Wir führen an der Universitätsfrauenklinik Frankfurt seit 1984 Refertilisationen sowie Tubenanastomosen wegen anderer Ursachen unter zusätzlicher Anwendung von Fibrinkleber durch. Über die Zweckmäßigkeit dieses Vorgehens ist ausführlich diskutiert worden, sie soll nicht Gegenstand dieses Beitrags sein.

In den letzten Jahrzehnten ist eine weltweite Zunahme ektoper Schwangerschaften (EUG) zu beobachten. Verschiedene Ursachen werden hierfür verantwortlich gemacht: Optimierung der Diagnostik, Verwendung des IUD, Veränderungen im Sexualverhalten etc..

The world-wide increase in extrauterine pregnancies induced us to grow trophoblastic elements obtained from ectopic locations in tissue cultures in order to determine whether the tubal implantation of the blastocyst could be caused by chromosomal aberrations. In addition, we investigated for what period of time trophoblastic tissue from ectopic sites is capable of producing HCG in culture. This was done in view of an eventual use of this method as a model for the testing of the effect of antitrophoblastic agents in vitro. Finally, the concentration of several tumor markers in the culture medium was measured. The karyotype could be determined in 16 out of 20 tissue specimen subjected to tissue culture; in one case a chromosomal aberration was recognized, two times there was evidence of increased fragility of the chromosomes. The ratio of female to male karyotypes was 10 to 6. HCG was found to be produced for 6 to 9 days in the tissue cultures. The concentration of the tumor markers CEA, CA 19-9, CA 12-5 and CA 15-3 in the culture medium was low as compared to cultures containing additional tubal mucosa. We are concluding that chromosomal aberrations do not seem to play a causal role in the genesis of EUP. The assay of HCG production by trophoblastic cells in tissue cultures could eventually be used for the testing of agents which might ultimately be employed for the non-surgical treatment of certain cases of EUP.

Journal Article Problems in the localization of androgen-producing tumors. Elevated levels of T and 17-OHP in the suprarenal vein in a case of Sertoli-Leydig cell tumor Get access R Baumann, R Baumann Zentrum für Radiologie, FrankfurtKlinikum der J.-W.-Goethe-Universität, Frankfurt Search for other works by this author on: Oxford Academic Google Scholar H Kuhl, H Kuhl Zentrum für Radiologie, FrankfurtKlinikum der J.-W.-Goethe-Universität, Frankfurt Search for other works by this author on: Oxford Academic Google Scholar R Rauber, R Rauber Abteilung für gynäkologische Endokrinologie, FrankfurtZentrum für Radiologie, FrankfurtKlinikum der J.-W.-Goethe-Universität, Frankfurt Search for other works by this author on: Oxford Academic Google Scholar O Jürgensen, O Jürgensen Abteilung für gynäkologische Endokrinologie, FrankfurtZentrum für Radiologie, FrankfurtKlinikum der J.-W.-Goethe-Universität, Frankfurt Search for other works by this author on: Oxford Academic Google Scholar R Humke, R Humke Abteilung für gynäkologische Endokrinologie, FrankfurtZentrum für Radiologie, FrankfurtKlinikum der J.-W.-Goethe-Universität, Frankfurt Search for other works by this author on: Oxford Academic Google Scholar H-D Taubert H-D Taubert Abteilung für gynäkologische Endokrinologie, FrankfurtZentrum für Radiologie, FrankfurtKlinikum der J.-W.-Goethe-Universität, Frankfurt Search for other works by this author on: Oxford Academic Google Scholar Acta Endocrinologica (Norway), Volume 104, Issue 4_Supplement_b, Dec 1984, Pages S51–S52, https://doi.org/10.1530/acta.0.107S051-a Published: 01 December 1984

A highly active LH-RH-analog (D-Ser(TBU)6-LH-RH-(1-9)-nonapeptide-ethylamide = HOE 766) was administered to normally cyclic and ovulatory women in a double-blind study. Each woman received from day 1 through day 14 of the cycle according to a randomization plan either 10 microgram HOE 766 i.m. or a placebo. Ovulation was inhibited for at least two weeks in all subjects receiving HOE 766. The initially very marked release of LH measured 4 hourse after the injection decreased within 3 days by approximately 50%, and remained at this level for the remainder of the experiment while the initially high FSH response was abolished during further treatment. In 3 out of 5 women receiving the analog, serum estradiol was severely suppressed, in the remaining 2 slightly. Within 5 days after the discontinuation of treatment, the pituitary had regained the capacity to respond normally to LH-RH. It is postulated that follicular maturation is disturbed by the unphysiologic pattern of gonadotropin secretion during administration of HOE 766.A LH-RH analog (luteinizing hormone-releasing hormone) was studied in a double-blind trial to test its effectiveness as an ovulation inhibitor. It was administered to 10 healthy female volunteers, aged 22-34 years, with regular, ovulatory cycles. Each volunteer received from Day 1-14 of cycle an intramuscular injection of a coded ampoule by a randomized plan. 3 consecutive cycles were covered in the study; blood samples were drawn for hormone determinations, and basal body temperature data were used to determine ovulation along with the hormonal profiles. HOE 766 (D-Ser(TBU)-LH-RH-(1-9)-nonapeptide-ethylamide) inhibited ovulation for at least 2 weeks in all subjects receiving the agent in the injection (i.e., 5 of 10). Starting at 4 hours postinjection, a marked release of LH (luteinizing hormone) was recorded which decreased within 3 days by approximately 50% and then remained at this level for the remainder of the experiment. FSH (follicle stimulating hormone), however, though initially very high after treatment, was completely abolished for the remainder of the study. Estradiol was severely depressed in 3 of 5 women in the study; 2 women showed slightly depressed estradiol levels. Pituitary capacity returned within 5 days of cessation of intramuscular injections of the LH-RH analog. The mechanism of action is thought to be disruption of follicular maturation caused by the unphysiological pattern of secretion which occurs under HOE 776 therapy.

The displacement by various LH--RH analogs and fragments of 125I-LH--RH specifically bound to plasma membranes isolated from rat anterior pituitaries was investigated. The addition of increasing amounts of unlabelled LH--RH resulted in an increasing displacement of bound 125I-LH--RH. When some fragments of LH--RH or of an analog with little biological activities were incubated, a much weaker affinity for LH--RH binding sites could be observed. No correlation between biological effectiveness and binding affinity was, however, found when several highly active LH--RH analogs were tested. The potent analogs competed much less efficiently for specific binding sites on isolated plasma membranes than LH--RH. Binding experiments with iodine-labelled (D-Ser(But)6-LH--RH(1--9)-nonapeptide-ethylamide indicated that the small binding affinity of the superactive analog may be due to a lower association rate while the dissociation rate is comparable to that of LH--RH. Contrary to LH--RH, no binding equilibrium was reached during 2 h of incubation of the analog with plasma membranes. The physiological role of LH--RH binding sites on isolated pituitary plasma membranes remains to be elucidated.

Luteinizing hormone-releasing hormone (LH-RH) was administered to prepubertal male rats (intact, castrate or castrate-adrenalectomized, 60 g body weight) for 28 days (1 microgram LH-RH/day, s.c.), at a 10-fold physiological dose, as compared to the minimal FSH-releasing dose of 100 ng/rat s.c. In intact rats, serum LH and weight of androgen-dependent organs (vented prostate, seminal vesicles) were reduced after 14 days of treatment. In castrate rats, the postcastration rise in serum LH was abolished by treatment. Pituitary LH content, FSH secretion and prolactin secretion were not suppressed. Hypothalamic LH-RH was increased at 14 and 21 days. In castrate adrenalectomized male rats, LH secretion was also suppressed by 1 microgram LH-RH s.c. x 28 days. The hypothalamic LH-RH content did not increase. The pituitary LH-RH receptor level was not down-regulated after 14 days treatment either in intact or castrate male rats. Pituitary inhibition (LH release) in rats by a supraphysiological dose of LH-RH given for 28 days indicates that the optimal regime for chronic treatment has to be determined by monitoring LH release at regular intervals. Direct pituitary inhibition by LH-RH may explain some of the unexpected antifertility effects observed with high doses of LH-RH.