The clinical administration of estrogen to women following the cessation of ovarian function and the permanent end of menstruation, primarily to alleviate vasomotor symptoms, prevent urogenital atrophy, and mitigate the accelerated bone loss associated with estrogen deficiency. This therapy requires careful risk stratification and is often combined with progesterone in women with an intact uterus to protect the endometrium. It is a cornerstone of managing the menopausal transition.
Origin
The term combines “postmenopausal,” defining the patient’s physiological state, with “estrogen therapy,” specifying the intervention. Its use dates back decades, but the clinical approach has been profoundly refined by major studies that established the importance of timing, dose, and route of administration for maximizing benefits and minimizing cardiovascular and oncological risks. This practice is now guided by personalized medicine principles.
Mechanism
Exogenous estrogen molecules bind to and activate estrogen receptors (ER-alpha and ER-beta) in various target tissues, mimicking the action of the endogenous hormone. In the bone, this activation suppresses osteoclast activity, slowing bone resorption and maintaining mineral density. In the brain, it supports neuroprotection and mood regulation, and in the vasculature, it maintains endothelial function and nitric oxide production, contributing to cardiovascular health.
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