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

A cohort of 2586 asymptomatic women, 98% over the age of 45, 78% Caucasian, was screened using commercially available devices for endometrial mucosal sampling and cytohistological techniques; 1567 returned for rescreening one year later, and 187 for a third time. The prevalence of endometrial carcinoma was 7 per 1000 and the incidence 1.7 per 1000 woman-years. An unexpected observation suggested that endometrial hyperplasia does not necessarily precede or accompany endometrial carcinoma in asymptomatic women aged 50 or more. Occult endometrial carcinoma is a detectable disease, but the study did not permit the evaluation of the effect of its detection on mortality from the disease.
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PMID:Screening for endometrial cancer. 357 Apr 12

This article deals with a 6-yr mass screening program for the early detection of endometrial cancer, which took place 1978-1983. The diagnostic accuracy of endometrial cytology and the possibility of integrating this technique with the hysteroscopy and endometrial biopsy were studied. The authors analyzed 2,504 outpatients, all over the age of 45. The results of endometrial cytology were compared with those found using hysteroscopy and endometrial biopsy. Endometrial cytology showed high sensitivity in diagnosing endometrial cancer (97.7%) and high specificity in diagnosing true negatives. However, this technique was not adequate in identifying benign endometrial pathology, e.g., endometrial hyperplasia, polyps, or submucous fibromas. Epidemiological and clinical data in our series were fundamental in establishing mass screening for the early detection of endometrial cancer using integrated techniques. These data should be taken into consideration for creating new projects. The significantly high prevalence of endometrial neoplasia even in asymptomatic women over 45 years of age (4 per 1000) and the possibility of improving the accuracy of endometrial diagnosis using hysteroscopy and endometrial biopsy were the cornerstones of this project.
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PMID:Endometrial cytology: six years of experience. 366 87

To evaluate the risk of transformation of atypical endometrial hyperplasia (AEH) into endometrial cancer, a group of 190 women who underwent treatment for AEH was followed up. The group included 53 women of child-bearing age, 81 in the premenopausal period, and 56 in the postmenopausal period. The most frequent clinical manifestation of AEH was metrorrhagia. The patients with mild or moderate AEH received conservative treatment, while the patients with severe AEH complicated by other gynecological diseases (uterine myoma or adenomyosis) received surgical treatment. Conservative hormonal treatment included cyclic administration of infecundin, bisecurin, hydroxyprogesterone caproate. The average duration of hormone therapy was 12 months. The 1st follow-up examination was conducted 3 months after the onset of the treatment. Of 53 patients of child-bearing age, 18 had recurrence of AEH (1 within 6 months after the initiation of the treatment, 5 within 6 months, 10 within 1-3 years, 1 within 5 years, and 1 within 9 years). Endometrial cancer was diagnosed in 2 patients (7 and 10 years after treatment of AEH). Of 81 patients in the premenopausal period, 29 developed recurrence of AEH within 3 months to 3 years of the treatment; endometrial cancer was detected in 2. Of 56 patients in the postmenopausal period, 16 developed recurrence within 3-6 months of the treatment; endometrial cancer was diagnosed in 3 patients. These findings indicate that majority of the patients with AEH can be cured by hormonal therapy, but the high risk of cancer development (3.7%) requires longterm follow-up.
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PMID:[Results of treatment of atypical endometrial hyperplasia]. 368 27

This investigation pursued the question of how many patients with precancerous endometrial hyperplasia were not recommended for screening programs solely because of the lack of risk factors. The median age of precancerous hyperplasia patients in Erlangen is 54, 8 years before the median age for endometrial carcinoma. Just under 10% (8.5%) of precancerous endometria occur before the age of 45. Only 18.3% of all precancerous patients do not suffer from overweight. Because age and adiposity were missing from the list of risk factors, one quarter (23.9%) of the women studied in Erlangen had not been included in a screening program. One-fifth (19.1%) of the precancerous stages in the risk patients would not be determined cytologically because nuclear criteria were either missing or deeply situated. Consequently, a minimum failure rate of 38.5% for precancerous patients must be reckoned with when using a cytological screening routine with risk patients. In the period under study, it is surprising to note that six times as many endometrial carcinoma as precancerous endometrial were treated. There is no universally suitable treatment for all precancerous patients. Certainly, an individualized, conservative form of treatment would seem to offer more hope of success than surgical therapy, which would always be aggressive.
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PMID:[Incidence of the risk factors age and obesity in patients with endometrial hyperplasia]. 374

Unopposed oestrogen replacement therapy increases the risk of endometrial cancer in post-menopausal women. However, the addition of progestogen to the oestrogen therapy reduces the risk of endometrial carcinoma by preventing and effectively treating hyperplasia of the endometrium. In a 5-yr prospective study with a further 4 yr of follow-up (1975-83), 31 adenocarcinomas of the endometrium were detected over 27243 patient-years of observation, for an incidence of 113.8:100 000 women. The first report on the results of the study appeared in 1978; this paper presents further results. The lowest incidence of endometrial cancer (49.0:100 000) was observed among the oestrogen-progestogen users and the highest (390.6:100 000) among the unopposed oestrogen users. Not only was the incidence of endometrial carcinoma significantly lower in the oestrogen-progestogen users than in those using unopposed oestrogens (P less than or equal to 0.0001), but it was also significantly lower than that among the non-hormone users (245.5:100 000 with P less than or equal to 0.0005). Endometrial hyperplasia had been diagnosed previously in 12 of the 31 patients with adenocarcinoma (38.7%) from 4 mth to 8 yr before the detection of cancer. When given for 7-10 days each month progestogens are effective in reversing hyperplasia and restoring a normal endometrium in 94.5% of patients treated within 3-6 mth. The progestogen challenge test was devised to identify post-menopausal women at greatest risk for adenocarcinoma of the endometrium. It is concluded that the use of this test will reduce the risk of endometrial cancer in both oestrogen-treated post-menopausal women and women with increased endogenous oestrogens.
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PMID:Prevention of endometrial cancer with progestogens. 374 49

The authors evaluated the diagnostic effectiveness of a triple specimen technique (cyto-histologic) performed by the Perma device. The incidence of endometrial hyperplasia (according to Dallenbach-Hellweg's classification) was estimated in 254 climacteric women selected from outpatients who come spontaneously to the Menopause Clinic of the Obstetrics and Gynecology Department (Bologna University). The selection criterion was the evidence of risk factors for endometrial carcinoma, climacteric bleedings (obesity, late menopause, high blood pressure, diabetes), or endometriotropic estrogen therapy in the postmenopause. Results showed that the cyto-histologic sampling is most useful for diagnosing endometrial hyperplasia and early carcinoma (diagnostic effectiveness: 89.0-93.8%). Also, endometrial hyperplasia was found to have a significant incidence in the group we examined. This incidence was highest in women with climacteric bleedings, secondly in women using high-dose estrogens, and thirdly in women with risk factors for endometrial carcinoma. When evaluating the different kinds of endometrial hyperplasia, we never found adenomatous hyperplasia in women on estrogen therapy. Affinity between histologic and cytologic classes was around 50% in endometrial hyperplasia and 100% in early carcinoma. This emphasizes that both samplings are needed to perform an accurate diagnosis.
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PMID:Cyto-histologic evaluation of the endometrium in climacteric women at risk for endometrial carcinoma. 376 24

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

Megestrol acetate, 20 to 40 mg/d, was given continuously to 70 postmenopausal women with a variety of endometrial hyperplastic changes. All patients were followed up with periodic endometrial biopsies. The study was conducted for 14 years with mean patient follow-up of more than 5 years. In 65 patients (93%), surgery was avoided due to this protocol. No patient developed endometrial carcinoma, and there were no major side effects. This regimen proved to be most effective in preventing hysterectomy in postmenopausal patients who presented with surgical risk factors and endometrial hyperplasia.
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PMID:Hormonal therapy for lesions of the endometrium. 379 26

The contact hysteroscope gives a clear view only upon contact with the observed surface. There are 6mm and 8mm diameter models. A total of 172 contact hysteroscopic examinations were performed to view the uterine cavity. The following results were obtained: After the previous observation with the panoramic hysteroscope, the rate of correct diagnosis with the 6mm model was 83.3% and that with the 8mm one was 98.5%. The rate of correct diagnosis with the 8mm model was 85.3% and that with the 6mm one was 92.7%, when used initially. The main disadvantages of the contact hysteroscope were a lack of perspective view and occasional existence of a dead angle just above the internal os. Among the contact hysteroscopic diagnosis, that of endometrial polyp was the most difficult, followed by those of slightly bulging submucous myoma and endometrial hyperplasia, while diagnosis of IUD, hydatidiform mole and endometrial carcinoma were easier. After acquiring the necessary experience, the 6mm model also gave very accurate results, requiring no cervical dilatation in multiparous cases. The 6mm model should therefore be a useful instrument to use in outpatient diagnosis.
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PMID:[Contact hysteroscopic exploration of the uterine cavity]. 381 4

This paper reviews epidemiologic evidence regarding the association between exposure to oral contraceptives (OCs) and the development of 4 cancers involving the reproductive system: breast, ovarian, endometrial, and cervical. Most knowledge in this area has been derived from cohort or case-control studies. Currently available evidence suggests that OC use does not influence breast cancer risk either adversely or favorably, although there may be a favorable influence on tumor growth. In view of the long latency of effect seen with known risk factors such as radiation exposure, age at menarche, and age at 1st full-term pregnancy, further studies are needed in this area. The epidemiologic evidence consistently supports the prediction that OC use makes the ovaries less susceptible to malignant change, perhaps by a mechanism similar to the protective effect of pregnancies. The magnitude of the effect is considerable, and should have a significant impact on the future incidence of ovarian cancer. In terms of endometrial cancer, there is evidence that sustained estrogenic stimulation unopposed or inadequately opposed by progestogen leads to endometrial hyperplasia and an increased longterm risk of malignancy. In currently used OC formulations, however, the progestogenic component has the predominant effect on the endometrium, and this effect is protective. It remains unknown whether OCs increase cervical cancer risk directly, or whether the association is an indirect one linked to some aspect of sexual behavior that is not being controlled. On the other hand, it seems reasonable to conclude that longterm OC users have an above average risk of cervical cancer and should have regular screening by cervical cytology. It should be kept in mind that recent changes in OC formulations and use patterns render epidemiologic data now available obsolete. It will be many years before sound data will be available on the low-dose estrogen OCs now in almost universal use.
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PMID:Oral contraception and cancer of the female reproductive system. 389 28


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