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Objective: We sought to compare vascular resistance and plasma lipids in postmenopausal women assigned to tibolone (a synthetic estrogen replacement steroid) therapy or continuous combined hormone replacement therapy., Study Design: Pulsatility and resistance indexes in pelvic arteries (color Doppler transvaginal ultrasonography) and lipids were monitored in this double-blind 1-year trial of 100 women randomized to either 2.5 mg tibolone or 2 mg 17beta-estradiol plus 1 mg norethindrone acetate daily., Results: Both indexes of the arcuate arteries (uterine arteries) were significantly reduced beyond 3 and 6 months (12 months) from baseline, respectively, by the combined regimen compared with tibolone alone. Tibolone increased the resistance index of arcuate arteries but did not affect uterine arteries. There was no effect of either regimen on the internal iliac arteries. The medians of the percentage changes from baseline of high-density lipoprotein cholesterol (triglycerides) were significant between groups after 1 year, as follows: -17% (-16%) in the tibolone group and -4% (+15%) in the combined group, respectively. Both regimens similarly reduced total and low-density lipoprotein cholesterol and lipoprotein Lp(a)., Conclusion: Hormone replacement therapy may induce different or opposite changes of both vascular resistance and lipids. It is unknown whether these findings may modify cardiovascular risk.

Hormonal replacement therapy (HRT) is generally regarded as first choice for pharmacological prevention of osteoporosis in women. We reviewed recent studies of HRT regimens and selective oestrogen receptor modulators (SERMs), including controlled trials of at least one-year duration published since 1995 until February 2000 providing data on bone mineral density (BMD) or fractures. Natural and synthetic oestrogens exert a continuum of positive effects on BMD in a dose-dependent, though non-proportional, fashion independent of age and mode of administration. Bone loss may be largely prevented by 25 microg transdermal patch oestradiol, 0.3 mg conjugated equine or 0.3 mg esterified oestrogens. Progestogens neither attenuate nor augment the effect of oestrogens; sole use of tibolone prevents bone loss. Both the SERMs, tamoxifen and raloxifene, slightly increase BMD. There are no adequately powered fracture trials for any HRT regimen. Raloxifene 60 mg daily decreases the relative risk of vertebral fractures by at least 30%, as demonstrated by one 3-year fracture study of osteoporotic women. In conclusion, the recommendation to use oestrogen for postmenopausal osteoporosis, given both the lack of fracture trials and the rare trials on long-term use of HRT in (late) postmenopausal women, is not well supported. Fracture trials could overcome shortcomings of the current level of evidence.

We restudied histologically and immunohistochemically 17 endometrial carcinomas, 2 malignant mixed tumors and 180 endometria with benign changes during or after tamoxifen therapy. The carcinomas were subtyped according to the 1994 WHO-classification. Endometrial biopsies were taken only if the endometrial thickness was > 8 mm sonographically, when a polyp was seen, or for postmenopausal bleeding. About half of the endometrial specimens showed simple or cystic atrophy, 55-76% had cystic-atrophic polyps or regressive hyperplasia. Depending upon the dose of tamoxifen, 7-19% (30 mg) to 27-36% (20 mg) showed moderate glandular proliferation. 20-33% had foci of mucinous, clear cell or serous-papillary metaplasia. 68-70% revealed diffuse extensive fibrosis of the endometrial stroma. None of 11 patients biopsied before starting tamoxifen therapy had advanced endometrial glandular proliferation in the second endometrial biopsy after tamoxifen treatment. None of the 19 endometrial neoplasms after tamoxifen therapy was of the endometrioid type: 11 were mucinous adenocarcinomas, 4 clear cell carcinomas, 2 serous-papillary carcinomas, one carcinosarcoma and one malignant Mullerian mixed tumor. The reasons for discrepancies between suspicious sonograms and endometrial atrophy are discussed.

Hormone replacement therapy may increase the quality of life of postmenopausal women. Any regimen need to offer long-term endometrial safety. It is a standard to consider the co-administration of a sequential progestogen when estrogen replacement should be initiated in non-hysterectomized women. It is almost impossible to decide which combination of an estrogen and a progestogen seems to be optimal as individual tolerance of HRT may very well limit acceptability despite metabolic benefits and proven endometrial safety of a given combination. Several combinations of oral and transdermal estradiol or conjugated equine estrogens, oral progestogens, transdermal norethisterone acetate and levonorgestrel, and intrauterine levonorgestrel may achieve endometrial safety. It is noteworthy that there is no uniform correlation between the timing of onset of bleeding induced by any sequential estrogen and progestogen replacement and a certain pattern of histology. Therefore, although it is likely, there is no absolute reassurance that regular bleeding on or after day 11 of progestogen administration rules out abnormal histopathology. Transvaginal sonography seems not to be of pivotal importance to screen asymptomatic women on replacement therapy for detection of serious abnormal endometrial findings such as hyperplasia and endometrial cancer. Continuous combined hormone replacement therapy or the use of tibolone may be an alternative in postmenopausal women, who do not want any uterine bleedings after menopause. However, spottings or bleedings most often occur at the beginning of treatment. Vaginal administration of estriol and estradiol for urogenital symptoms of estrogen deficiency may stimulate the endometrium unintentionally. Available data suggest that use of oral estriol may be associated with endometrial hyperplasia and endometrial carcinoma relatively more often compared to sequential HRT. Raloxifene, a benzothiophene derivative acting as a selective estrogen receptor modulator approved for prevention of vertebral osteoporosis, rarely causes uterine bleeding. There is no ideal therapy available to suit women looking for a permanently bleed-free hormonal replacement therapy today.

The purpose of this study was to analyze the midvertebral area of lumbar vertebrae in osteoporotic and nonosteoporotic female patients and to find out whether the midvertebral area may be used as an additional parameter in the diagnosis of osteoporosis. In 195 peri- and postmenopausal patients (average age 51.7 +/- 5.2 years) trabecular and cortical bone mineral density (BMD) were determined using quantitative CT (QCT) in L2-4. In addition, midvertebral cross-sectional area was measured in a standardized fashion on the CT sections and the height of the second lumbar vertebra was determined on the lateral digital radiographs. Body height and weight were obtained and vertebral fracture status was determined. According to WHO criteria 29 patients (average age 57.2 years) were considered osteoporotic, 93 osteopenic (average age 52.2 years) and 73 normal (average age 48.6 years). Body weight and size did not show significant differences between the individual groups. Average midvertebral area was 1278 +/- 173 mm2 in the osteoporotic patients, 1186 +/- 125 mm2 in the osteopenic patients and 1126 +/- 127 mm2 in the normals. A correlation of r = -0.39 (p < 0.05) was obtained between BMD and area. Thirty-six of 195 patients showed osteoporotic vertebral fractures. Midvertebral area in these patients was 1266 +/- 171 mm2 versus 1159 +/- 133 mm2 in the nonfractured females (p < 0.05). We therefore conclude that the lumbar midvertebral area is larger in osteoporotic and osteopenic patients compared with women with normal BMD. In contrast to biomechanical considerations midvertebral area seems not to be suited as an additional measure of bone strength in vivo.

Objective: To evaluate endometrial thickness and the incidence of uterine bleeding in postmenopausal women using either tibolone 2.5 mg or continuous combined 2 mg estradiol and 1 mg norethisterone acetate (E+NETA) daily as hormone replacement therapy., Design: We compared diary records of self-reported uterine bleeding and measurements of endometrial thickness, area, and volume by transvaginal sonography at baseline and after 1, 3, 6, and 12 months in a 1-year, prospective, randomized, double-blind, single-center trial of 100 postmenopausal women aged 46-69 years. Bleeding frequencies and endometrial thickness were assessed by Chi-square tests and analysis of covariance, respectively., Results: Self-reported bleeding was significantly less in the tibolone group. Bleeding episodes were reported by 27.7% of women in the tibolone group and by 59.2% in the E+NETA group. The mean number of days with bleeding was 5.8 +/- 27.0 in the tibolone group and 35.6 +/- 58.6 in the E+NETA group. Six women in the tibolone group and seven in the E+NETA group discontinued the study; three in the E+NETA group because of bleeding. The mean endometrial thickness at baseline was 2.56 +/- 0.81 mm in the tibolone group and 2.58 +/- 1.04 mm in the E+NETA group. After 1 year, the corresponding figures were 3.32 +/- 1.58 mm and 3.07 +/- 1.68 mm. Thus, 86% of women in the tibolone group and 93% in the E+NETA group had an endometrial thickness of less than 5 mm., Conclusions: Use of tibolone 2.5 mg daily for 1 year was associated with significantly less bleeding and spotting compared with daily continuous combined 2 mg estradiol and 1 mg norethisterone acetate in postmenopausal women in the presence of both minimal and nonprogressive increase of endometrial thickness associated with the two regimens.

Urogenital aging is given a low priority in the medical community and is an entity not well known to the general public. Many women are not aware of the possible disorders of the lower urinary tract and the vagina because of estrogen deficiency. These changes are perceived often as a normal part of the general aging process not associated with the possibility of medical attention, diagnosis, and treatment. Access to the information that certain urogenital dysfunctions, in particular incontinence, and vaginal discomfort respond to estrogen replacement therapy is not available for every woman. In addition, physicians and patients may hesitate to address these issues because of feelings of shame and embarrassment, feelings commonly encountered and specific for the complex of urogenital aging. Educational efforts and promotion of information with use of various media might help to improve knowledge and remove the taboo attached to urogenital aging in both health care providers and the general public. Thus a better understanding of urogenital aging would be achieved and the potential of estrogen replacement extended.

We report the third case of a prenatal diagnosis of Larsen's syndrome, which is the first report affecting both a 37-year-old primiparous caucasian woman and her fetus not considered to have Larsen's syndrome until the finding of bilateral clubfeet was demonstrated on screening ultrasound at 23 weeks of gestation. History and physical examination of the pregnant woman revealed severe impairment in the mobility of hip, elbow and knee joints starting in early childhood. Additional findings were spatulate thumbs and a flat nasal bridge. The mother of the pregnant woman demonstrated similar joint symptoms. The differential diagnosis of Larsen's syndrome was considered for the first time in both women. The patient wished to terminate her pregnancy, as the potential early onset of the same disorder was suggested by the finding of clubfeet. An intraamniotic instillation of ethacridinic acid was performed. On pathological examination including radiography of the male stillborn, various anomalies of the face, and upper and lower extremities were demonstrated compatible with Larsen's syndrome.

Intracranial tumours, often presenting with progressive hydrocephalus, are rare congenital diseases accounting for 0.5-1.5 per cent of all cases of brain tumours diagnosed during childhood. The differential diagnosis includes vascular malformations, infarctions, and haemorrhages. Sonographic signs suggestive of glioblastoma, teratoma, and astrocytoma do not establish the histological diagnosis, however. We report a case of an undifferentiated fetal glioma detected at 29 weeks' gestation. The diagnosis of an undifferentiated brain tumour was suspected by sonography because of the lack of normal brain structures in conjunction with a diffuse echogenic central lesion and an external hydrocephalus. Because of the very poor prognosis, we induced labour by intravaginal and intravenous administration of prostaglandin E2 and achieved the vaginal delivery of a stillborn child whose head circumference corresponded to 38 weeks of pregnancy. Histological and immunochemical features of this undifferentiated congenital glioma (glioblastoma) are presented.

We assessed the resistance index (RI) and pulsatility index (PI), peak and average systolic velocities in uterine, arcuate and radial arteries, and endometrial thickness (ET) by transvaginal B mode and color Doppler sonography in patients on continuous combined hormonal replacement therapy (HRT) and controls. HRT consisted of 2 mg estradiol, 1 mg estriol and 1 mg norethisterone acetate daily (n = 33) compared to controls, who received none of these (n = 21). Age was 61 +/- 6 and 59 +/- 9 years (mean +/- standard deviation) in the HRT and control groups, respectively. The duration of HRT was 5 +/- 2 years, with a minimum of 1 year. We found that the uterine RI and, to a lesser extent, the uterine PI were significantly lower and the radial peak systolic velocities were significantly higher in the HRT group compared to controls. The highest uterine PI values were measured in controls with the shortest life-time exposure to endogenous estrogens, i.e. late menarcheal age or early menopause. The endometrial thickness of 2.8 +/- 1.8 mm in the HRT group was not significantly different from that in the controls (4.2 +/- 5.6 mm). In conclusion, the alteration in blood flow parameters demonstrated in this study would suggest that the long-term use of continuous oral estradiol 2 mg, estriol 1 mg and norethisterone acetate 1 mg daily is associated with a slight increase of flow in the uterine arteries compared to controls matched for (postmenopausal) age. Endometrial thickness does not increase with duration of use of continuous combined HRT.

The occurrence of uterine bleeding usually associated with hormonal replacement therapy is not acceptable for many women. Our objective was to review data on compliance and bleeding patterns in 70 postmenopausal women on oral replacement with estradiol 2 mg, estriol 1 mg, and norethisterone acetate 1 mg daily administered in a continuous combined fashion to avoid withdrawal bleeding. After 1 year, compliance was 97%, after 5 and 9 years 76% and 58%. The most common reason for discontinuation was spotting. Reproductive history, body weight and pretreatment estradiol and FSH concentrations were not different between the subgroups with bleeding-19%- and without bleeding-81%. The probability to maintain amenorrhoe on HRT did not increase with the length of the postmenopausal interval or weight. Endometrial histology revealed one case of a highly differentiated in situ adenocarcinoma of the endometrium. In the women with bleeding, induced serum estradiol levels were significantly and pretreatment SHBG-levels lower compared to the non-bleeders. Whether these findings may be significant for election of patients for continuous combined HRT remains to be determined. In conclusion, we demonstrate that adherence to this treatment regimen apparently provides a choice patients considering long-term HRT should be informed about. However, the lack of parameters to elect patients in conjunction with the problem of uterine bleeding does not permit the recommendation to regard continuous combined HRT as first line therapy for long-term HRT. Criteria need to be developed when to obtain an endometrial histology once uterine bleeding occurs, as the optimal surveillance of this mode of HRT is presently unknown.

Objective: Estrogens are known to exhibit antioxidative effects. At present little information exists on the influence of co-administered progestins upon this effect. Therefore we investigated the influence of levonorgestrel, a potent antiestrogenic progestin, on the inhibition of the low-density lipoprotein (LDL) oxidation by 17 beta-estradiol or 17 beta-estradiol valerate in vitro and ex vivo., Methods: After isolation from blood, the in vitro oxidation of LDL was induced by copper ions and measured continuously by monitoring the formation of conjugated dienes. In 21 female ovariectomized White New Zealand rabbits the antioxidative action of 17 beta-estradiol alone or in combination with levonorgestrel after subcutaneous infusion for 3 days was determined using the copper-induced LDL-oxidation as an endpoint. Eleven postmenopausal women were exposed to sequential estrogen-progestin replacement therapy (day 1-21:2 mg estradiol valerate/day, day 10-21: 0.15 mg levonorgestrel/day). Blood samples were collected at three times: on day 1, on day 10, on day 22 (after the combination phase). The lag time of ex vivo oxidation of LDL, the plasma estradiol and estrone levels were estimated., Results: In the chosen cell-free system, 17 beta-estradiol increased the lag time of the LDL-oxidation in a dose-dependent manner. Levonorgestrel showed neither pro-oxidative nor antioxidative effects when administered alone in different concentrations. Co-administration of different doses of levonorgestrel did not modify the antioxidative action of estrogen either. The two ex-vivo models confirmed these results. In rabbits the co-administered 19-nortestosterone derivative levonorgestrel did not impair or reverse the estradiol-dependent effect. In postmenopausal women the daily oral administration of levonorgestrel in conjunction with 17 beta-estradiol valerate did not diminish the antioxidative action of this estrogen given for the first 9 days., Conclusion: The antioxidative potential of estradiol and estradiol valerate is maintained in the presence of levonorgestrel.

Epidemiological data strongly suggest a substantial improvement of quality of life for post-menopausal women using hormonal replacement therapy (HRT). Nevertheless, reluctance of women to choose HRT is high. Various attempts to develop regimens with substantially better acceptance are being investigated. Sequential and continuous combined regimens, oral and transdermal routes of administration are available; however, no regimen nor any mode of administration has proven superior with regard to patients' compliance. Research on the specific problems of compliance in HRT has not yet offered solutions to the medical community about optimal conditions concerning long-term hormonal therapy. Unless metabolic profiles of the various modes of treatment are defined in long-term trials, general recommendations are difficult to justify. As long as the occurrence of uterine bleeding is associated with any concept of HRT in non-hysterectomized women, adherence has been reported to be very low. Persisting endometrial atrophy has not been achieved by any type of HRT. New regimens not stimulating endometrial growth are essential, since women in most cultures do not accept uterine bleeding after cessation of ovarian function. Educational programs should be developed to inform women about the physiology of menopause in general and the rationale of HRT. The occurrence of uterine bleeding due to the present types of HRT needs to be specifically addressed. Risk-benefit assessments are to be explained to patients to reach an informed decision on HRT, and fears of women about actual or alleged negative metabolic impacts of HRT need to be discussed.

Objective: We assessed compliance, relief of climacteric symptoms, and impact on lumbar bone mineral density in two groups of 140 patients treated with a sequential estrogen-progestogen or a continuous combined replacement therapy in comparison with controls., Study Design: Patients were randomized to 2 mg of estradiol valerate daily and 5 mg of medroxyprogesterone acetate daily for 12 days per month sequentially to induce withdrawal bleeding (group A) or 2 mg of estradiol, 1 mg of estriol, and 1 mg of norethisterone acetate daily continuously to maintain amenorrhea (group B) or a control group (group C)., Results: Compliance was 93% after 1 year and 73% after 2 years in group B and 66% and 49% in group A after 1 and 2 years, respectively. Improvement of climacteric symptoms was similar in groups A and B. Uterine bleeding in 24% of patients in group A and 3% in group B was the most frequent reason for discontinuation of drug intake. Only continuous combined therapy (group B) increased bone mineral density after 1 and 2 years compared with baseline: +13% and 17% (p = 0.01). In groups A and C no significant changes in bone mineral density were recorded. Compliance was unrelated to the age of menopause., Conclusion: Continuous combined therapy is superior to sequential estrogen progestogen replacement in compliance and prevention of bone loss but not with regard to relief of climacteric symptoms.

The term 'aneurysm of the vein of Galen' encompasses a range of different midline arteriovenous fistula malformations. Prenatal real-time and Doppler sonography can contribute to the differential diagnosis of fetal cerebral cystic lesions of various origins, pineal and choroid tumors, and intracerebral hematoma. Regardless of the type of treatment, perinatal morbidity and mortality are high, often due to cardiac failure. A case of spontaneous delivery at 36 weeks of gestation by a 30-year-old woman presenting with a fetal aneurysm of the vein of Galen is described. As the extrauterine cardiac function was normal and a steal phenomenon was not present, expectant management was justified. Five arterial embolizations within the following 4 years were performed as a means of treating the primary lesion. Our case illustrates the fact that elective spontaneous vaginal delivery followed by serial embolization is possible in cases of arteriovenous fistula malformation without signs of cardiac insufficiency.

At least one of four women will suffer from osteoporosis with fractures of vertebrae, forearm or hip. Maintenance of bone mass is a crucial argument for long-term estrogen replacement for prophylaxis of osteoporosis. 2 mg estradiol or 0.625 mg conjugated estrogens orally or 50 to 100 micrograms estradiol percutaneously are equally sufficient for prevention of osteoporosis. The additional use of a progestogen in women with intact uterus may support the antiresorptive effects of estrogens. Improvement of patients' compliance-administered today by only 25% of postmenopausal women in Germany through sufficient information upon estrogen replacement therapy provided by the medical community is a rewarding task for physicians and scientists engaged in the field of menopause and prevention of osteoporosis.

Quantitative CT of the axial skeleton (aQCT) may serve as an example of the evaluation and interpretation of bone densitometric data as it is the only state-of-the-art technique with valid longitudinal observations. The value of bone density measurements in interindividual cross sections refers to a grading derived from a representative reference population and provides an evaluation of fracture risk. The presence and rate of any bone loss can only be evaluated in an intraindividual longitudinal follow-up. Adequate follow-up for trabecular bone requires at least 3 to 5 years intervals to discriminate between different loss rates. Bone losses induced by steroid therapy or immobilisation may have faster kinetics apparent within months; bone density increase due to hormone substitution may be significant after one to two years. Morphological data allow critical evaluation of the quantitative measurements, eliminating false values and differentiating between rarefying and destructive osteopenia.

An oral estrogen-progestogen replacement therapy consisting of 1 mg estradiolvalerate +2 mg estriol/day for 21 days in combination with 0.25 mg levonorgestrel/day for the last 10 days sequentially may be sufficient to maintain lumbar trabecular bone density in climacteric pre- and postmenopausal women as demonstrated by serial bone density measurements (single-energy quantitative computed tomography of the lumbar spine) in 7 individuals with longitudinal follow-up for up to 5 years. At present, only postmenopausal women with induced estradiol levels of at least > or = 220 pmol/l (> or = 60 pg/ml) provided by estrogen replacement therapies containing higher daily estradiol doses as the above described preparation have been shown to be protective against loss of trabecular bone at the lumbar spine. Preliminary pharmacokinetic results obtained from 14 postmenopausal women being treated with the low-dose estrogen-progestogen replacement demonstrated peak estradiol concentration of 120-160 pmol/l (32-43 pg/ml) 10 hours after oral ingestion, suggesting bone preserving properties by these considerably lower estradiol concentrations.

At least one of four women is suffering from osteoporosis with fractures of vertebrae, forearm or hip. Maintenance of bone-mass is a crucial argument for long-term estrogen replacement for prophylaxis of osteoporosis. 2 mg estradiol or 0.625 mg conjugated estrogens, or 50-100 micrograms estradiol percutaneously are equally sufficient for prevention of osteoporosis. The additional use of a progestagen in women with intact uterus may support the antiresorptive effects of estrogens. Improvement of patients' compliance of estrogen substitution--administered today in only 25% of postmenopausal women in Germany--by sufficient information upon estrogen replacement therapy provided by the medical community is an awarding task for physicians and scientists engaged in the field of menopause and prevention of osteoporosis.

Prophylaxis of postmenopausal osteoporosis is of major importance if estrogen replacement therapy is considered. Assessment of clinical symptoms, (standardized) x-ray analysis, and bone densitometry contribute to the final diagnosis. Incidence of osteoporotic fractures is rising due to alterations in life style and dietary habits. One out of three to four women eventually suffer from osteoporosis in the European countries, United States and Japan. Prevention of postmenopausal osteoporosis is achieved by adequate estrogen replacement therapy carried out for years, maintaining peripheral estradiol concentrations of 220 pmol/l. Doses of 2 mg estradiol or 0.625 mg of conjugated estrogen or 50-100 micrograms percutaneous estradiol/day are equally effective for prevention. The additional administration of a progestogen may be of specific value to increase the antiresorptive effect of estrogens. We distinguish between estrogen replacement in a cyclic or continuous way combined with a sequential or continuous progestogen in women with intact uterus.

One in the three women develops osteoporosis--low bone mass and structural deterioration leading to fractures. Pre- and postmenopausal deficiency states are main causes. Estrogens prevent bone loss: Oral doses of 2 mg estradiol or 0.625 conjugated estrogens/day or 50-100 micrograms transdermal estradiol/day substantially reduce vertebral, forearm, and hip fractures. Certain progestins may enhance this effect. Calcium as a prerequisite for attainment of peak bone mass will not substitute for estrogen replacement. Selection of patients actually being at risk for postmenopausal osteoporosis needs to be improved substantially; there is no sensitive single test or testing system for osteoporosis. As individual history and physical exam or biochemical markers of bone resorption and formation rarely provide the early diagnosis of osteoporosis, prophylactic estrogen replacement therapy has to be considered in the majority of postmenopausal women to achieve prevention of postmenopausal osteoporosis. Compliance of replacement therapy in the European countries is poor, only 5-25% of postmenopausal women use estrogen replacement therapy for more than one year. Major compliance problems are alleged weight gain, resumption of withdrawal bleeding and fear to develop breast or endometrial cancer.

The diagnostic ranking of trabecular morphology for the evaluation of osteoporosis in quantitative CT (QCT) is presented. 5 patterns of cancellous bone correlating with trabecular density may be discerned. However, these patterns may indicate osteoporotic changes in particular cases only, by confluent rarefactions if the density is still within the normal range. There is neither a predictive value for the degree of spontaneous or therapy-induced bone loss, nor for therapy response. The trabecular appearances remain unchanged in short term even under strong quantitative changes and are therefore of no value for follow-up.

In this double blind cross-over study, 20 infertile men, who had sperm antibodies detected by the mixed antiglobulin reaction (MAR test) in the ejaculate and by the tray agglutination test (TAT) in serum, were treated with 40 mg/day prednisolone or placebo from days 1 to 10 of the partners' menstrual cycle. Patients were randomly allocated to different treatment groups. While group 1 started with placebo followed by verum for three consecutive cycles, group 2 began with verum and continued with placebo. All patients had regular intercourse (n = 19) or intra-cervical insemination at ovulation (n = 1). A post-coital test or a sperm penetration test was performed during verum and placebo regimes. Blood samples were drawn from the male partner at this time to control the efficacy of prednisolone treatment by checking the TAT titre. No pregnancy occurred during prednisolone or placebo treatment. In eight of 12 patients, post-coital testing showed little improvement and antibody titres decreased in seven of 16 patients. Side-effects from medication were reported by eight patients (seven verum and one placebo cycle) and caused treatment to be discontinued in two cases. Five patients' partners conceived at a later stage by intrauterine insemination with spermatozoa prepared by 'swim up' (n = 3) or by in-vitro fertilization (IVF n = 2). Thus high dose corticosteroid therapy was ineffective in achieving pregnancies induced by infertile men positive for antisperm antibodies. Since side-effects of corticosteroids should not be underestimated in otherwise healthy men, other reproductive techniques such as intrauterine insemination or IVF should be offered to such couples.

Osteoporosis is a disease of the elderly characterized by a loss of bone mass causing fractures in presence of an inadequate trauma. Osteoporosis has to be considered as a significant ailment in our population. This review outlines epidemiology, pathogenesis and risk factors of primary osteoporosis. The physiological role of sex hormones, especially of estradiol, for the development and maintenance of skeletal bone mass is explained. Principles of preventive estrogen(-progesterone) application for the prophylaxis of postmenopausal osteoporosis are specified by several estrogen replacement studies in postmenopausal women. Individual replacement therapy for the compensation of a long-lasting estrogen deficit in the reproductive age group, in pre- and postmenopausal women is the assignment of the gynecologist in order to protect the skeletal system.

Idiopathic osteoporosis mainly affects postmenopausal women. The normal trabecular volume of the lumbar vertebrae in a sample of healthy perimenopausal women was established by monoenergetic computed tomography. Early diagnosis of diminished bone mass is crucial for the identification of women at risk for involuntary osteoporosis following climacteric estrogen depletion. Body weight, endogenous levels of sex steroids, renal calcium and hydroxyproline excretions are not related to individual bone mass in the lumbar spine.

The effect of continuous intrauterine administration of prostaglandin F2 alpha (PGF2 alpha) or indomethacin or indomethacin together with PGF2 alpha and PGE2 or vehicle on fertilization of rabbits was studied. These substances and vehicle were delivered into the cornua of the uterus via an Alzet minipump for 11 days. The animals were inseminated vaginally. Compared with controls (104 eggs of which 88.5% were fertilized) a reduction of the fertilization rate was observed with indomethacin (74 eggs of which 70% were fertilized). Exogenously added PGF2 alpha did not change the fertilization rate. The administration of indomethacin together with PGE2 raised the fertilization rate to 86% (63 eggs of which 54 were fertilized). The application of PGF2 alpha together with indomethacin showed a fertilization rate of 85% (59 eggs of which 50 were fertilized). The indomethacin application was associated with a reduction of prostaglandin production in several tissues from the female genital tract, showing that indomethacin is taken up by the endometrium of the rabbit. The ovary, oviduct, cervix and vagina were mainly affected by this treatment. The route of transport of this drug is not known, however. The reduction of the total number of eggs together with the decrease of the fertilization rate after indomethacin administration point towards multiregional sites of interference of prostaglandins in reproductive functions. PGF2 alpha seems to be the more important factor since PGE2 may be converted to PGF2 alpha in reproductive tissues.

The authors present a case of an interstitial extrauterine pregnancy in the intramural portion of the left oviduct after preceding ipsilateral adnectomy. Sonographic diagnosis was confirmed by the site at operation.

Healthy perimenopausal women (152) were examined by QCT to quantify the mineral content of the axial skeleton. The density was measured in the spongiosa of the L2-4, using single energy technique and the Cann-Genant calibration phantom. The women, aged 37 to 64, had no history of pathological fractures, ovariectomy, metabolic disease, or hormone therapy. The age-related mean values were 25 mg K2HP04/cm3 lower than the normal values reported by Genant et al. for 203 healthy American women. The 95% confidence interval was distinctly narrower (+/- 40 mg/cm3) than the American confidence interval (+/- 60 mg/cm3). To evaluate the relationship of the BMC to mechanical stress, the BMC was compared with body weight, body mass index (weight/height2), and the lumbar muscle mass estimated from cross sections of the paravertebral muscles in the CT images. The assumption that higher mechanical stress results in higher bone mineralization could not be confirmed.