The spontaneous pattern of pituitary gonadotropins and ovarian steroids and their response to dynamic tests were measured in 12 women with polycystic ovarian syndrome (PCO) and the results compared to those from 6 normal women during the early follicllar phase of the cycle (controls). As judged by serial measurements of urinary total estrogen and pregnanediol over a 12-week period, in PCO patients 75% of cycles were anovulatory (anovulatory PCO) as compared to 100% ovulatory in controls. The basal concentrations of LH, androstenedione and estrone were significantly higher and the concentration os FSH significantly lower in anovulatory PCO than in the controls (P less than .05). In PCO patients the concentration of LH was lower following an ovulatory cycle than that following a period of anovulation. Negative and positive feedback responses to an estrogen provocation test (200 microgram ethinyl estradiol per day for 3 days) were normal in anovulatory PCO although the LH peak occurred 24 h earlier than in the controls. The amplitude of the pulses of LH was significantly greater in anovulatory PCO than in the controls and was suppressed in both groups after ethinyl estradiol. The peak release of LH in response to 56 microgram LRF in ovulatory PCO was similar in controls but LH responses in anovulatory PCO were significantly greater. It is suggested that the abnormalities in gonadotropin secretion in PCO are secondary to excessive and prolonged extraglandular production of estrogen from androstenedione.
Welsh mountain sheep of known conceptual age (term 148 days) were given a spinal anaesthetic (2 ml 20% procaine). A hind leg artery was catheterized, the foetus was exposed by Caesarian section, allantoic and amniotic fluids were collected and a catheter inserted into a tributary of an umbilical artery. Blood samples were taken within 15 min of anaesthesia. The heparinized plasma was separated immediately in the cold and stored at \m=-\15 \ s=deg\ C. Luteinizing hormone (LH) and 17\g=b\-oestradiol were determined by radioimmunoassay (Naftolin & Corker, 1971) and competitive binding assay (Corker & Exley, 1970). The oestradiol method removes oestrone and oestriol, but 17\g=a\-oestradiolwould interfere if present in quantities approaching those of 17\g=b\-oestradiol.No, or just detectable, LH activity was found in plasma from mothers or from older foetuses (Table 1). Measurable LH was present in the plasma of 10 out of 11 foetuses aged 117 days or less. There was a wide range in levels. In two animals (484/70 and 477/70) two consecutive samples gave similar values. However a sample taken from animal 477/70 after a large haemorrhage gave a much lower value. Oestradiol was not measurable in either foetal or maternal plasma from early gesta¬ tions (Table 1), but significant quantities were present in some of the older animals from 130 days onward. Particularly high values were found in animals 500/70 (near term) and C/70. The latter may have also been near term; the estimate of its age was based upon weight and length only. No LH was found in any of the foetal fluids except for traces ( < 0-5 ng/ml) in 487/70 and 485/70 (amniotic fluid) and 485/70 and 490/70 (allantoic fluid). Traces of oestrogens were found in three of six amniotic and five of seven allantoic fluids (0-3-2 ng/100 ml).The low levels of LH in maternal plasma late in pregnancy resembled those seen in dioestrous ewes (Bjersing, Hay, Kann, Moor, Naftolin, Scaramuzzi, Short & YoungLai, 1972). The presence of LH, particularly in the plasma of younger foetuses, has also been reported by Foster, Roach, Karsh, Norton, Cook & Nalbandov (1972) with post-mortem material. The fall in LH occurred when measurable levels of 17/?-oestradiol first appeared. Thus 17/?-oestradiol may suppress LH secretion. Since LH was present in foetal but not maternal blood it must be of foetal origin and the J Present address:
Testosterone tablets of crystal size 2\p=n-\5\g=m\mwere administered orally for 10 dags to 3 human subjects with low endogenous serum testosterone (se-T) levels. Fifty mg testosterone increased se-T slightly, while one daily dose of 200 mg maintained the se-T level within normal range for men for more than 12 h. No cumulative effect was seen.Seven further subjects with low androgen production ingested 100 or 200 mg testosterone of crystal size 125\p=n-\400\g=m\m.Blood samples were taken frequently during the 24 h period following administration of the testosterone and se-T levels determined. Testosterone levels in serum increased in 6 patients and was maintained within the normal male range for 5\p=n-\7h. In one subject a slight but significant increase in se-T was observed although the level did not reach the normal male range. Although it has been shown that it is possible to use orally administered testosterone to maintain se-T levels in the normal male range, the convenience to the patient must be balanced against the cost and possible side effects of the large doses required.
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