SUMMARYSerum androgen levels, including dehydroepiandrosterone sulphate (DHAS) which is thought to be solely of adrenal origin, are elevated in women with the polycystic ovarian syndrome. We have investigated the possibility that this may be due to a mild form of congenital adrenal hyperplasia by measuring basal and stimulated levels of ACTH in women with this condition and have compared them to levels in normal women. We found no difference in the diurnal rhythm of ACTH between patients and normal subjects nor any difference in stimulated levels achieved after a single‐dose oral metyrapone test. Thus there is no evidence from this study to support the idea that these patients might have congenital adrenal hyperplasia. There are two alternative hypotheses to explain the elevated DHAS levels. They may be associated with the high oestrogen levels, which interfere with the enzyme 3β‐hydroxysteroid dehydrogenase, or there may be alteration of the factors controlling adrenal androgen secretion.

Summary The technique for and results of 100 laparoscopic ventrosuspensions are described; patients were followed for an average of 40 months and in all but 11 the uterus was anteverted at the end of the follow‐up period. The presenting symptoms of dyspareunia, dysmenorrhoea or sacral backache were almost always improved as a result of the operation. The authors thank Professor H. C. McLaren, Mr J. Kelly, Mr W. G. Mills, Mr H. O. Nicholson and Mr H. Roberts for allowing their patients to be studied.

SUMMARY The effect of the administration of oestradiol benzoate and of progesterone on the subsequent response to LHRH has been investigated in women with hyperprolactinaemia. There was an amplification in the release of LH in four out of ten patients and of FSH in one out of ten patients at 44 h after the administration of 2·5 mg oestradiol benzoate. The average amount of LH released before and after oestrogen 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 oestradiol concentration in serum at the time of the LHRH tests but there was a negative correlation between the FSH released and the oestradiol 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 oestrogen concentrations and the amount of LH and FSH released. As in normal subjects, bowever, a significant suppression of basal FSH concentrations, persisting until 44 h, was produced by the oestrogen ( P < 0.01). Seven out of eleven patients showed an amplification of LH response and six out of eleven 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 oestradiol which in patients with hyperprolactinaemia are significantly less than those found in the mid follicular phase of the cycle ( P < 0.05). These results indicate that in women with hyperprolactinaemia oestrogen negative feedback, necessary for cycle initiation, is normal: failure of ovulation may be related to failure of positive feedback to oestrogen. Oestrogen‐negative feedback is unopposed and this may explain the follicullar development and lack of oestrogen in the mid‐follicular phase.

SUMMARYExogenously administered oestradiol or progesterone was found to induce augmentation of LH and FSH release in response to LHRH administration in patients with the polycystic ovary (PCO) syndrome. The effect of oestradiol upon LH release in the patients was significantly less than the augmented release induced in normal women (P < 0.02). In contrast, progesterone induced a significantly greater LH release in PCO patients than normal women studied during the early follicular phase (P < 0.001) but less than that in normal women studied during the mid‐follicular phase of the cycle (P < 0.01). The effects on FSH release in the PCO patients were less marked but similar to those in normal women with comparable basal steroid levels.The results suggest that both oestradiol and progesterone can modify the hypothalamic‐pituitary axis in the PCO syndrome in a manner similar to that observed in normal women and a failure of these ‘positive feedback’ mechanisms does not appear to be the cause of the ovulatory deficiency in this syndrome.

SUMMARYThe response to synthetic luteinizing hormone‐releasing hormone was studied in eighteen patients with the polycystic ovary syndrome. The release of follicle‐stimulating hormone was similar to that found in normal women. The mean response of luteinizing hormone was similar to that found in the luteal phase, but significantly greater (P<0.02) than that found in the early follicular phase of the normal menstrual cycle. Basal serum levels of FSH and LH, estimated in twenty‐five patients, were similar to those found in normal subjects. The sex hormone binding globulin capacity was reduced in twenty‐four of them. Basal serum testosterone levels were elevated in twelve of twenty‐two patients and the mean level was significantly greater (P<0.01) than the mean level of normal women. Basal serum androstenedione levels were elevated in nine of twenty‐two patients and the mean level was also significantly greater (P<0.02) than normal. There was a highly significant negative correlation (r=−0.86; P<0.001) between basal testosterone and LH levels. These data suggest that the pituitary gland of patients with the polycystic ovary syndrome contains adequate amounts of LH but that the ovulatory surge of LH which occurs in normal women is inhibited by testosterone acting on either the pituitary or, more probably, on the hypothalamus.