par L'Hermite, Marc
Référence Maturitas, 12, 3, page (215-246)
Publication Publié, 1990
Article révisé par les pairs
Résumé : Contrary to widespread irration belief, estrogen replacement therapy (ERT) bears very little risk and, on the contrary, exerts a protective effect against atherosclerosis and cardiovascular disease. This protection most likely results from one or both of the following mechanisms: (1) a drive of the lipidic metabolism towards a 'favorable', profile (decrease of total- and LDL-cholesterol and increase in HDL-cholesterol levels); (2) a favorable prostacycline/thromboxane balance towards vasodilatation and anti-aggregation. This is the case when natural estrogens are used, synthetic estrogens (namely ethinylestradiol) overstimulate the hepatic production of proteins, such as renin substrate and angiotensinogen, with an increased risk of hypertension, vasoconstriction and platelet aggregation. Conjugated equine estrogens are not truly physiologic for human use and some of their estrogenic components can also predispose to hypertension and accumulate. Non-orally administered natural estrogens have less - almost no - metabolic impact and this could hypothetically result in an impaired protective effect against cardiovascular disease; the presently available estrogen implants are not satisfactory and their use frequently leads to estrogen accumulation. Hypertension and diabetes are no longer considered to be contra-indications to ERT: natural estrogens can even improve hypertension as well as glucose tolerance. Estrogen use, at least by the oral route, slightly increases the incidence of gallstones. The sole other well-documented risk of unopposed (i.e., without administration of any progestogen) ERT resides in a 2x - 3x greater risk of developing a carcinoma of the endometrium, the effect being dose- and duration-dependent. A progestogen challenge test is mandatory before initiating ERT and the addition of a progestogen must be considered in case of long-term ERT. Furthermore, patients having received ERT remain at increased risk for endometrial carcinoma development for many years and thus require careful post-treatment surveillance. As far as breast cancer is concerned, and despite the clear involvement of exogenous estrogens in its etiology, the bulk of the data offers reassurance that low-dose exogenous estrogens will not dramatically increase its incidence. However, it remains controversial whether or not high doses and long duration could still, however, slightly increase the risk. Therefore, regular breast screening (X-ray) is mandatory and it is recommended to use the lowest estrogen dose possible that can treat menopausal complaints and/or prevent osteoporosis. In this respect, estrogen doses could perhaps still be reduced (to the equivalent of 0.3 mg conjugated equine estrogens), provided additional measures such as calcium supplementation and physical exercise are taken.