Jorge Soria

Studies on the luteinizing hormone- and follicle-stimulating hormone-releasing mechanism in the testicular feminization syndrome: Hypothalamic-pituitary responsiveness to clomiphene, luteinizing hormone-releasing hormone, gonadectomy, and sexual steroids

Abstract The follicle-stimulating hormone (FSH) and luteinizing hormone (LH) secretory response to various stimuli was studied in 4 adult siblings with the complete form of testicular feminization. Before gonadectomy, the 4 patients had elevated serum levels of both LH and FSH. Clomiphene administered for 7 days did not change the serum levels of gonadotropins. LH-releasing hormone (LH-RH) administration resulted in FSH release above the range observed in normal adult men and women; however, the maximum LH increase was not different from that of normal adults. Gonadectomy elicited a further and significant elevation of both FSH and LH levels. After castration, serum levels of LH and FSH exhibited a further increase following LH-RH administration comparable quantitatively to that before castration. The FSH secretory response to LH-RH was greater than that of LH. The administration of progesterone alone to the 4 patients already castrated did not result in any major change in the serum levels of FSH and LH. Estrogen administration decreased the high levels of gonadotropins. The relative decrease for FSH was greater than for LH, and, when progesterone was given following 4 weeks of estrogen treatment, an increase in the serum levels of LH was found; there was also a small increase in FSH concentration. It is concluded from this study that in testicular feminization: (1) There is a partial gonadal feedback control of both FSH and LH secretion; (2) hypothalamic receptors are not sensitive to the stimulatory effect of clomiphene; (3) there is an unusually large amount of FSH released by the pituitary after intravenous LH-RH; (4) FSH and LH secretion are readily suppressed by estrogen administration; (5) there is a positive feedback effect of progesterone upon serum gonadotropins in estrogen-primed castrated patients with testicular feminization.

Pituitary FSH and LH reserve in women with isolated gonadotropin deficiency.

Six women with isolated gonadotropin deficiency were stimulated with 50 μg of synthetic luteinizing hormone-releasing hormone (LH-RH) and their response was compared with that obtained from 10 eumenorrheic women. Patients with hypogonadotropic hypogonadism had low serum LH levels and normal or near

Further observations on postpartum ovarian refractoriness: effect of gonadal stimulation in women receiving bromocryptine.

It has been reported previously that the administration of human menopausal gonadotrophins (HMG) to lactating and non‐lactating women from day 5 to day 9 postpartum elicited no significant elevation of urinary oestrogens or serum oestradiol within 15 days after delivery. In order to study further the role of prolactin on this ovarian refractoriness, five women receiving 7.5 mg of bromocryptine (CB‐154) daily were given HMG at a dose of 300 iu per day, from day 5 to day 10 postdelivery. In all women serum oestradiol and urinary oestrogens showed no significant elevation within the 2 weeks after delivery. Serum prolactine was elevated in all cases and fell to normal nonpregnant levels immediately after CB‐154 was administered. The suggestion that prolactin may possess antigonadotrophic activity at the ovarian level is not supported by the data presented here. The deficient ovarian response to gonadotrophin stimulation could be due to either the intraovarian effect of the high amounts of circulating steroids produced during gestation or to some unknown mechanism.

Prolactin Responsiveness to TRH in Amenorrheic Women with and without Galactorrhea

Abstract. Sixty women were given intravenous injection of 200 μg TRH to assess its diagnostic potential as a stimulus to PRL release. Following the administration of TRH, there was a prompt increase in serum PRL to 614.6%, to 296%, to 282.1 %, and 34% in normal women, amenorrheic patients, non tumoral galactorrhea cases, and patients with pituitary tumors respectively. The TRH response above baseline of PRL levels was statistically significant in all groups, but the women with pituitary tumors which showed a blunted response. The per cent of increment of PRL levels after TRH was similar in amenorrheic women regardless the presence or not of galactorrhea; this increase was significantly greater than in patients with pituitary tumors (p < 0.01). The per cent of increment above baseline of PRL was significantly greater in menstruating women than in amenorrheic patients (p < 0.001). In basis of present data: 1) there is a diminished PRL secretion after TRH in amenorrheic women regardless the presence of galactorrhea or hyperprolactinemia; 2) a blunted response to TRH in hyperprolactinemic women may be indicative of a pituitary tumor.

Long-Term Administration of Thyrotropin-Releasing Hormone and its Effect on Gonadotropin Secretion in Eumenorrheic Women

Thyrotropin-releasing hormone (TRH) was administered orally in doses of 60 mg/day to six women for two consecutive menstrual cycles. Daily serum samples were obtained for radioimmunoassay of luteinizing hormone, follicle-stimulating hormone, prolactin (PRL), and 17beta-estradiol secretory response. TRH was ineffective in interfering with normal gonadotropin and estradiol secretion, and failed to inhibit ovulation. The length of the luteal phase was not affected by TRH in the two cycles of treatment as demonstrated by basal body temperature, pregnanediol excretion, and endometrial biopsy. Long-term TRH administration induced an elevation of PRL serum levels that were not persistent and showed wide spikes. From these studies it is concluded that oral TRH at a dosage of 60 mg/day is unable to modify gonadotropin secretion and ovarian responsiveness in normally menstruating women.