a premature LH surge and no laparascopy for follicle punction could be performed. A treatment with Buserelin nasal spray was started on the onset of menstrual bleeding: 4 x daily 300Mg-AH patients have given the written consent to the treatment performed. Blood was taken for LH during a time period of 2 hrs in 15 min. intervals after the morning application of Buserelin. If no single value of LH exceeded the 2s range of the intraassay variation LH fluctuation was found to be negative. To test the endogenous reaction to increasing estrogens 1 mg estradiolbenzoate was injected i.m. and blood was taken again for LH measurement 48 hrs. later. The E 2-test was found to be negative when no significant increase in LH ocurred 48 hrs. after estradiolbenzoate application.
De 1966 a 1983 un total de 586 transfusions fœtales intrauterines ont ete realisees sur 268 fœtus. 149 fœtus (56%) ont survecu. La survie a augmente a 63% pendant les 5 dernieres annees
Ovarian stimulation with hMG/hCG is most effective in hypogonadotropic patients. In normogonadotropic/estrogen-positive patients in whom gonadotropin therapy is also indicated after failure of other forms of treatment, it is much more difficult and considerably less effective. The objective of this study was to change the endocrine status in patients from a normogonadotropic and estrogen-positive status, by administration of a GNRH analogue, to a hypogonadotropic, estrogen-negative status, in order to create better conditions for gonadotropin stimulation. For this purpose Buserilin was administered either intranasally or intravenously and the endocrine reaction was observed. The endocrine changes observed were very varied. In the majority of cycles a fall in plasma FSH concentrations resulted (20 out of 28), in 2 a rise, while in 6 of the 28 there was no change. In 12 out of 28 cycles the plasma LH concentration decreased; it rose in 3 and was unchanged in 13. The LH fluctuation was suppressed or irregular in all cases. Estrogen secretion was unaffected in 16 cycles; it increased continuously in 6 cycles and temporarily in a further 6. The reaction to the hMG injections did not show the hoped-for improvement with simultaneous administration of an RH analogue. A complete and constant suppression of pituitary function, and thus the creation of a hypogonadotropic state, could not be achieved by medication with 8 X 300 micrograms Buserilin or intravenous injection of 5 and 10 micrograms every 90 minutes.
Thirty-two infertile patients with basal FSH/LH ratios of less than 0.5 were treated with a pure human urinary FSH preparation in various doses, in 57 cycles. With initially low FSH doses and increase in the dose according to the individual reaction (analogous to hMG therapy) ovulation and a normal luteal phase were achieved in 22 out of 25 cycles, and 6 pregnancies. In one cycle there was a clinical overstimulation syndrome in early pregnancy. Treatment with high doses of FSH at the beginning of the cycle proved unsuitable: normal follicle stimulation, ovulation and luteal phase only occurred in 12 out of 23 cycles, and there was no pregnancy. The combination of FSH therapy with initially high doses and subsequent stimulation with hMG resulted in ovulation in 9 out of 10 cycles without ensuing pregnancy. The behaviour of the endogenous LH under FSH therapy varied: with an initially high dose of FSH there was a clear drop in serum LH concentrations in 8 out of 23 cycles, and with an initially low dose in 5 out of 25 cycles. In 5 cycles the serum LH concentrations rose under FSH therapy. The results of the investigation confirm earlier observations that ovarian stimulation with FSH is possible in cases with low endogenous FSH/LH ratios, and that it is best accomplished by individualized therapy with an initially low dose. However, because of the different reaction of endogenous LH secretion, a better ovarian reaction than with hMG therapy could not be achieved with regard to ovulation and pregnancy rate, course of the luteal phase and overstimulation.
Between 1966 to 1984 a total of 636 intrauterine foetal transfusions were performed at the Hamburg University Hospital on 280 foetuses suffering from severe erythroblastosis. 54.6% of these foetuses survived. Ascitic fluid was found in 29,6% of the foetuses at the beginning of therapy. The survival rate improved to 22%.
The therapeutic effect of glucocorticoid therapy in infertile patients with hyperandrogenemic ovarian insufficiency was verified in a clinical study and compared with the results of other forms of therapy. Of 40 patients treated with 0.5 mg/d dexamethasone only one conceived. Of 47 patients treated with 7.5 mg/d prednisone 6 became pregnant. A combination therapy of dexamethasone and clomiphene resulted in 3 pregnancies among 20 patients; a combination of prednisone and clomiphene in 18 patients led to one pregnancy. In the majority of these patients previous treatment with clomiphene only had been unsuccessful. In the patient in whom both clomiphene and glucocorticoid therapy was unsuccessful, hMG/hCG therapy was applied. The pregnancy rate, 24% in the dexamethasone group and 36% in the prednisone group, was much higher. Plasma testosterone concentrations were not significantly suppressed under corticoid therapy. Neither at the beginning of a cycle nor at the time of ovulation were FSH and LH levels changed by the administration of corticoids. There was no significant correlation between the plasma testosterone values and the length of the cycle, the duration of the follicular phase, the duration of the rise in basal temperature or the length thereof. There was a significant correlation between testosterone and the LH/FSH quotient at the beginning of the cycle both in the spontaneous cycles and under corticoid therapy, though not under clomiphene therapy. In the control cycles there was a significant correlation between testosterone and LH; in the corticoid cycles it was not significant, and under corticoid therapy there was no correlation. A negatively significant correlation between testosterone and FSH was found in the control cycles. This correlation was not significant under glucocorticoid therapy and there was no correlation under clomiphene therapy. As testosterone concentrations increased a decrease in the percentage of biphasic cycles was observed in all groups. Regardless of the testosterone concentration, the pregnancy rate in patients showing signs of androgenization, at 22%, was higher than in patients without these symptoms. In patients who conceived under corticoid therapy there was no uniform correlation either to the pretherapeutic testosterone levels or to the degree of testosterone suppression. Neither the initial testosterone level nor the degree of its suppression is of any prognostic value for corticoid therapy. The more pronounced the clinical symptoms in hyperandrogenemic patients, the more effective a corticoid therapy will be; this applies both to signs of androgenization as well as to the degree of ovarian insufficiency.