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(1.7 cm, p < 0.025), and placental weight (136 g, p < 0.02) in those patients with high initial SD ratio. For the 12 women with extreme initial SD ratio, aspirin therapy did not result in a significantly different pregnancy outcome, suggesting that in these cases the
placental lesion and fetal effect were too far advanced to reverse. Maternal ingestion of aspirin affects the maternal and fetal circulation.4 We have demonstrated that the pathology of placental insufficiency that is identified by doppler study of the flow velocity waveform in the umbilical artery is present in the fetal umbilical placental circulation.2 Sometimes there is associated vascular disease in the maternal uteroplacental circulation.3 Our results support the hypothesis that the benefits of aspirin result from its actions in the fetal circulation. Studies of flow velocity waveforms from branches of the maternal uterine artery in the placental bed were normal in our patients. We do not advocate the widespread use of aspirin in all pregnancies in which the fetus might be considered at risk on the basis of obstetrical history or associated maternal disease. Our study demonstrated fetal benefit when umbilical placental insufficiency was defined early by doppler flow study. Accordingly aspirin treatment is better reserved for these cases.
Fetal Welfare Laboratory, University of Sydney at Westmead Hospital, Westmead, New South Wales 2145, Australia
BRIAN TRUDINGER COLLEEN-M. COOK ROSEMARY THOMPSON WARWICK GILES ANITA CONNELLY
Trudinger BJ, Cook C-M, Thompson RS, Giles WB, Connelly A. Low dose aspirin therapy improves fetal weight in umbilical placental insufficiency. Am J Obstet Gynecol (in press). 2. Giles WB, Trudinger BJ, Baird P. Fetal umbilical artery flow velocity waveforms and placental resistance: Pathological correlation. Br J Obstet Gynecol 1985; 92: 31-38. 3. Trudinger BJ, Giles WB, Cook CM. Flow velocity waveforms in the maternal uteroplacental and fetal umbilical placental circulation. Am J Obstet Gynecol 1985; 1.
152: 155-63. 4. Ylikorkala O, Makila U, Kaapa P, Vinikka L. Maternal ingestion of acetylsalicylic acid inhibits fetal and neonatal prostacyclin and thromboxane in humans. Am J Obstet Gynecol 1986; 155: 345-48.
POLYCYSTIC OVARIAN SYNDROME TREATED BY LASER THROUGH THE LAPAROSCOPE
SIR,-Bilateral ovarian wedge resection is still widely accepted in the management of the polycystic ovary syndrome (PCO).l Treatment by ovarian electrocautery through the laparoscope has been reported by Gjonnaess.2 This method reduces the risk of adhesions, the main complication of wedge resection. Lasers have the advantages over electrocautery of a reduced area of damage and haemostasis during sharp dissection. Furthermore, tissue regeneration is greater after laser treatment than after electrocautery.3 Because the placebo effect of surgical procedures in PCO remains unresolved4 we evaluated laparoscopic laser treatment in two groups of patients with PCO, one being studied by laparoscopy for diagnosis only (group A) and the other scheduled to receive laser treatment at laparoscopy (group B). All the patients had an LH/FSH ratio of 2 or more with macroscopic confirmation of enlarged sclerocystic ovaries. The study was not, therefore, randomised. Patients were told of the possibility of normal menstrual cycles and pregnancy arising after the procedure and the women in group B were informed about the ovarian excision procedure. We used
an
neodymium (Nd:YAG) laser with
a
flexible
fibre,
introduced through a third endoscopic puncture. Bilateral incision of the ovary was carried out for a distance of around 5 mm on the opposite of the mesovarium. In each ovary the laser incisions were done three, four, or five times to a length of 5-1 mm and a depth of 4 mm. Before the procedure clomiphene failure had been recorded in all patients, and testosterone, androstendione, and dehydroepiandrosterone were raised in most of them. All women had hirsutism and oligomenorrhoea. Spontaneous menstrual bleeding occurred 2-10 days after the procedure in all patients in group B. In group A menstruation occurred in only 2 cases, both 12 days after laparoscopy. No follicular maturation could be demonstrated in group A by daily monitoring of LH and oestradiol whereas in group B 5 patients ovulated spontaneously, and in 3 cases ovulation could be achieved
by clomiphene 2 months after the laser treatment. In these 3 cases LH and androgen levels were raised again after one cycle with an established ovulation. In the remaining 5 patients, the menstrual cycle was monitored for 2 months by endocrinological testing (LH, oestradiol), after that, basal body temperature was recorded. We now have follow-up data over about 6 months. All 5 patients now have a biphasic basal body temperature record, although none have yet become pregnant. In group A, despite the 2 cases of menstrual bleeding, ovulation could not be documented by basal body temperature measurement. These results confirm that endoscopic wedge resection is clinically relevant and does not act merely as a placebo. The incision of polycystic ovaries seems to be a new application for this kind of laser. First Department for Gynaecology and Obstetrics, University of Vienna, 1090 Vienna, Austria
J. HUBER J. HOSMANN J. SPONA
EY, Rock JA, Guzick D, Wentz AC, Jones GS, Jones HW Jr. Fertility following bilateral ovarian wedge resection: a critical analysis of 90 consecutive cases of the polycystic ovary syndrome. Fertil Steril 1981; 36: 320-25 2. Gjonnaess H. Polycystic ovarian syndrome treated by ovanan electrocautry through the laparoscope. Fertil Steril 1984; 41: 20-25. 3. Goldzieher J, Green JA. The polycystic ovary: Clinical and histologic features. J Clin 1. Adashi
Endocrinol Metab 1962; 22: 325-38. 4. Shearman RP, ed. Clinical reproductive Livingstone, 1985.
endocrinology. Edinburgh: Churchill
ASSESSING THE HYPOTHALAMO-PITUITARY-ADRENAL AXIS SiR,—Dr Stewart and colleagues (May 28, p 1208) propose the of the short ’Synacthen’ (synthetic corticotropin) test rather than the insulin tolerance test for the assessment of hypothalamopituitary-adrenal function in patients with hypothalamo-pituitary disease but not in patients who have been treated with a glucocorticoid. I cannot agree that the insulin tolerance test should be used routinely for those who have received glucocorticoid use
therapy. Stewart and colleagues did not in fact study patients on glucocorticoid therapy. They excluded patients with Cushing’s syndrome, those taking glucocorticoids, and those within 15 days of an acute pituitary insult. Thus their recommendation is based on the work of others. However, other reports do not support this exclusion. In general, the maximum response of the plasma cortisol level to corticotropin corresponds to the maximum plasma cortisol level observed during the induction of general anaesthesia and surgery in patients who have received glucocorticoid therapy.l-4 This occurs after a rapid intravenous injection of synthetic corticotropin with measurement of the plasma cortisol level 30 min2 or 60 min1 after the injection, or after a 6 h infusion of COrtlCOtropln.3’4 Thus a normal preoperative response to corticotropin is unlikely to be followed by impaired secretion of cortisol during anaesthesia and surgery in glucocorticoid-treated patients. It is true that patients have occasionally been reported in whom the response to corticotropin is normal but the response to insulin-induced hypoglycaemia or metyrapone is abnormal. 5,6 However, these studies did not systematically compare their findings with the response to a physiological stress such as the induction of general anaesthesia and surgery. (In one instance where this was done, a patient had normal corticotropin and cortisol responses to the stress of a vasovagal attack, but failed to respond to subsequent hypoglycaemia.6) Without such information, the comparison between a corticotropin test and an insulin tolerance or metyrapone test is difficult to interpret. It is possible, for example, that the hypoglycaemic stimulus was not adequate in the insulin tolerance test since normally there is variation between subjects in the plasma cortisol response to hypoglycaemia.7 It is also possible that the insulin tolerance or metytrapone test is too sensitive, rather than that the corticotropin test is insufficiently sensitive. Thus systematic studies consistently demonstrate the value of a corticotropin test in the assessment of hypothalamo-pituitaryadrenal function in patients who have been treated with glucocorticoids. As Stewart et al argue, for patients with hypothalamo-pituitary disorders the short synthetic cortcotropin