Objective: To evaluate the role of endogenous feedback in monofollicular growth during low-dose gonadotrophin therapy in polycystic ovary syndrome (PCOS) by measuring FSH levels in a group of patients cotreated with a GnRH agonist (GnRH-a) (group B) compared with patients not cotreated with an agonist (group A).
Design: Prospective randomized study.
Setting: University tertiary care Reproductive Endocrinology Unit.
Patients: Women with clomiphene citrate-resistant PCOS.
Main outcome measures: Follicle-stimulating hormone, E2, and inhibin levels, follicular growth.
Results: In group A, FSH levels decreased significantly from 7.3 mIU/mL (conversion factor to SI unit, 1.00) at day -5 to 5.9 mIU/mL at day 0 (day that hCG was administered) despite a constant dose, whereas they remained at a level of 7.4 mIU/mL in group B. The rate of monofollicular growth was significantly higher in group A (80%) than in group B (22%). No significant differences in E2 levels or inhibin levels were found between the groups.
Conclusions: The absence of a decrease of FSH during GnRH-a treatment in association with a lower rate of monofollicular growth suggests that endogenous feedback during low-dose step-up ovulation induction in PCOS plays an important role. The absence of this feedback mechanism in the presence of normal inhibin levels suggests that negative feedback control by inhibin during follicular stimulation is minimal.