RESUMO
AIM OF THE STUDY: The objective of this study was to assess the impact of tadalafil on endometrial growth, the uterine artery pulsatility index (PI) and the uterine artery resistance index (RI) in patients under clomiphene ovarian stimulation for intrauterine insemination (IUI). METHODS: This randomized crossover study included 30 patients with a normal endometrium over 53 cycles, and 46 of those cycles in 23 patients were included in the analysis. In group A the patients were under 100 mg clomiphene daily for five days (2-6) and 5 mg tadalafil daily for 7 days (4-10). For Group B (control) the patients only received clomiphene. Measurements of the endometrium, PI, RI and estradiol determinations were taken on cycle days 4, 8 and 10. RESULTS: We observed a better endometrial growth in Group A compared to Group B: 7.5 ± 2.1 mm vs 5.5 ± 1.2 mm, P < 0.0002 and 8.9 ± 1.8 mm vs 6.3 ± 1.8 mm, P < 0.0002 on days 8 and 10, respectively. Additionally, a progressive decrease in the RI was observed in Group A but not in Group B from day 8 (0.77 ± 0.15 vs 0.85 ± 0.18, P = 0.059) to day 10 (0.74 ± 0.20 vs 0.87 ± 0.14, P < 0.017). However, no differences were observed in PI or serum estradiol between Group A and Group B. CONCLUSION: The use of tadalafil improved endometrial growth in patients under clomiphene ovarian stimulation with no significant effect on the uterine artery Pulsatility Index and serum estradiol.
RESUMO
BACKGROUND: Since in rodents anti-Müllerian hormone (AMH) has been shown to inhibit antral follicle responsiveness to FSH, we aimed at verifying whether a relationship exists between serum AMH levels and antral follicle responsiveness to exogenous FSH in normo-cycling women. METHODS: Serum AMH, estradiol (E(2)) and FSH levels were prospectively measured on cycle day 3 in patients undergoing controlled ovarian hyperstimulation (COH) with a time-release GnRH agonist and standardized FSH doses. In 162 patients, follicles were counted after pituitary suppression and before FSH administration (baseline; small antral follicles; 3-8 mm), and on the day of hCG (dhCG; pre-ovulatory follicles; 16-22 mm). Antral follicle responsiveness to FSH was estimated by the Follicular Output RaTe (FORT), determined by the ratio pre-ovulatory follicle count on dhCG × 100/small antral follicle count at baseline. RESULTS: Serum AMH levels were positively correlated with the number of small antral follicles at baseline (r = 0.59; P < 0.0001) and pre-ovulatory follicles on dhCG (r = 0.17; P < 0.04). Overall, FORT was 47.5 ± 1.4% and failed to be influenced by the woman's age, BMI or basal E(2) and FSH level. Conversely, multiple regression analysis showed that FORT was negatively correlated with AMH levels (r = -0.30; P < 0.001), irrespective of duration of COH and total FSH dose. CONCLUSIONS: The percentage of follicles that effectively respond to FSH by reaching pre-ovulatory maturation is negatively and independently related to serum AMH levels. Although the mechanisms underlying this finding remain unclear, it is in keeping with the hypothesis that AMH inhibits follicle sensitivity to FSH.