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Estrogens with or without progestins should be prescribed at the lowest effective doses and for the shortest duration consistent with treatment goals and risks for the individual woman.
There is no evidence that the use of natural estrogens results in a different endometrial risk profile than synthetic estrogens of equivalent estrogen doseAdding a progestin to postmenopausal estrogen therapy has been shown to reduce the risk of endometrial hyperplasiawhich may be a precursor to endometrial cancer.
The metabolism of estrogens may be increased by concomitant use of substances known to induce drug-metabolising enzymesspecifically cytochrome P450 3A4CYP3A4enzymesThereforeinducers or inhibitors of CYP3A4 may affect estrogen drug metabolismInducers of CYP3A4such as StJohn’s wortHypericum perforatumpreparationsphenobarbitalphenytoincarbamazepinerifampicinrifabutinnevirapineefavirenz and dexamethasonemay reduce plasma concentrations of estrogenspossibly resulting in a decrease in therapeutic effects and/or changes in the uterine bleeding profileInhibitors of CYP3A4such as cimetidineerythromycinclarithromycinketoconazoleitraconazoleritonavirnelfinavir and grapefruit juicemay increase plasma concentrations of estrogens and may result in side effects.
In women who are not taking hormone replacement therapy or women who switch from a continuous combined hormone replacement therapy producttreatment may be started on any convenient dayIn women transferring from a sequential hormone replacement therapy regimentreatment should begin the day following completion of the prior regimen.
The WHI estrogen plus progestin substudy reported increased risks of DVTpulmonary embolismPEstroke and myocardial infarctionMIin postmenopausal women50 to 79 years of ageduring 5.6 years of treatment with daily oral CE0.625 mgcombined with medroxyprogesterone acetateMPA2.5 mgrelative to placebosee WARNINGS AND PRECAUTIONSand Clinical Studies
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