THE CONTROL OF GONADOTROPHIN RELEASE IN WOMEN WITH HYPERPROLACTINAEMIC AMENORRHOEA: EFFECT OF OESTROGEN AND PROGESTERONE ON THE LH AND FSH RESPONSE TO LHRH

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Abstract
The effect of the administration of estradiol benzoate and of progesterone on the subsequent response to LHRH [luteinizing hormone-releasing hormone] was investigated in women with hyperprolactinemia. There was an amplification in the release of LH [luteinizing hormone] in 4 of 10 patients and of FSH [follicle-stimulating hormone] in 1 of 10 patients at 44 h after the administration of 2.5 mg estradiol benzoate. The average amount of LH released before and after estrogen did not change, but there was a significant decrease in the amount of FSH released. There was no correlation between the LH released and the estradiol concentration in serum at the time of the LHRH tests, but there was a negative correlation between the FSH released and the estradiol concentration (r = 0.507; P < 0.05). These results contrast with those obtained in normal subjects in the follicular phase of the cycle when there is a positive correlation of estrogen concentrations and the amount of LH and FSH released. As in normal subjects, however, a significant suppression of basal FSH concentrations, persisting until 44 h, was produced by estrogen (P < 0.01). Out of 11 patients, 7 showed an amplification of LH response and 6 of 11 an FSH response 20 h after the administration of 25 mg progesterone. The mean amplifications are not significantly different from those of normal subjects tested in the early follicular phase of the cycle, but are significantly less than those tested in the mid follicular phase of the cycle (LH P < 0.001; FSH P < 0.01). This may be related to the serum concentrations of estradiol which in patients with hyperprolactinemia are significantly less than those found in the mid follicular phase of the cycle (P < 0.05). In women with hyperprolactinemia estrogen negative feedback, necessary for cycle initiation, is probably normal: failure of ovulation may be related to failure of positive feedback to estrogen. Estrogen-negative feedback is unopposed, and this may explain the follicular development and lack of estrogen in the mid-follicular phase.