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

The treatment regimens are described in 74 patients with endometrial disease among 850 climacteric women receiving oestrogen therapy. Cystic hyperplasia was associated with unopposed oestrogen therapy without progestagen. Two courses of 21 days of 5 mg norethisterone daily caused reversion to normal in all 57 cases of cystic hyperplasia and 6 of the 8 cases of atypical hyperplasia. 4 cases of endometrial carcinoma referred from elsewhere demonstrated the problems of inappropriate and unsupervised unopposed oestrogen therapy and the difficulty in distinguishing severe hyperplasia from malignancy. Cyclical low-dose oestrogen therapy with 7--13 days of progestagen does not seem to increase the risk of endometrial hyperplasia or carcinoma.
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PMID:Prevention and treatment of endometrial disease in climacteric women receiving oestrogen therapy. 8 11

Dr Thom and her colleagues (Sept. 1, p. 455) are incorrect when they state that the U.S. case-control studies of endometrial cancer and oestrogen use "are open to criticism on grounds of selection of patients, poor medical supervision, inappropriate hormone therapy, and lack of clarification of the pathology by the addition of progestagens." It is not the studies which are open to criticism on the grounds stated but the way in which oestrogen therapy had been administered before the publication of these studies. A case-control study compares the frequency of exposure to a suspect carcinogen (oestrogens, in the example of endometrial carcinoma) to that of a control group. Since it was not at all a common practice to prescribe oestrogen with a progestagen when these studies were done, few histories of this combined regimen were found in either the cases or controls. But it is a great mistake to conclude that the absence of data on the risk of combined oestrogen and progestagen therapy means that there is no risk attached to combined therapy. The case-control studies that have thus far been reported shed no light on this risk because the regimen was too rarely used for these studies to have picked up a risk if indeed it was present. Thom et al. suggest that treatment with progestagen is effective in preventing or reversing endometrial hyperplasia. It is not yet well established that hyperplasia is a precursor to neoplasia. Thom et al. may be correct in believing that the combined regimen is safe but we must be perfectly clear about the meaning of the results of our case-control study, the largest reported to date. Our results do not put the combined regimen beyond suspicion but rather point up the need for continued monitoring of this regimen for cancer risk until the issue can be settled one way or the other. Meanwhile, the unfortunate experience with widely prescribed unopposed oestrogens should serve as a warning that any recommendations about prolonged use of these substances should be made with considerable caution.
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PMID:Oestrogen-replacement therapy. 9 Aug 98

Initial evidence suggested that estrogen therapy increases the risk of endometrial carcinoma. It was then suggested that some studies may have exaggerated the hazard of estrogen therapy by including patients with atypical endometrial hyperplasia among those having endometrial carcinoma. Three internationally recognized pathologists reviewed the histology slides available from the Ziel and Finkle study, which originally reported a risk ratio of 7.6 for estrogen users. At least one of the pathologists concurred with the original diagnosis in all but one case. Furthermore, all pathologists aggreed that 74 per cent (66/89) were correctly diagnosed. In the 66 patients with unanimous diagnosis, 61 per cent (40/66) had used conjugated estrogens, versus 57 per cent (54/94) in the original study. On the basis of 66 patients and 132 matched controls, the revised risk-ratio estimate is 8.1 (with a one-sided 95 per cent lower confidence limit of 4.5), validating the original estimate.
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PMID:Estrogen and endometrial carcinoma. An independent pathology review supporting original risk estimate. 19 95

Estrogens and progesterone seem to have at times antagonistic, at times synergetic action on breast and uterine tissues. While estrogens stimulate cell proliferation, progestrerone favors secretion. While estrogens favor myometrial and endometrial hyperplasia, progesterone seems to dominish congestive phenomena caused by estrogens, especially on breast tissues. Women who experience menopause at 55 have a twice as high risk of breast cancer than women who menopause at 45. Breast and endometrial cancer are often associated with a history of menstrual disorders, and it is very possible that endometrial hyperplasia and cystic mastosis are connected. While treatment with estrogens helps to avoid vaginal atrophy and to arrest osteoporosis, it is doubtful whether the treatment should be systematic over 45. Breast examination and a thorough gynecological examination are essential once a year.
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PMID:[Menopause, estrogens and genital cancer]. 24 20

The epidemiology of cancer of the endometrium has been reviewed by going through the literature in order to find a high risk category. A particular type seems to be discernable: obestiy, endometrial hyperplasia, and the contribution of endogenous or exogenous oestrogens and lack of progesterone are the most marked elements. These factors for cancer of the endometrium are similar to those for cancer of the breast. It has been astonishing to find that these two hormone dependent cancers have a very similar background.
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PMID:[Cancer of the endometrium. The evaluation of high risk cases (author's transl)]. 38 9

Because of adverse publicity regarding increased risk of endometrial cancer in women receiving estrogen therapy, a 2-year prospective study was conducted in 1976 to determine the incidence of endometrial cancer in postmenopausal women. A retrospective study for the year 1975 was also added. A postmenopausal survey card for each patient recorded the patient's visit and clinical data, as well as hormone therapies (estrogen, progestogen, androgen). Postmenopausal women never treated with hormones were also provided survey cards. A total of 2088 patient-years of estrogen use was recorded during the combined 3-year study period (1975-77). 8 of the estrogen users had a diagnosis of adenocarcinoma of the endometrium for an annual incidence rate of 3.8/1000 women. 2 endometrial cancers were detected in the estrogen-progestogen users for a cancer incidence rate of 0.5/1000 (3792 patient-years of observation); this finding suggests that progestogen provides better protection against endometrial cancer compared to estrogens. This difference between estrogen users and estrogen-progestogen users was statistically significant (p ? 0.01). 1 endometrial malignancy occurred among estrogen vaginal cream users, giving an incidence of 1.7/1000. The patient used Premarin vaginal cream (1 gm thrice weekly) for 7 months before the cancer was diagnosed. No endometrial cancer was diagnosed in both the progestogen and androgen groups. Overall, 14 endometrial cancers out of 8170 years of observation were diagnosed in this clinic; annual incidence rate for the study period was 1.7/1000. 199 women with endometrial hyperplasia (a precancerous lesion) were treated with progestogens for 3 to 6 months. The hyperplastic endometrium returned to normal in 96.5%. It was suggested that all postmenopausal women with intact uterus be given the Progestogen Challenge Test and that progestogens be given to the women each month as long as bleeding follows. This should prevent the development of endometrial cancer in most women.
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PMID:Reduced incidence of endometrial cancer among postmenopausal women treated with progestogens. 46 50

Histological analysis of 266 hyperplastic endometria obtained by curettage revealed the following forms of hyperplasia: simplex 29.3%, cystic 50%, adenomatous 18.4, and atypical 2.2% (according to the classification accepted by the authors). Mild forms of endometrial hyperplasia (simple and cystic) recede in most cases spontaneously or after therapy and rarely turn into endometrial adenocarcinoma, whereas severe forms of hyperplasia (adenomatous and atypical), unless treated, often turn into endometrial carcinoma. The etiology, some clinical manifestations, and therapy of this condition of the endometrium are reviewed.
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PMID:[Histopathological diagnosis and clinical significance of endometrial hyperplasia]. 55 15

8 papers, based on the results of retrospective studies performed in the U. S., have dealt with the effects of treatment of postmenopausal women with unopposed estrogens. The studies are unanimous in showing that such treatment is associated with increased risks of developing uterine cancer. The increase in risk is related to dose and duration of treatment. The studies have produced essentially similar risk radios, which have survived independent reevaluation of the original histopathological diagnoses. Prospective clinical studies have also shown the dose and duration of unopposed estrogens to be related to increased risk of endometrial hyperplasia, the most severe form of which is believed to be a precursor to endometrial cancer.
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PMID:Hormone replacement therapy. 55 41

A 22 year-old phenotypic female with a 45,x/46,x, r(x) mosaic complement had anovulatory cycles, histologically normal ovaries, and atypical endometrial hyperplasia which, when clinically followed by repeated biopsies, was found to progress to locally invasive endometrial carcinoma. This was successfully managed by the induction of ovulation with Clomid, which resulted in conversion of the endometrium to a normal secretory pattern for two subsequent years.
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PMID:The reversible behavior of locally invasive endometrial carcinoma in a chromosomally mosaic (45,X/46,Xr(X)) young woman treated with Clomid. 58 62

We investigated the serum activity of the fifth fraction of L-lactate: NAD-oxidoreductase (E.C.1.1.1.27) and serum alkaline phosphatase activity prior to diagnostic curettage in patients with abnormal and atypical endomertial hyperplasia. We also determined them in 75 patients with carcinoma of the endometrium, 80 patients with glandular cystic endometrial hyperplasia and a "normal" control group of 70 patients. In the statistical evaluation we found a significantly high incidence of low AP activity and elevated LDH5 in the group of patients with glandular cystic endometrial hyperplasia, as well as in patients with precancerous lesions of the endometrium and carcinoma of the endometrium. The findings raise the question of whether these changes in the serum activity of the given enzymes are only a response to a given hormonal modulation.
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PMID:Alkaline phosphatase activity in relation to LDH5 (L-lactate: NAD+ - oxidoreductase, E.C.1.1.1.27) in patients with precancerous conditions of the endometrium. 61 58


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