Abstract
In women, oral menopausal hormonal therapy (MHT) is associated with adverse effects including an increased incidence of thromboembolic events, classically attributed to an increase in several liver-derived coagulation factors due to hepatic first pass. While platelets are central players in thrombus constitution, their implication in women treated with estrogens remains incompletely characterized. Platelets and their medullar progenitors, megakaryocytes, express estrogen receptors (ER) that may explain, at least in part, a sensitivity to hormonal changes. The purpose of this review is to summarize our current knowledge of estrogen actions on platelets and megakaryocytes in mice following in vivo administration and in women using MHT.
Highlights
Menopause is defined as a permanent cessation of menstruation and ovulation due to ovarian aging
These symptoms could be alleviated by the administration of menopausal hormonal therapy (MHT), at first based on oral administration of natural estrogens extracted from the urine of pregnant mares, and later from the synthesis of the natural estrogen, 17β-estradiol (E2), especially using the transdermal route
The Women’s Health Initiative (WHI) study investigated the potential risks and benefits associated with oral MHT by including around 16,000 postmenopausal women treated with conjugated estrogens (CE) in combination with medroxyprogesterone acetate (MPA)
Summary
Menopause is defined as a permanent cessation of menstruation and ovulation due to ovarian aging. The Women’s Health Initiative (WHI) study investigated the potential risks and benefits associated with oral MHT by including around 16,000 postmenopausal women treated with conjugated estrogens (CE) in combination with medroxyprogesterone acetate (MPA) This hormonal combination was associated with an increased incidence of thrombotic events, coronary disease, and breast cancer [2]. Several observational studies suggest that, contrary to the transdermal route, the oral administration of estrogen is a major determinant of the increase in thrombotic events with a higher risk of VTE under oral MHT [5,6,7]. In addition to these nuclear, called genomic actions of ER, estrogens have been found to induce rapid effects occurring within minutes following administration These effects are mediated through receptors associated with the plasma membrane, a process termed “nongenomic”, “membrane-initiated steroid signaling” (MISS), or “extranuclear” effects [12]. We will summarize our current knowledge of estrogen actions on platelets and MK in mice and women following in vivo administration
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
