EFFECTS OF HORMONE REPLACEMENT THERAPY ON GLUCOSE-METABOLISM

Objective. To evaluate the relationship between hormone replacement th erapy and glucose metabolism, and the possible role played by the admi nistration route. Design. Prospective randomized study. Materials and methods. Eighty-four patients in either surgical or spontaneous menopa use were randomly allocated into four groups: 15 patients in surgical menopause were treated with estrogens alone administered transdermical ly (17 beta-estradiol, 50 mu g/day); 15 patients in surgical menopause were treated with Oral conjugated equine estrogens (0.625 mg/day); 18 patients in spontaneous menopause were treated with transdermic estro gens plus oral progestagen (17 beta-estradiol 50 mu g/day, acetate med rosyprogestogen 10 mg/day for IZ days per month); 16 patients in spont aneous menopause were treated with oral conjugated equine estrogens (0 .625 mg/day) plus oral progestagen (10 mg/day for 12 days per month). Twenty patients not given any medication represented the control group , Before starting the trial and after six months of therapy, glucose a nd insulin levels before and after an oral glucose loading test were e valuated, Data analysis was performed by means of Student's ''t''-test , ANOVA was used to compare mean levels between the groups, Significan ce was set at p < 0.005. Results. Dosages made after 6 months of thera py showed comparable basal glucose levels in all the studied group, wh ile basal insuline levels in patients taking estrogen alone were lower (76.88 +/- 23.66 vs 95.91 +/- 24.57 in group 1, 80.51 +/- 13.34 vs 96 .91 +/- 18.97 in group 2) than pretreatment values, No significant dif ference in glucose levels was found after glucose load in the four gro ups. Conclusion. Women treated with estrogen alone have a tendency to a lower insulin response, which could indicate a greater insulin sensi tivity, This effect seems to be more evident in transdermic administra tion than with oral administration, The addition of progestagen seems to wane the increase in insulin sensitivity induced by estrogens.