Cushing's disease even when biochemically stable has long-term adverse effects on mood and social functioning. We hypothesize that this may be related to irreversible changes in central neural function. Further studies are necessary to define the precise pathways involved.
Several biological changes take place during the menopause transition. The number of oocytes declines progressively from before birth but reaches a critically low level by the time of the menopause. The regular pattern of the menstrual cycle becomes disrupted and the frequency of normal ovulatory cycles declines. Rising gonadotrophin levels, particularly of follicle stimulating hormones (FSH), and declining estrogen levels are thought to characterize the menopausal transition. It now appears that declining levels of inhibin may play an important role in maintaining estrogen levels until just before the menopause, while causing increased levels of gonadotrophins. Wide variations in hormonal profiles between and within individuals occur. The clinical responses to this endocrine instability include vasomotor symptoms, psychological symptoms, sexual dysfunction and irregular menstrual bleeding. Estradiol deficiency induces a rapid phase of increased bone turnover in the early postmenopausal period, which can contribute to osteoporosis later in life. Similarly, changes in lipid profiles, particularly high-density lipoprotein (HDL) and triglycerides, can also occur.
Summary. Our experience of ovarian electrocautery for the treatment of polycystic ovarian syndrome (PCOS) in ten women is described. We found that nine responded favourably, either ovulating spontaneously or becoming more responsive to ovulation induction. There was a significant and persistent fall in serum testosterone levels, and a transient fall with subsequent rise in inhibin. We recommend that laparoscopic ovarian electrocautery is considered as an alternative to ovulation induction with gonadotrophins, in women with PCOS who fail to respond to clomiphene citrate.
We have identified a group of women with infertility and regular menses who have persistently raised FSH levels and probable incipient ovarian failure (IOF). Thirteen such women (19 cycles) had serum samples taken for RIA of LH, FSH, estradiol, and progesterone (P) 3 times a week over 1 menstrual cycle. Sixty infertile women with normal ovulatory cycles (as determined by hormones and ultrasound scan) served as controls. Overall, the FSH was higher (P less than 0.01) on all days of the cycle in the IOF group, serum LH was raised on days-14 to-5 before and days 5-11 after the LH surge. There was no difference between estradiol and P levels in the two groups. Ultrasound scanning showed failure of normal ovulation in the IOF group. Inhibin, measured by RIA in 9 cycles in the IOF group was lower (P less than 0.01) during the follicular phase than in 43 normal cycles. The highest inhibin level was seen in the luteal phase, as in normal cycles, but levels were still lower (P less than 0.01) in the IOF group. Inhibin was inversely correlated with FSH (P less than 0.05) during the follicular and luteal phases and was correlated with P during the luteal phase (P less than 0.05) in the IOF group. After 3 weeks of suppression (39 cycles) with an estrogen-progestogen preparation in the IOF group, LH and FSH fell to normal values. Ovulation occurred in 22 cycles on withdrawal of suppression in the presence of high FSH levels and low inhibin levels. No pregnancies occurred. These findings are consistent with the suggestion that diminished ovarian inhibin secretion may contribute to the elevated FSH levels of IOF and indicate that ovulation in the rebound cycle after suppression occurs in the presence of high FSH and low inhibin levels. Such cycles, however, still appear to be subfertile.
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