Percutaneous estrogen therapy. Endometrial response and metabolic effects.

A hydroalcoholic gel containing estradiol-17 beta (0.6 mg/g) for percutaneous application was used for estrogen replacement therapy in postmenopausal women. During treatment the serum concentrations of estrogens were significantly increased and stable. The conversion of estradiol into estrone was far less pronounced after percutaneous vis-à-vis oral therapy. In terms of FSH suppression the estrogenic potency of percutaneous estradiol-17 beta 3 mg daily was similar to that of oral estradiol-17 beta 2 mg. The serum concentrations of three estrogen-sensitive liver proteins--sex hormone binding globulin (SHBG), pregnancy zone protein (PZP) and ceruloplasmin--were unchanged during percutaneous treatment, whereas during oral therapy all three proteins showed a marked increase. The endometrial response was quantified by morphometry. The mean relative endometrial gland volume increased from 10% to 40% and was correlated to serum levels of estradiol-17 beta. Single-cell growth did not reveal the same correlation and the sequential addition of lynestrenol, 5 mg daily for ten days, did not reduce the estrogen-induced endometrial growth. No obviously harmful local effects were observed in skin samples. Topical application of estradiol-17 beta may develop into an alternative treatment for climacteric complaints and may even have some metabolic advantages over oral treatment.