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Query: UMLS:C0003128 (anovulation)
 1,718 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

At the Wilford Hall U.S. Air Force Base Medical Center, Texas, about 4000 postmenopausal women received estrogen replacement therapy during 1975. Of these, 2700 took estrogens only and 1240 were given a progestogen along with estrogen. Hysterectomy had been done previously on 1700 patients (42%), leaving 2300 with intact uteri and a risk of endometrial cancer. Adenocarcinoma of the endometrium was diagnosed in 7 patients. Of these, 6 had received estrogen therapy. There was 1 endometrial malignancy in a patient also receiving a progestogen. Among 510 untreated postmenopausal women with intact uteri, 1 adenocarcinoma of the endometrium was found. Type and dosage of estrogen were unrelated to endometrial malignancy. In addition to the 7 endometrial cancers from the clinic, 22 cases were diagnosed elsewhere and referred for treatment, 11 of these had received no hormones. 10 were taking estrogens and 1 was receiving Oracon for birth control. The incidence of endometrial malignancy in the U.S. is reported to be 21/100,000 women/year. There is a 3-fold to 9-fold increased risk of endometrial cancer associated with obesity alone. The probability that untreated postmenopausal women with intact uteri will develop carcinoma of the endometrium is 1/1000/year. With estrogen users, it is reported to be increased -7.6/1000 women/year. In the author's clinic during 1975, the incidence among those receiving only estrogen was 4.7/1000. Among those also receiving a progestogen the incidence was .8/1000. Unopposed estrogens apparently have a role in the etiology of endometria hyperplasia and neoplasia through incomplete shedding of the endometrium. Progesterone produces more complete sloughing of the endometrium and also converts all degrees of hyperplasia into secretory endometrium. Nulliparity, infertility, and anovulation are predisoposing factors to endometrial carcinoma. Progestogens are palliative therapy for endometrial cancer.
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PMID:Estrogens, progestogens and endometrial cancer. 19 79

This lengthy discussion of possible associations between both endogenous and exogenous estrogens and progestins to occurrence of human cancers begins by discussing endogenous metabolism of the 2 sex steroid types. For example, the endogenous production of estrogen is associated with anovulation and endometrial cancer, although clearly other risk factors are associated with these diseases, and breast cancer, which account for some or all of the sex hormones apparent carcinogenic effect. Also discussed are the modulating effects of estriol on response of the breast and endometrium to estradiol and estrogens, and the modulating effects of androgens on development of breast cancer. The bulk of the monograph concerns summaries of data on the correlations of exogenous sex hormones and human cancers. Attention is also paid to the use of exogenous sex hormones for treatments of human cancers. Estrogens have been used to treat endometrial cancer, breast cancer, and benign breast disease. Side effects of hormonal contraception discussed include gross and microscopic changes in the breast, benign breast disease, and breast cancer; in the uterus, exogenous hormonal contraception is associated with neoplastic changes in the cervix, cervical neoplasia, endometrial cancer, trophoblastic tumors, and uterine fibroids. Ovarian effects include nonneoplastic and benign lesions and ovarian cancers. Oral contraception may also correlate with incidences of pituitary and melanoma malignancies. Liver effects include both benign neoplasms and malignant tumors.
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PMID:Oestrogens and progestins in relation to human cancer. 39 83

Precanceroses and early screening of endometrial carcinomas are reviewed. Measures are evaluated on how to prevent this malignancy with administration of gestagens in hyperplastical endometrial changes in climacteric conditions and manifestations of endometrial estrogenization in postmenopause. On the basis of clinical, laboratory and histological investigations, the total of 31 female subjects with dysfunctional bleeding was given medroxyprogesterone acetate (Provera Upjohn tbl.) in 10 mg daily doses for up to 10-13 days cyclically prior to the onset of menopause. Under the mentioned treatment any of them experienced the rebleed, and no endometrial carcinoma had been diagnosed with control vacuum curettage within one year of observation. In a total of 196 women operated on to endometrial carcinoma, the occurrence of risk-factors for the development of mentioned tumour (obesity, late menopause, i.e. menopause after 50 years of age, sterility and dysfunctional bleeding backed with anovulation, long-term estrogen administration, feminizing ovarian tumours, liver diseases, glycide metabolic disorders and hypertension) was evaluated. The present work was aimed on the screening of asymptomatic group of women. Two important signs (obesity and late menopause) were invariably determined with the addition of any other risk factor. Mentioned women are supposed to undergo regular yearly histological investigation of endometrium. Of most benefit the vacuum curettage is believed by authors as a result of comparing the validation of cytological and histological methods in order of early evidence.
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PMID:[Precanceroses and endometrial carcinoma]. 184 15

Data from previous studies suggest that infertility is a risk factor for endometrial cancer. We used data from the Cancer and Steroid Hormone Study to further characterize this relationship. The subject group comprised 399 women ages 20-54 with newly diagnosed epithelial endometrial cancer ascertained through six cancer registries. The control group comprised 3040 women in the same age range selected by random-digit telephone dialing from the same geographic areas where cancer patients resided. Compared with women who reported no fertility problem, women with physician-diagnosed infertility who had reported at least 2 years of infertility had an odds ratio for endometrial cancer, adjusted for age, of 1.7 (95% confidence interval 1.1-2.6). Women who reported infertility resulting from ovarian factors had an adjusted odds ratio of 4.2 (95% confidence interval 1.7-10.4). These results suggest that factors such as anovulation may explain much of the increased risk of endometrial cancer found among subgroups of infertile women.
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PMID:Infertility-associated endometrial cancer risk may be limited to specific subgroups of infertile women. 198 11

To investigate whether a history of infertility affects a woman's risk of developing breast cancer, the authors analyzed case-control data collected between 1980 and 1982 as part of the Cancer and Steroid Hormone Study. The 4,730 cases were women aged 20-54 years with a first diagnosis of breast cancer ascertained from eight population-based cancer registries; the 4,688 controls were women randomly selected from the general population of these same eight areas. After controlling for age, age at first birth, and parity, the odds ratio (OR) for breast cancer associated with infertility was 1.01 (95% confidence interval (CI) 0.89-1.15) among gravid women. Controlling for age, the odds ratio was 0.82 (95% CI 0.59-1.14) among nulligravid women. Women who reported that the reason for their infertility was a problem with their ovaries had a risk similar to that for women without a history of infertility (OR = 0.75, 95% CI 0.48-1.24). Women whose physicians reported that the reason for their infertility was anovulation or Stein-Leventhal syndrome also had risks similar to those for women without a history of infertility (OR = 1.26 (95% CI 0.67-2.34) and OR = 1.13 (95% CI 0.46-2.78), respectively). Menopausal status, age at menarche, history of spontaneous abortions, drinking or smoking behavior, use of exogenous hormones, or family history of breast cancer did not appreciably alter the observed odds ratios. If infertility has an effect on breast cancer that is independent of age at first birth, then the effect is small.
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PMID:Infertility and breast cancer: a population-based case-control study. 240 11

Medroxyprogesterone acetate (Provera) is a drug that is commonly given to young women with cancer during chemotherapy and radiation to control heavy bleeding associated with anovulation. Because hypothalamic-pituitary-ovarian suppression has been associated with ovarian protection from the effects of chemotherapy and medroxyprogesterone acetate has been identified as a radiosensitizing agent, we explored the effects of medroxyprogesterone acetate on a rat model with known radiation injury characteristics. Sprague-Dawley rats were treated with medroxyprogesterone acetate or vehicle from day 22 to day 37 of life and were either irradiated or sham-irradiated on day 30 of life and then killed on day 44. Radiation with medroxyprogesterone acetate administration produced a greater loss in preantral and healthy control follicles than in control follicles. No suppression of luteinizing hormone or follicle-stimulating hormone had occurred by day 30 but ovarian glutathione content was reduced. These findings indicate that the administration of medroxyprogesterone acetate with radiotherapy may enhance ovarian injury.
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PMID:The effect of medroxyprogesterone acetate (Provera) on ovarian radiosensitivity. 252 68

A case-control study incorporated within a cohort study was undertaken to test the hypothesis that anovulation or decreased luteal function is associated with increased risk of breast cancer. A large population (n = 12,000) of apparently healthy women aged 40-49 collected a specimen of urine on day 22 of 3 consecutive menstrual cycles, or, in cases of amenorrhea, on 3 arbitrarily chosen days. These samples were stored at -20 degrees C. Subsequent screening of the women by mammography revealed 34 cases of breast cancer, and over the next 4 years a further 34 cases were reported to the cancer registry. Urine samples from 53 of these cases were assayed for pregnanediol and creatinine, and the results were compared with those for an equal number of matched controls. No differences between these groups were found in the pregnanediol/creatinine ratio. We conclude that our results do not support the hypothesis that women with luteal insufficiency are at increased risk for breast cancer. However, since breast cancer patients tend to have a later menopause than controls, the possibility cannot be excluded that breast cancer patients continue to have ovulatory cycles for a longer period during reproductive life. Such a finding--opposite to the working hypothesis--would complicate the interpretation of the results.
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PMID:A prospective study on corpus luteum function and breast cancer risk. 272 7

The literature concerning endogenous hormonal profiles in women with breast cancer and breast-cancer risk has been critically reviewed. The many published reports have been divided into 11 groups, with each group centered on a particular hypothesis that has been either explicitly formulated by the authors of the reports or perceived by other workers as a unifying hypothesis in certain studies. The hypotheses reviewed are: the adrenal androgen insufficiency hypothesis, the anovulation/luteal inadequacy hypothesis, the estriol hypothesis, the ovarian androgen excess hypothesis, the thyroid dysfunction hypothesis, the prolactin hypothesis, the estrone hypothesis, the estrogen-window hypothesis, the estrogen-excess hypothesis, the melatonin hypothesis, and the estrogen hydroxylation hypothesis. It is concluded that there remain, at present, only four viable hypotheses: the hypotheses of increased risk with adrenal androgen deficiency, ovarian dysfunction (luteal inadequacy and excessive ovarian androgen secretion), increased 16 alpha-hydroxylation of estradiol, and the hypothesis of decreased risk with pregnancy-induced lowering of prolactin levels. Adrenal androgen deficiency seems to be pertinent only in premenopausal cancer patients, and may be a genetic defect. Ovarian dysfunction seems to be pertinent to both premenopausal and post-menopausal patients and may also have a strong genetic component. Increased estradiol hydroxylation likewise seems to have a genetic component. The prolactin effect differs from the others, in that it is clearly environmental, rather than genetic, and may represent a permissive effect rather than a true risk-promoting effect.
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PMID:Hormonal profiles in women with breast cancer (review). 305 48

"Dysfunctional uterine bleeding" is not a generic term for abnormal uterine bleeding. Rather, it refers solely to bleeding caused by an ovarian endocrinopathy. Estrogen withdrawal and inappropriately sustained estrogen production are the two mechanisms responsible. The latter mechanism produces estrogen breakthrough bleeding, which is common in women with chronic anovulation. Treatment of estrogen withdrawal bleeding depends on when in the menstrual cycle bleeding occurs. Anovulatory bleeding is best treated with progestin. Estrogen therapy is contraindicated, except in patients with profuse anovulatory bleeding unresponsive to progestin treatment, because it increases the risk of endometrial hyperplasia and cancer.
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PMID:Dysfunctional uterine bleeding. Clarifying its definition, mechanisms, and management. 394 5

A clinicopathological review of 106 cases of premenopausal endometrial carcinoma has confirmed the good prognosis in such patients. Women less than 40 years old were more likely to be nulliparous, over 80 kg in weight, and to present with irregular or heavy and irregular bleeding, than women 40 years or older. Seven patients developed malignancies at other sites. A detailed pathological review of 32 cases revealed poor prognostic features in 30% of patients; corpora lutea were identified in the ovaries of 13 patients. It is suggested that factors other than anovulation are related to the development of endometrial cancer in the over 40 age group.
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PMID:Endometrial carcinoma in premenopausal women: a clinicopathological study. 397 91


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