Endocrine Abstracts

The history of hormone replacement therapy (HRT) has been marked out by successive ‘earthquakes’, the perception of which has been reflected by the evolution of prescription curves. Early hormonal treatment protocols included estrogens only and have lead to an increased relative risk of endometrial cancer. This risk returns to baseline if a progestin is associated to estrogens for at least 12 days/28.Then based on interventional studies as well as in vitro data, animal studies, and surrogate markers suggesting a protective effect of HRT on vascular disease, HRT has been widely prescribed, including to women with vascular risk factors. Data from the HERS then showed that HRT had no protective effect in women with coronary heart disease. These results were then confirmed in women without known coronary heart disease, in the WHI. Finally, reanalyses of the WHI and other studies such as the Nurses health study have shown that HRT could have protective vascular effects in women without abnormalities of the arterial wall and treated early in menopause. Deep vein thrombosis (DVT) has been recognized as an adverse event of HRT in the early 1960s. Recently, the cohort study ESTHER has suggested that transdermal estrogens do not increase DVT risk. Breast cancer (BC) risk evaluation in post-menopausal women receiving HRT has gone through different revolutions as well. The relative risk of BC has been shown to increase regularly with treatment duration. The negative role of the progestin component has been shown by the WHI. The E3N cohort study has recently suggested that the use of progesterone instead of a synthetic progestin may be an advantage. Step by step, the prescription of HRT is progressively moving to a personalized scheme in early post-menopausal women with climacteric symptoms. This scheme must be based on a global, yearly renewed evaluation, in collaboration with the woman.