ABSTRACT
Hormonal replacement therapy is currently used for the control of climacteric symptoms, and for the prevention of long-term consequences of menopause. Chronic hypoestrogenism in post-menopausal years causes a critical decrease in bone mineral density (BMD) that is an important determinant of fracture risk 1-5 . Estrogen replacement therapy prevents the lowering of BMD related to peri-and post-menopausal hypoestrogenism 4-7 . In addition, post-menopausal estrogen supplementation can exert cardioprotective effects with substantial reduction of morbidity and mortality for cardiovascular disease 8-16 . During estrogen therapy, progestin supplementation is mandatory to prevent endometrial hyperstimulation 17-23 . However, the administration of progestogens can jeopardize the beneficial effects of estrogens on cardiovascular protection 24 , 25 . The metabolic effects depend on the type and dose of progestogens. Dydrogesterone (DD) is a potent orally active progestogen, similar to endogenous progesterone in its molecular structure and biological actions, and devoid of any androgenic, anabolic or estrogenic effect 26-31 . Sequential DD administration was reported to antagonize the estrogenic effect on endometrial profferation 26-31 . In the present paper we report clinical and metabolic effects of the long-term administration of DD in combination with conjugated estrogens (CE) in early post-menopausal women.
