. Citations from
the literature
Int. J. Gynecol. Obstet. 47 (1994)
the human has not been investigated to date. In this study we examined the presence and the hormonal regulation of different complement components and receptors in the human endometrium at various phases of the menstrual cycle of normally cycling women with no pelvic pathologic abnormalities. Study design - Endometrial tissue was obtained from normally cycling women, and immunohistochemistry was performed by means of monoclonal antibodies against C3, factors B, decayaccelerating factor, membrane cofactor protein, and complement receptor types I, 2, and 3. The tissue was incubated with minimal essential media without methionine containing methionine labeled with sulfur 35. Immunoprecipitations were performed on the media with goat antihuman C3 antibody, and the proteins were analyzed by sodium dodecyl sulfate polyacrylamide gel electrophoresis. Results - C3 was found to be present in the glandular epithelial cells of luteal endometrium. Biosynthesis as analyzed by immunoprecipitation with anti-C3 antibody was found to increase during the luteal phase of the cycle and to be minimal in the proliferative phase. Like C3, factor B and decay-accelerating factor were localized to the luteal glandular epithelial cells. In contrast, membrane cofactor protein was found to be present in the glandular epithelium throughout the menstrual cycle, and complement receptor type I was present only in the stromal compartment of luteal endometrium. Complement receptor type 3 was present only in the infiltrating leukocytes in the luteal endometrium, whereas complement receptor type 2 was undetectable. Conclusions These findings suggest that several components of the complement system exist in the human endometrium in a hormonedependent manner and may play a role in normal reproductive function. The hypothalamic-pity-ovarian axis in patients with eodometriosis is suppressed by Ieoprolide acetate but not by dnnazol
193-201
197
Tii of the endometriaI biopsy may be critical for the accurate diagnosis of IuteaI phase deficiency
Castelbaum A.J.; Wheeler J.; Coutifaris C.B.; Mastroianni L. Jr.; Lessey B.A. USA
FERTIL STERIL 1994 61/3 (443-447) Objective - To determine the optimal time to perform the endometrial biopsy for the detection of ‘out-of-phase’ endometrium. Design: Two endometrial biopsies were performed during a single menstrual cycle in each subject. The patient’s chronological day was determined by counting forward from the midcycle LH surge, as assessed by urinary LH detection. The ‘early’ biopsy was done on day LH + 7.4 f 0.8, and the ‘late’ biopsy on day LH + Il.6 & 0.7. Each biopsy was independently read by two pathologists and was considered out of phase if the histologic date was 2 3 days delayed compared with the chronological date. Setting: Infertility practice of an academic teaching hospital. Patients - Thirty-three ovulatory women seeking evaluation for infertility. Main Outcome Measure - Number of patients with out-of-phase endometrium detected by the early versus the late biopsy. Results - There was a significantly greater detection rate for out-of-phase endometrium using the early biopsy (12.1% to 18.2% incidence depending on the observer) compared with the later biopsy (6.1% to 9.1% incidence). A majority of the early out-of-phase biopsies corrected by the time of the later biopsy. Conclusion - Our findings indicate that an endometrial biopsy performed in the midluteal phase may detect a greater number of women with delayed endometrial maturation during the temporal window of embryo implantation. The observation that most of the women with out-of-phase midluteal biopsies had normal late luteal endometrium may represent a cryptic form of luteal phase deficiency.
Sakata M.; Ohtsuka S.; Kurachi H.; Miyake A.; Terakawa N.; Tanizawa 0.
Hemostatic sod metabolic variables in women with polycystic ovary syndrome
JPN
Dahlgren E.; Janson P.O.; Johansson S.; Lapidus L.; Lindstedt G.; Tengborn L.
FERTIL STERIL. 1994 61/3 (432-437) Objective - To investigate the effects of leuprolide acetate (LA), a GnRH agonist (GnRH-a), and of danazol on the hypothalamic-pituitary-ovarian axis in patients with endometriosis. Design: Ten patients were divided into LA and danazol treatment groups. Measures: Serum levels of Ez, immunoreactive and bioactive LH. pulsatility of LH, and gonadotropins release by GnRH. Changes in serum E, levels by hMG administration during LA treatment. Results Serum Ez level decreased to near castrated levels during the LA treatment, while it remained unchanged during the danazol treatment. Leuprolide acetate administration resulted in a significant suppression of the serum level of bioactive LH, of the pulsatility of LH release, of the pituitary response to GnRH injection. and of the elevation in the serum E, level by hMG administration, but danazol treatment did not show these suppressive effects. Conclusion - Our results suggest that the hormonal actions of LA and danazol on endometriosis are different from each other, especially in the suppression of serum E, level.
SWE
FERTIL STERIL 1994 61/3 (455-460) Objective - To study whether a previously demonstrated increased morbidity in cardiovascular disease (CVD) and diabetes mellitus in women with polycystic ovary syndrome (PcoS) is associated with certain hemostatic variables that are known to be markers for CVD. Design: The study was a transsectional follow-up study from a cohort of women with PcoS. Setting - The women with PcoS were recruited from hospital clinics and referents were randomized from a population study of women from the same area. Participants - The investigation involved 28 women aged 43 to 62 years diagnosed to have PcoS on ovarian histopathology at wedge resection 25 to 34 years previously and 56 referents who were matched by age and body mass index. Main Outcome measures -- In connection with a clinical investigation, the hemostatic variables fibrinogen, von Willebrand factor antigen, factor VII procoagulant activity, factor VII antigen, and plasminogen activator inhibitor as well as the metabolic variables serum insulin