Endometrial hyperplasia

In breast cancer patients, total PR status is measured for hormonal treatment. The presence of PR is associated with increased survival rates and hormonal responsiveness of mammary tumors. PR agonists are widely used in contraception, HRT, breast cancer, and endometrial hyperplasia. Antiprogestins such as RU486 are used for blocking ovulation and preventing implantation, and in addition they are in clinical testing for the induction of labor and to control various neoplastic transformations. 

For most conditions associated with primary and secondary amenorrhea, estrogen (along with a progestin to minimize the risk of endometrial hyperplasia) is provided. 

Women who have an intact uterus should be prescribed a progestin in addition to estrogen in order to decrease the risk of endometrial hyperplasia and endometrial cancer. 

In women who have not undergone hysterectomy, a progestogen should be added because estrogen monotherapy is associated with endometrial hyperplasia and cancer. 

Several progestogen regimens to prevent endometrial hyperplasia are shown in Table 31-3. 

Low-dose hormone therapy (conjugated equine estrogen 0.45 mg and medroxyprogesterone acetate 1.5 mg/day) has demonstrated equivalent symptom relief and bone density preservation without an increase in endometrial hyperplasia. Whether such lower doses will be safer (cause less venous thromboembolism and breast cancer) remains to be seen. 

An estrogen dose equivalent to at least 1.25 mg conjugated equine estrogen (or 100 meg transdermal estradiol) is needed to achieve adequate replacement in young women, and a progestogen should be given for 12 to 14 days per calendar month to prevent endometrial hyperplasia. 

The effects of pure antiestrogens in the uterus have also been extensively studied, since it is an estrogen-dependent organ and the target of the main side effects of tamoxifen therapy, such as endometrial hyperplasia, hypertrophy of glandular epithelium, or even focal cellular atypia (Sourla et al. 1997). 

At present, the only SERMs routinely used in clinical practice are tamoxifen and raloxifene. Tamoxifen is used essentially as adjuvant treatment in women with breast cancer. Its use is related to estrogenic effects on the uterus. Specifically, tamoxifen can be associated with an increase not only in endometrial hyperplasia and cancer risk but also in uterine leiomyoma dimensions and in a risk of developing active endometriotic lesions. 

Endometrial hyperplasia Prolonged unopposed estrogen therapy may increase risk... 

Endometrial hyperplasia - To reduce the incidence of endometrial hyperplasia in nonhysterectomized postmenopausal women receiving 0.625 mg conjugated estrogens. 

Prevention of endometrial hyperplasia - Give as a single daily dose in the evening, 200 mg orally for 12 days sequentially per 28-day cycle, to postmenopausal women with a uterus who are receiving daily conjugated estrogen tablets. 

Prevention of endometrial hyperplasia IM 200 mg in evening for 12 days per 28-day cycle in combination with daily conjugated estrogen. 

Hormone replacement therapy PO 5-lOmgfor 12-14 consecutive days a month, beginning on day 1 or 16 of cycle given as parf of regimen with conjugated estrogens. Endometrial hyperplasia PO 2.5-10 mg/day for 14 days. 

Women (9%-l%) Genital itching, vaginal discharge, endometrial hyperplasia orpolyps... 

Adverse effects of pharmacological doses of androgens include, as one would expect from male hormones, hirsutism with acne and other signs of virilization, along with adverse lipoprotein profiles, endometrial hyperplasia in women, and an increased risk of cardiovascular disease. Some compounds are particularly likely to cause liver disorders. 

Some helpful evidence comes from related fields. It should be borne in mind, for example, that the question of an increased risk of endometrial hyperplasia and endometrial cancer also arises in patients with estrogen-producing tumors of the ovaries, obesity, and polycystic ovarian syndrome (101) and in patients with breast cancer who are using tamoxifen (102). 

The minimum dose of continuously administered nor-ethindrone acetate needed to reduce significantly the incidence of endometrial hyperplasia associated with the use of 17-P-estradiol 1 mg/day has been investigated in a large, controlled, comparative study in 1146 women over 12 months (107). The results suggested that continuous norethindrone acetate at doses as low as 0.1 mg/day is fully effective, at least during the first year of treatment. 

Lethaby A, Suckling J, Barlow D, Farquhar CM, Jepson RG, Roberts H. Hormone replacement therapy in postmenopausal women endometrial hyperplasia and irregular bleeding. Cochrane Database Syst Rev 2004 (3) CD000402. 

Kurman RJ, Felix JC, Archer DF, Nanavati N, Arce J, Moyer DL. Norethindrone acetate and estradiol-induced endometrial hyperplasia. Obstet Gynecol 2000 96(3) 373-9. 

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