Endometrial Hyperplasia
Estrogen Replacement Therapy after Endometrial Cancer
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Estrogen replacement therapy can be used safely in patients who have had endometrial cancer. This suggestion is based on the fact that patients with a disease with a good prognosis, although estrogen-progesterone receptor positive, nevertheless have no remaining cancer cells after their treatment. Those patients with a lesion with a poor prognosis are usually receptor poor; therefore, replacement therapy theoretically would have no impact on development of recurrences. There are now five studies in the literature (none of them prospective and randomized), and all suggest that hormone replacement therapy is not detrimental to these patients. Some investigators will start the patient taking estrogen replacement therapy immediately after primary therapy for her cancer, although others think that waiting a number of months or even years is necessary to be safe. A Committee Opinion of the American College of Obstetricians and Gynecologists stated that in women with a history of endometrial carcinoma, estrogens can be used for the same indications as they are used for any other woman, except that the selection of appropriate candidates should be based on prognostic indicators and the risk that the patient is willing to assume. A prospective, randomized study of estrogen replacement therapy in endometrial cancer patients is anticipated to begin shortly under the auspices of the Gynecology Oncology Group. The experience over the last 10-15 years would suggest that if estrogen replacement therapy is detrimental to patients with endometrial cancer, the risk is extremely small. Because most patients with endometrial cancer are long-term survivors, the risks of cardiovascular disease and osteoporosis appear to be significant and higher than the risk of recurrence of the endometrial cancer. Benefits of estrogen replacement therapy, therefore, appear to greatly outweigh the theoretical risk in patients who have had endometrial cancer.
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Endometrial Hyperplasia
Both the diagnosis and management of endometrial hyperplasia have generated tremendous confusion. The natural history would suggest that some of these lesions revert to normal spontaneously or with medical therapy, some persist, and a few will progress to endometrial adenocarcinoma. Most endometrial hyperplasias are thought to result from persistent or prolonged estrogenic stimulation of the endometrium, either endogenously (anovulatory cycle or hormone-producing tumor) or with unopposed exogenous estrogen. In the mid-1980s, a new classification was developed by the International Society of Gynecologic Pathologists, which eliminated a plethora of terms that carried different connotations.
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The diagnosis of endometrial hyperplasia is made pathologically, usually on an endometrial biopsy that is obtained because of irregular or postmenopausal bleeding. Four categories of hyperplasia are now recognized: simple, simple atypical, complex, and complex atypical. It would appear that only those patients with atypical hyperplasia are at risk of developing endometrial cancer if the hyperplasia is allowed to go untreated for varying periods (up to and more than 10 years). The diagnosis of atypical hyperplasia is based on cytologic atypia. Architectural changes that previously were thought to indicate high risk for developing endometrial cancer no longer carry that implication unless atypia is present. Even when complex atypical hyperplasia is present, data suggest that only one fourth to one third of these patients might develop endometrial adenocarcinoma some years in the future.
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In the patient who has atypical hyperplasia on an endometrial biopsy, a thorough curettage is usually recommended because as many as one third of these patients will have a coexistent adenocarcinoma. In the patient with hyperplasia without atypia, curettage is usually not warranted. Hyperplasias, both with and without atypia, can be treated successfully in most instances with progestins. Various progesterone regimens (ie, use of medroxyprogesterone acetate or its equivalent for a few months) have been effective. The younger patient usually needs a higher dose. The goal is to make the endometrium atrophic, and a rebiopsy is recommended 2-3 months after commencement of the pro-gestin therapy. If hyperplasia persists on biopsy, progestin may be continued for another period. In many patients with atypical hyperplasia, particularly if they are postmenopausal, a simple hysterectomy and bilateral salpingo-oophorectomy have been advocated. These surgical patients may use estrogen replacement therapy postoperatively.