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

Perimenopausal and postmenopausal substitutive estrogen treatment is valuable if prescribed according to proper indications and in the proper manner. Studies have shown a correlation between menopausal estrogen treatment and endometrial cancer. Siiteri hypothesized that estrone was the estrogen with a specific carcinogenic effect. A study undertaken in California indicates, however, that conjugated estrogens are associated with a lower risk of endometrial cancer. There is also strong indications that certain factors predispose a woman to endometrial cancer during menopausal estrogen treatment: obesity, the Stein-Leventhal syndrone, the Turner syndrome, hirsuitism caused by increased androgen activity, and family history of endometrial cancer. Menopausal estrogen treatment is prescribed in cases of menstrual disturbances, neurovegetative or vaso-motor disturbances, psychological disturbances, atrophy of the urogenital tract, or cases of calcium or fat metabolism disturbances which could lead to osteoporosis or arteriosclerosis.
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PMID:[Estrogen substitution and endometrial carcinoma]. 21 33

20 postmenopausal patients with serious and painful decalcifying osteosis were treated with an association of estrogens, progesterone, calcium and phosphates. Symptomatology disappeared completely in 7 cases, and was enormously improved in 9 cases. Improvement was very rapid, beginning after only 4 weeks of treatment. 2 patients did not receive any benefit from the treatment, and 2 more had a relapse after initial improvement. Estrogen therapy does reduce bone resorption and has a definite preventive and curative action whenever there is lack of estrogens. It is imperative, however, to eliminate from this kind of treatment patients with risk of breast or endometrial cancer.
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PMID:[Oestrogen therapy of osteoporosis (author's transl)]. 43 26

One in the three women develops osteoporosis--low bone mass and structural deterioration leading to fractures. Pre- and postmenopausal deficiency states are main causes. Estrogens prevent bone loss: Oral doses of 2 mg estradiol or 0.625 conjugated estrogens/day or 50-100 micrograms transdermal estradiol/day substantially reduce vertebral, forearm, and hip fractures. Certain progestins may enhance this effect. Calcium as a prerequisite for attainment of peak bone mass will not substitute for estrogen replacement. Selection of patients actually being at risk for postmenopausal osteoporosis needs to be improved substantially; there is no sensitive single test or testing system for osteoporosis. As individual history and physical exam or biochemical markers of bone resorption and formation rarely provide the early diagnosis of osteoporosis, prophylactic estrogen replacement therapy has to be considered in the majority of postmenopausal women to achieve prevention of postmenopausal osteoporosis. Compliance of replacement therapy in the European countries is poor, only 5-25% of postmenopausal women use estrogen replacement therapy for more than one year. Major compliance problems are alleged weight gain, resumption of withdrawal bleeding and fear to develop breast or endometrial cancer.
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PMID:Identification and treatment of postmenopausal women at risk for the development of osteoporosis. 149 Jul 69

Fifty years ago Albright contributed the following to understanding osteoporosis: (1) He recognized it as a deficiency of formation, not of mineralization of bone matrix; (2) he observed that 40 of 42 patients with osteoporosis before age 65 were women past menopause or young women postoophorectomy; (3) he concluded that estrogen stimulates osteoblasts (a conclusion later challenged); (4) he demonstrated by metabolic balance studies that estrogen causes a positive calcium balance in postmenopausal osteoporosis; (5) he introduced periodic progesterone to prevent or treat endometrial hyperplasia from prolonged estrogen therapy; and (6) he showed that long-term therapy arrested vertebral damage and height loss in postmenopausal osteoporosis and prevented them if started early. Since Albright's time, more sensitive methods of assessing bone density have replaced conventional roentgenograms. Some large scale trials of estrogen have indicated increased bone density and fewer fractures. Unopposed estrogen increases risk of endometrial cancer and decreases mortality from other cancers, myocardial infarction, stroke, and osteoporosis. Trials of calcitonin, diphosphonates, fluoride, vitamin D, and high calcium intake have not proved more effective than estrogen.
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PMID:Fuller Albright. His concept of postmenopausal osteoporosis and what came of it. 186 30

In the past decade, we observed progress in the differential diagnosis of osteoporosis, mainly because of advanced radiological and laboratory procedures, including new bone markers. Loss of bone can also be related to primary and secondary forms of osteoporosis. Consequently, secondary osteoporosis (and osteomalacia) should be treated primarily according to the original disease. Although etiopathology of primary osteoporosis is still unclean differential therapy should be applied to the different subgroups (juvenile, postmenopausal, and senile osteoporosis). Furthermore, even patients of the same age and sex can be at risk for osteoporosis or have definite osteoporosis. This can be differentiated in "low or high turnover osteoporosis" and should be diagnosed and treated as described. Conjugated estrogens in combination with progesterone decrease the rate of endometrial carcinoma and have been established to be very effective in the treatment of high turnover osteoporosis and patients at high risk of developing manifest osteoporosis. In combination with calcium (1 g/day) total doses of estrogen can be reduced to 0.3 g/day. The same applies for the treatment of low turnover (mostly manifest) osteoporosis with fluoride. Daily doses of fluoride can be decreased from 80 mg sodium fluoride to 50g in combination with calcium. These reductions of daily fluoride doses decreases the rate of side effects and allows longer control periods, provided that bone measurements demonstrate a beneficial long-term effect. The control periods depend on the sensitivity of the bone density measurements. Special indications, modifications, alterations and additions of further drugs are discussed for the individual patient.
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PMID:[Differential therapy of osteoporosis]. 208 55

Estrogen replacement therapy is the most effective single means of preventing and treating osteoporosis. The most common objection by patients, the resumption of menses if the uterus is present, may be eliminated by providing estrogen and progestin continuously. An additional concern, endometrial carcinoma, appears to be largely alleviated by coadministration of progestin. Evidence indicates that concomitant progestin administration actually reduces the incidence of endometrial carcinoma to less than that in untreated women. An incidental but potentially more important benefit is protection against coronary artery disease. Optimal management includes initiation of estrogen therapy shortly after menopause, long-term continuation and calcium supplementation.
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PMID:Estrogen replacement therapy for the prevention of osteoporosis. 267 51

The menopause is the physiologic cessation of normal, cyclic ovarian function. The development of vasomotor symptoms, atrophic changes in the genito-urinary system and osteoporosis are associated with oestrogen deficiency. Osteoporosis is the most important consequence of ovarian failure because it causes considerable morbidity and mortality. There is no simple screening test for detecting postmenopausal women who are at risk of developing osteoporosis. Oestrogen replacement therapy affects lipid metabolism and may be associated with the risk of developing endometrial cancer, breast cancer and thromboembolic disease. The addition of a progestogen regime have shown to reduce the risk of endometrial pathology. The most consistent and beneficial effect of oestrogen is the prevention of osteoporosis and subsequent fractures. Non-hormonal treatment regimes for postmenopausal osteoporosis include calcium, calcitonin and 1-alpha hydroxyvitamin D. It may be possible to use hormonal treatment for the optimal control of menopausal symptoms and non-hormonal treatment as long term prophylaxis.
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PMID:Geriatric gynaecology. 329 37

The pathophysiology of primary osteoporosis and the various therapeutic regimens that have been used are reviewed. Osteoporosis is a major public health problem because the incidence of hip, wrist, and vertebral fractures associated with bone loss is high. Postmenopausal women are at increased risk for developing osteoporosis because bone mineral content is lower in women than in men, dietary calcium intake is frequently insufficient, intestinal absorption of calcium decreases with age, and the rate of bone loss accelerates at menopause. The efficacy of many single and combination therapies in preventing or treating osteoporosis has been studied. Differences in study design and diagnostic techniques and the heterogeneous nature of osteoporosis make evaluation of clinical trials difficult. Exercise helps to maintain skeletal mass, but amenorrhea caused by vigorous activity may be harmful. The efficacy of estrogen replacement therapy is documented best; many studies have shown that estrogens slow the rate of bone loss and reduce the incidence of fractures, but the association of estrogen use with endometrial cancer and breast cancer is of concern. Progesterones may protect against endometrial cancer, but undesirable effects of oral contraceptives have resulted in a hesitancy to use combination hormonal therapy. All adults should meet daily nutritional requirements for calcium, but this intake may be insufficient for elderly persons and is below recommended doses for treating osteoporosis. A daily intake of at least 1000-1500 mg of elemental calcium has been shown to slow the rate of bone loss. Nutritional requirements for vitamin D should be met, but benefits from pharmacologic doses have not been demonstrated. The role of fluoride, calcitonin, anabolic steroids, and vitamin D metabolites is unclear. Fluoride has the potential to increase bone mass, but effects on bone histology and fracture rates require further study. The major goals for the management of osteoporosis are maintenance of bone mass and prevention of fractures. An adequate intake of calcium and regular weight-bearing exercise are important preventive measures. Despite the documented effectiveness of estrogens, risks associated with long-term use are of concern.
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PMID:Pathogenesis and management of primary osteoporosis. 352 28

Prevention of osteoporosis involves a variety of health promotion strategies: good nutrition with an emphasis on non-animal sources of protein; an adequate intake of calcium; and an active lifestyle with plenty of weight-bearing activity. Cigarette-smoking and excessive intakes of alcohol and caffeine can accelerate the development of osteoporosis and should be avoided. In many cases hormonal replacement is also essential. The risk of endometrial carcinoma as a consequence of estrogen replacement is reduced by adding a progestogen on a cyclic basis. The most desirable estrogen/progestogen combination involves the use of a progestogen for at least 10 days every month and the use of estrogen on a cyclic basis with several days each month during which neither hormone is taken.
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PMID:Osteoporosis: strategies for prevention. 376 62

Osteoporosis is the most common bone disorder in the United States. Bone mass is decreased, and porosity and fragility are increased. Dual-beam photon absorptiometry is currently considered the best detection technique. Prevention involves increased calcium intake and avoidance of diets high in protein and phosphates, excessive alcohol consumption and smoking. Estrogen therapy is recommended for most oophorectomized or postmenopausal women, at least for a few years. The addition of progestins to the regimen reduces the risk of endometrial cancer.
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PMID:Osteoporosis. 406 Dec 40


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