Comparison between Human Urinary Follicle-Stimulating Hormone and Human Menopausal Gonadotropin Treatment in Polycystic Ovary

Human menopausal gonadotropins have been used, with varying results, for induction of ovulation in patients with polycystic ovary disease. The present authors have reported earlier that follicular growth, ovulation, and pregnancy can be achieved by administration of pure urinary follicle-stimulating hormone to such patients. In the present study, the effects of the two hormones on the same patients with polycystic ovary disease are compared. Five patients suffering from chronic anovulation and amenorrhea for at least 6 months, due to polycystic ovaries, were treated. They received six cycles of clomiphene citrate, but ovulation was not achieved. The patients showed high levels of serum androgens and luteinizing hormone, with the ratio of luteinizing hormone to follicle-stimulating hormone constantly above 3. Two types of treatment were administered next, one with human urinary follicle-stimulating hormone and the other with human menopausal gonadotropin. There was an interval of at least 6 months between the two treatments, but no particular order of treatment was adhered to. The gonadotropins were administered daily, beginning on the fourth or fifth day of a progestin-induced menstrual period. When the follicular diameter was greater than 19 mm, 5000 IU of human chorionic gonadotropin were administered to the patient. In the five urinary follicle-stimulating hormone cycles, there were four ovulations; in the human menopausal gonadotropin cycles, there were five. One pregnancy occurred in the follicle-stimulating hormone cycles but resulted in abortion. In the menopausal gonadotropin cycles, two pregnancies, one ectopic and one resulting in abortion, were observed. No hyperstimulation was seen in either treatment. Adequate follicular development was obtained in both treatments, without substantial differences. In each follicle-stimulating hormone treatment, however, ovulatory follicle diameter greater than 19 mm was always achieved less than 24 hours earlier than in the human menopausal gonadotropin. FSH plasma levels increased during both treatments, and no significant differences were seen (Fig. 1). The estradiol serum concentrations showed an initial slow, progressive rise in all subjects (latent phase), followed by a rapid increase to a peak (active phase), without marked contrast between the hormone profiles in the two treatments. Nevertheless, administration of human urinary follicle-stimulating hormone induced a greater increase of estradiol, and a more precocious appearance of the active phase than did the administration of human menopausal gonadotropin. At human chorionic gonadotropin administration, estradiol levels in follicle-stimulating hormone treatment were 1428 ± 325 pg/ml and higher than in menopausal gonadotropin treatment (557 ± 85 pg/ml; P < 0.05) (Fig. 1). Estrone plasma levels were different in basal conditions and showed a pattern similar to that of estradiol, but with no significant differences between the two types of treatment. The plasma levels of LH were always high under basal conditions. LH dropped with a clear-cut profile in both types of treatment, but the fall was greater (P < 0.05) during urinary follicle-stimulating hormone treatment (Fig. 1). A spontaneous LH peak was observed in both treatments in four of the five patients but did not occur in the same subjects. Prolactin and 17-hydroxyprogesterone serum concentrations showed an increase in both treatments, particularly in the active phase, but no significant differences were seen. Progesterone plasma concentrations did not show any variation up to LH peak. All patients were hyperandrogenic. Plasma concentrations of testosterone, 5α-dihydrotestosterone, and androstenedione showed similar profiles in both types of treatment, with wide daily fluctuations. Testosterone and 5α-dihydrotestosterone did not show significant differences. Only androstenedione increased and was higher in urinary follicle-stimulating hormone treatment than in human menopausal gonadotropin treatment, both in basal conditions and in treatment cycles; P < 0.05). A sharper increase of these steroids was often evident at spontaneous or human chorionic gonadotropin-induced LH peaks. A marked turnover of follicles with diameters not exceeding 10 mm was observed in ultrasound scanning, and multiple follicles were often found at human chorionic gonadotropin administration in both treatments. A greater incidence of multiple follicles is not clearly correlated with