Estrogen Therapy (ET) is a clinical intervention involving the administration of estrogen compounds to women experiencing symptoms related to estrogen deficiency, most commonly due to menopause or surgical removal of the ovaries. This therapy is primarily used to manage vasomotor symptoms like hot flashes, prevent urogenital atrophy, and mitigate accelerated bone loss. Estrogen, a steroid hormone, exerts wide-ranging effects on numerous tissues, including the cardiovascular system, brain, and skin. Clinical practice requires careful assessment of individual risk factors and selection of the appropriate estrogen type, dosage, and delivery route.
Origin
The therapeutic use of estrogen dates back to the early 20th century, but the widespread clinical application, particularly for menopausal symptoms, became common mid-century. The term “Estrogen Therapy” became a standard clinical designation, later often referred to as Hormone Therapy (HT) or Hormone Replacement Therapy (HRT) when combined with progestogen. Its etymological root comes from oistros, meaning “frenzy” or “gadfly,” referring to the estrous cycle in animals, and gen, meaning “producing.”
Mechanism
Estrogen Therapy functions by replacing the declining endogenous hormone, allowing estrogen to bind to its specific receptors (Estrogen Receptor alpha and beta) located in target cells throughout the body. Receptor binding initiates a cascade of intracellular signaling events that modulate gene transcription, restoring normal cellular function. In the bone, estrogen suppresses osteoclast activity, slowing bone resorption; in the brain, it supports neurotrophic factors and neurotransmitter balance. The therapeutic effect is achieved by restoring the physiological signaling that was lost due to ovarian senescence.
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