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[Current views on the epidemiology and etiology of endometrial carcinoma].


 Endometrial carcinoma (EC) shows a worlwide trend toward increase in industrialized nations which cannot be explained solely by the longer life expectancy of women although the incidence of EC increases at later age (10-20/100,000 women overall; 1/1000 women in 50-70 year olds). Mortality rate of EC has decreased and 5-year survival rate has increased. Besides age factors and individual disposition, endocrine factors are important in the etiology of EC. Obesity effects estrogen metabolism: in extraglandular aromatization fo androstanedione estrone is formed which, in turn, is metabolized to estradiol in the endometrium. A higher plasma level of estradiol is found in obesity with a correspondingly lower sex hormonebinding globulin capacity. Anovulation, corpus luteum insufficiency (as in the polycystic ovary syndrome) and nulliparity are risk factors because of uninhibited estrogen-induced endometrial proliferation with increased cell-turnover rate. This may lead to precancerous conditions and EC. Whearas estrogens of themselves are not carcinogenic they promote EC; epidemiologic studies have shown an increased risk and incidence of EC in postmenopausal women on longterm estrogen therapy. Although these studies are thus far inconclusive there appears to be a dose and time-dependent risk factor. Continued administration carries a greater risk than cyclic administration. Risk and incidence increase with duration of use; likewise, a 1.25 mg dose of conjugated estrogens carries twice the risk of a smaller dose. On the other had, estrogen-related EC is diagnosed earlier and treated more successfully (92% survival). Progestins inhibit estrogen-induced proliferation; the incidence of endometrial and/or ovarian carcinoma related to the use of hormonal contraceptives has dropped since the advent and use of combination pills with their low estrogen content.
