Topical Estradiol Research Articles

Effect of vulvovaginal estrogen on sensorimotor response of the lower genital tract: a randomized controlled trial

Objective: To assess the effect of vulvovaginal estrogen on mucocutaneous sensory threshold and circumvaginal motor strength. Methods: Thirty-nine postmenopausal, hypoestrogenic women with mixed lower-genitourinary-tract complaints were placed in four masked treatment arms by permuted-block randomization for 6 weeks. One group received topical estradiol (E 2) cream and pelvic muscle biofeedback training, the second received topical E 2 cream and sham biofeedback, the third received placebo cream and pelvic muscle biofeedback training, and the fourth received placebo cream and sham biofeedback. Circumvaginal muscle strength was measured by averaging maximum intravaginal pressure (mmHg) generated over a set of four pelvic muscle contractions. Absolute changes in von Frey threshold (mN) and maximum intravaginal pressure (mmHg) over 4 and 6 weeks were reported as summary measures. Of 39 subjects, 30 completed the study. Results: Topical estradiol cream significantly improved mechanical sensitivity of the vulvar vestibule to von Frey hairs, a −1.2-mN threshold decrease at 4 weeks ( F = 10.29; P = .004), and a −1.6-mN threshold decrease at 6 weeks ( F = 8.24; P = .009) compared with placebo cream. Stratification by age showed significantly greater improvement in mechanical sensitivity in the older (70–79 years) age group randomized to estrogen cream and a −5.49-mN threshold reduction ( F = 17.65; P = .002). Maximum intravaginal pressures during circumvaginal muscle contraction did not differ between estrogen and placebo cream users ( F = 0.00; P = .99). Conclusion: Improved sensation to mechanical stimuli can result from a rapidly acting, direct effect of topical E 2 cream on the vulvar vestibule.

Endothelial-dependent coronary vasomotor responsiveness in postmenopausal women with and without estrogen replacement therapy

Recently, Williams et al’ reported that acute administration of estrogen attenuates the coronary vasoconstrictor response to acetylcholine in atherosclerotic cynomolgus monkeys. These observations suggest that estrogen plays a fundamentally important role in the relationship between coronary vascular endothelium and vascular smooth muscle. This study examines the influence of current estrogen replacement therapy in postmenopausal women on endothelial-dependent and independent vasomotor responsiveness to acetylcholine. Ten postmenopausal women with exertional angina undergoing routine diagnostic coronary angiography or percutaneous transluminal coronary angioplasty were studied. The protocol was approved by the Clinical Research Practices Committee and each subject gave informed consent before the study, Four women were taking estrogen replacement therapy (PremarinB 0.625 to 1.25 mglday or topical estradiol 0.1 mg). None of the women were taking progesterone. All of the women had minimal coronary artery narrowings in the proximal portion of the left anterior descending or a nondominant circumflex coronary artery. Vasoactive medications were withheld for 12-24 hours before the procedure. A 3Fr infusion catheter was positioned in the proximal left anterior descending or proximal circumflex artery through the guiding catheter. After the baseline angiogram was recorded, 3 consecutive 2-minute infusions of acetylcholine were administered into the proximal coronary artery. The$ow rate (0.8 mllmin) was calculated to deliver a final estimated blood concentration of 10s, 10m7 and 10m6 M. After each acetylcholine infusion, repeat angiography was performed in an identical fashion to baseline. After the third acetylcholine in& sion and angiogram, a 50 pg bolus of nitroglycerin was administered and a final coronary angiogram was recorded. Heart rate, blood pressure and appropriate electrocardiographic leads were monitored during the infusions to verify the absence of any changes in hemodynamic status or evidence of &hernia. Proximal and midvessel segments of the coronary artery distal to the tip of the infusion catheter were analyzed without knowledge of the estrogen status using a quantitative coronary angiography method (Gammasonits, Chicago, Illinois). When possible, coronary segments from the noninfused half of the left coronary distribution