequent side effects. Moreover, decisions on the overall duration of hormone therapy should be based on possible side effects as well as on therapeutic response.
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PMID:Long-term toxicity in adjuvant treatment with tamoxifen. 926 12

In recent years, reports of favourable effects of estrogen therapy on cardiovascular morbidity and mortality have led to enthusiasm for widespread use of estrogens by postmenopausal women. Guidelines for estrogen therapy issued by the American College of Physicians include the statement "Women who have coronary heart disease are likely to benefit from hormone therapy". What evidence support this recommendation? More than 30 observation studies have examined the effect of estrogen replacement therapy on cardiovascular event and all cause mortality. In addition there have been 13 case controlled studies. The majority showed lower morbidity and mortality from coronary heart disease among users of postmenopausal estrogens than among non-users. Recently, 2 meta-analyses estimated the reduction in coronary heart disease associated with estrogen use to be in the range of 35 to 44%, respectively. All of these observational studies share a fatal flaw: Women who take estrogens are different from women who do not. Some differences have been measured, others have not. Women who take estrogens are on average better educated, healthier, have higher incomes and have better access to health care. These difference rather than the estrogens may account for much of the lower risk of heart disease. At this time we cannot tell from these observational studies what the real benefit of estrogens on coronary heart disease might be. Estrogen replacement therapy is not without risk. Estrogens increase the risk of endometrial carcinoma approximately 6-fold, an effect that is eliminated by the addition of progestins. Controversy continues over whether estrogen replacement increases the risk of breast cancer. A number of prospective randomized studies are now under way that will establish whether estrogen replacement therapy definitely reduces the risk of cardiovascular disease in women with and without coronary lesions and whether it increases the risk of breast cancer. Until the results of these trials are available claims on the definite usefulness of hormone supplementation to prevent coronary heart disease in postmenopausal women remain premature. In the light of the probable usefulness estrogen replacement therapy for the prevention of cardiovascular events should be recommended for women with increased risk for or definitively proven coronary heart disease.
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PMID:[Estrogens for prevention of coronary heart disease?]. 930 98

Cardiovascular disease is the leading cause of death in women of postmenopausal age. Data from observational studies suggest that the risk of coronary heart disease in postmenopausal women can be reduced by 30-50% by estrogen replacement therapy. The protective effect of estrogen is multifactorial, affecting lipids, carbohydrate metabolism, hemostasis, body-fat distribution and blood pressure. Although the unopposed use of estrogen is associated with an increased risk of endometrial cancer, this risk can be reduced or even neutralized by the addition of progestogen. The protection against cardiovascular disease provided by combined estrogen/progestogen treatment has been the subject of much debate. However, results from epidemiological studies, intervention trials and animal experiments now suggest that the addition of progestogen does not attenuate the beneficial effects of estrogen. While secondary prevention studies are needed to evaluate the various hormone regimens, the use of combined estrogen/progestogen therapy can be supported.
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PMID:Women at cardiac risk: is HRT the route to maintaining cardiovascular health? 938 12

Polycystic ovary syndrome (PCOS) is probably the most prevalent endocrinopathy in women and the most common cause of menstrual disturbances during the reproductive age. It is characterised by the presence of polycystic ovaries on ultrasound examination together with clinical and biochemical signs of hyperandrogenaemia. The majority of patients will seek medical advice because of menstrual disturbances, infertility or signs of hyperandrogeneamia (hirsutism, acne, alopecia). In obese patients the therapeutic mainstay is weight reduction. Anovulatory infertility is treated by stimulation of ovulation, laparoscopic electrocautery or IVF, while patients with menstrual disturbances without a wish to conceive should be treated with cyclic gestagen therapy or oral contraceptives in order to reduce the increased life-long risk of endometrial cancer. Additionally, hirsutism may be treated by epilation or antiandrogen therapy. PCOS is a common disease with an increased risk of NIDDM, hypertension, cardiovascular disease and endometrial cancer. Polycystic ovary syndrome is thus a disease which needs attention from the health system.
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PMID:[Polycystic ovary syndrome I. Clinical presentation and treatment]. 945 93


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