Decrease In Endometrial Thickness Research Articles

Monitoring of hormone replacement therapy in postmenopausal women by transvaginal sonography and color flow doppler: study in different phases of sequential therapy

Objective: To assess uterine artery blood flow and endometrial thickness in postmenopausal patients receiving sequential hormone replacement therapy (HRT) at different phases of the treatment. Design: Prospective controlled study. Setting: Ultrasound and menopause units of the obstetrics and gynecology department of the University of Tor Vergata, Rome, Italy. Patient(s): Forty postmenopausal women were treated with cyclic sequential HRT (transdermal E 2, 50 μg/d, days 1–21; and dydrogesterone, 10 mg/d, days 12–24). Intervention(s): All patients underwent transvaginal color Doppler sonography in the estrogen (phase E) and progestogen (phase E/P) phases and after uterine bleeding when no hormone was administered (phase 0). Main Outcome Measure(s): Endometrial thickness; systolic, diastolic, and mean velocities; and pulsatility and resistance indices of the uterine arteries. Result(s): No statistically significant difference in endometrial thickness between phase E (6.5 ± 1.6 mm) and phase E/P (6.0 ± 1.7 mm) was observed. In phase 0, compared with phases E and E/P, a statistically significant decrease in endometrial thickness was found (4.1 ± 1.2 mm). Doppler flow impedance parameters of uterine arteries during the different phases of the HRT cycle showed no differences between the phases considered. Conclusion(s): The decrease in endometrial thickness in phase 0 suggests a protective effect of our cyclic sequential regimen on the endometrium. Dydrogesterone does not interfere markedly with the vasodilatory effect of estrogen on uterine arteries.

Uterus and endometrium: The effect of local intrauterine levonorgestrel administration on endometrial thickness and uterine blood circulation

To evaluate non-invasively the role of levonorgestrel releasing devices in direct contact with the endometrium on menstrual spotting and endometrium inactivation, we inserted levonorgestrel releasing devices (20 micrograms/24 h) either into the cervical canal or the uterine cavity of 30 fertile women. Both before insertion and over the following 3 months, we used transvaginal sonography to measure the endometrial thickness in 20 of the women and Doppler flow to measure the uterine blood flow in the remaining 10 women. The women were asked to keep records of menstrual bleeding and they gave blood samples for the measurement of serum oestradiol, progesterone and levonorgestrel. By 10 weeks after insertion there was a significant decrease in endometrial thickness in both groups. Intracervical levonorgestrel release allowed the endometrium to maintain cyclic changes, whereas direct intrauterine levonorgestrel release eliminated the cyclical changes. The total number of spotting days was significantly less (P = 0.0249) in the intracervical release group at 3 months; 1.2 +/- 0.6 versus 8.1 +/- 1.8 (mean +/- SE). There were no significant differences in hormone concentrations between the groups. The pulsatility index did not change significantly during the study. We concluded that the inactivation process of the endometrium can be monitored by transvaginal sonography and that locally administered levonorgestrel does not change circulatory conditions detectable by Doppler flow. Our results also suggest that the inactivation process of the endometrium is different between intracervical and intrauterine levonorgestrel administration and may explain the difference in the number of spotting days.