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Using survey and archival data from 598 employees of a Fortune 100 financial services firm, this paper studies the antecedents and consequences of using goal selection as an impression management tool. We find that poor performance relative to performance targets in one period increased employees' desire to use goal setting as an impression management tactic in the next period. In addition, using goal setting as an impression management tactic causes employees to self-select less difficult performance goals, which in turn negatively impacts actual performance. Given the extensive use of goal setting in organizations, understanding its use and effects as an impression management tactic is important.

The administration of GnRH analogues is expected to improve treatment by avoiding hysterectomy, since problems connected with the surgical removal of leiomyomata are correlated with their size. In this study the GnRH analogue goserelin in its depot formulation (Zoladex, ICI, Plankstadt) was used for treating isolated leiomyomata of the uterus. All patients were treated for 3 months before myomectomy was performed. The complete regression of a large myoma (206 cm3) was observed in 1 of 11 patients. In 5 cases a reduction in volume of more than 50% was achieved. Ovarian function was suppressed by goserelin, after a short-term stimulation, within 7 +/- 3 days. Serum levels of 17 beta-oestradiol were found to be generally less than 25 pg/ml. All patients reported climacteric complaints, but in no case had therapy to be discontinued. After cessation of goserelin, restoration of ovarian function was observed in all patients.

Recently, GnRH antagonists (GnRHant) like cetrorelix and ganirelix have been introduced in protocols of controlled ovarian hyperstimulation for assisted reproductive techniques to prevent premature luteinizing hormone (LH) surges. Here we tested, whether the actions of cetrorelix and the GnRH agonist (GnRHag) triptorelin in gonadotrophs are dependent on the steroid milieu. Furthermore, we characterized the actions of cetrorelix and triptorelin on LH secretion and the total LH pool. Female rat pituitary cells were treated either with 0.1 nM triptorelin for 1, 2, 4 and 6 days or for 1, 3, 5 and 6 h or with 1, 10 or 100 nM cetrorelix for 1, 2, 3 and 5 h or for 10 min. Cells were stimulated for 3h with different concentrations of GnRH (10 pM-1 microM). For analysis of the total LH pool, which is composed of stored and released LH, cells were lysed with 0.1% Triton X-100 at -80 degrees C overnight. To test, whether the steroid milieu affects the actions of cetrorelix and triptorelin, cells were incubated for 52 h with 1 nM estradiol (E) alone or with combinations of 100 nM progesterone (P) for 4 or 52 h, respectively. Cells were then treated with 0.1 nM triptorelin for 9 h or 1 nM cetrorelix for 3 h and stimulated for 3 h with different concentrations of GnRH (10 pM-1 microM). The suppressive effect of triptorelin on LH secretion was fully accomplished after 3 h of treatment, for cetrorelix only 10 min were sufficient. The concentration of cetrorelix must be at least equimolar to GnRH to block LH secretion. Cetrorelix shifted the EC50s of the GnRH dose-response curve to the right. Triptorelin suppressed total LH significantly (from 137 to 36 ng/ml) after 1 h in a time-dependent manner. In contrast, only high concentrations of cetrorelix increased total LH. In steroid treated cells the suppressive effects of triptorelin were more distinct. One nanomolar cetrorelix suppressed GnRH-stimulated LH secretion of cells not treated with steroids from 10.1 to 3.5 ng/ml. In cells, additionally treated with estradiol alone or estradiol and short-term progesterone, LH levels were higher (from 3.5 to 5.4 or 4.5 ng/ml, respectively). In cells co-treated with estradiol and progesterone for 52 h LH secretion was only suppressed from 10.1 to 9.5 ng/ml. Steroid treatments diminished the suppressive effect of cetrorelix on LH secretion. In conclusion, the depletion of the total LH pool contributes to the desensitizing effect of triptorelin. The actions of cetrorelix and triptorelin are dependent on the steroid milieu.

In the current environment, an important firm asset is the employee knowledge base, which in a large part depends on employee willingness to share information. Yet prior research has noted that while employees are delighted to reveal success they are often reluctant to reveal errors. While there are many factors affecting managers’ reluctance to reveal errors, this study focuses on cultural differences between Chinese migrants and Anglo residents as well as the role of acculturation. This is particularly relevant given the very significant foreign direct investment into China, and migration of managers and high-end technical staff from portions of Greater China to the management and higher technical classes of the Anglo world. Prior studies including Chow, Harrison, McKinnon, and Wu (1999a). Accounting, Organizations and Society, 24, 561–582, Chow, Deng, and Ho (2000). Journal of Management Accounting Research, 12, 65–95, and Tinsley and Pillutla (1998). Journal of International Business Studies, 29(4), 711–728, provide conflicting views and evidence for differences in information sharing between Chinese and Anglo managers, and there is no accounting or management literature that deals with changes in information sharing behavior in the migration process. This study employs an experiment to test for differences in individuals’ willingness to share information about a prior costing error. Using a sample of students from two different nationalities drawn from a major Australian university (Australian and Hong Kong SAR, China), this study finds that migrant Chinese share less information than Anglo-Australians. This study further provides empirical evidence that the relative change in willingness to share this information when the supervisor is removed from the decision context is lower for the migrant Chinese than for the Anglo-Australians. Finally, this study finds evidence for acculturation as the willingness of migrant Chinese managers changes with the length of their stay in the new society. Acculturation occurs relatively quickly and highly acculturated Chinese information-sharing behavior is not significantly different from the Australian-born subjects.

The aim of this evidence-, consensus- and outcome-based good clinical practice guideline is to help physicians, and women in making appropriate healthcare decisions about the early detection of breast cancer. The principle of early detection of breast cancer comprises the detection and diagnosis of pre-malignant breast tumours (UICC stage 0, carcinoma in situ) with a possible cancer risk reduction and the detection and diagnosis of breast cancer at an early stage (UICC stage 1) with a scientifically proven 90% chance of cure. By establishing a nation-wide comprehensive quality assurance program for the early detection of breast cancer this guideline lays the foundation for a timely reduction of breast cancer mortality and achievement of cure with less impairment of patient's quality of life. It would appear that this guideline makes major improvements in women's healthcare feasible.

The present analysis focuses on the long term psychological reactions to early stage breast cancer. Two hypotheses were formulated. The first hypothesis draws a direct link between tumour size/survival chances and Quality of life (QoL): The better the survival chances, the better QoL ('biological danger model'). The second hypothesis assumes that localized early breast cancer has excellent prognosis (90% five year survival rate), and that therefore QoL differences between various forms of early breast cancer should be minimal ('medico-pragmatic model').In a defined rural area with 252.000 inhabitants (small-area-analysis), a total of n = 389 patients with primary breast cancer were recruited. For the present analysis we selected a subgroup (n = 269) from the cohort by tumour size (pTis, pT1a,b, pT1c, and pT2). QoL scores for global quality of life, emotional functioning and future perspective were computed according to the EORTC manual and compared to age-matched norm data of the German population.A total of 690 QoL questionnaires were obtained from n = 269 patients with comparable completion rates within the four subgroups (pTis, pT1a,b, pT1c, and pT2). For all four groups and in all scores there were improvements over time. Generally, pTis always scored highest, pT2 always lowest, the other two groups in between. After one year pTis patients had higher mean scores in global quality of life than the norm. In contrast, pT1a,b were considerably lower than the norm and the difference between these two was 17.2 score points. It seems that the small difference (3.5%) in five year survival chances between pTis and T1 a,b tumours transforms into marked differences regarding quality of life, thus supporting a biological danger model of the survival/QoL relationship.Our results show that physicians have to realise although their early breast cancer patients have excellent survival chances, psychological distress is present. From a clinical perspective we would recommend that early stage breast cancer patients, and especially patients with occult, pT1a,b tumours be informed about their excellent prognosis. In addition, cognitive therapy might help patients stop worrying about their cancer.

Objective The goal of this work was to study the anticancer activity of cetrorelix, a decapeptide with LHRH receptor antagonist properties in patients with platinum-resistant ovarian cancer. About 80% of primary ovarian cancers and cell lines bear LHRH receptors. Cetrorelix has anticancer activity in in vitro and in vivo ovarian cancer models. Methods Eligible patients with ovarian or mullerian carcinoma resistant to platinum chemotherapy received cetrorelix 10 mg subcutaneously every day. Eligibility criteria included age ≥ 18, PS ≤ 2, measurable disease, chemistries and blood counts in normal range, no estrogen replacement for at least 2 weeks, and no known allergic reactions to extrinsic peptide. In patients volunteering for a biopsy, tissue was taken to perform a LHRH receptor assay. Results Seventeen patients were treated. Median age was 58 years. Median performance status was 0. Median number of prior chemotherapies was 3. Three patients had partial remissions lasting 9, 16, and 17 weeks. Toxicities effects included grade 4 anaphylactoid reaction (one patient) controlled by cortisol and cimetidine, grade 2 histamine reaction (two patients), grade 2 arthralgia (one patient) 20% cholesterol increase (two patients, who did not require specific treatment), minor hot flushes, headache, and local skin reaction at the injection site. Six of seven samples were LHRH receptor positive for mRNA and/or ligand assay. Two responding patients were LHRH receptor positive. The patient who had no receptor did not respond. Conclusion Cetrorelix has activity against ovarian cancer in this refractory population, and has minimal toxicity, except for potential anaphylactoid reactions. Activity may be mediated through the LHRH receptor.

Clinical breast examination (CBE) refers to the traditional technique of physical examination of the breast by a health care provider. The examination comprises both systematic inspection and palpation of the nipple, breast, and lymph-draining regions in the axillae and supraclavicular and infraclavicular fossae. CBE is the least studied of the modalities for breast cancer screening. Whereas recommendations for mammography and breast self-examination (BSE) can be based on the findings of randomized screening trials, there have been no randomized trials of CBE alone on which to base recommendations. However, there is considerable indirect evidence from studies that CBE can be recommended as a method for detecting breast cancer for public health benefit. The examination by itself is inexpensive, as no special equipment is required. It is easy to perform, it can be readily taught to health care providers, and it can be offered ubiquitously. CBE should be part of any program for early detection of breast cancer worldwide, provided that follow-up medical and oncology care is available. Physicians and women should be informed about the advantages and disadvantages of this modality, especially as there are no data from randomized trials about the contribution of CBE in detecting breast cancer at an early stage and the absolute benefit of this modality in reducing breast cancer mortality and improving quality of life. Further research on CBE should be promoted, especially in countries with limited resources, to evaluate its efficacy and effectiveness in relation to age, ethnicity, and race.

The present study investigates the population of beta 2-receptors on lymphocytes in pregnant women with premature labor between the 29th and 34th week of pregnancy. The population of receptors on lymphocytes correlates with that on the myometrium, which is not accessible for study during pregnancy. Fourteen patients received a pulsatile tocolysis, while ten women received a continuous tocolysis with Fenoterol. Assuming an equal population of receptors in both groups before commencement of therapy, the numbers of receptors in the patients with continuous tocolysis fell to about 35% of the initial value after 72 hours. Under pulsatile tocolysis, the numbers of receptors remained unchanged for a period of three days and was still only just below 70% of the initial value by the seventh day. Our data demonstrate that continuous administration of the short-acting beta 2-agonist Fenoterol resulted in a substantial loss of beta 2-adrenoceptors on lymphocytes. In contrast, intermittent administration of the same beta 2-adrenergic agonist prevented the onset of receptor down-regulation in pregnant women with preterm labor. Further studies are required to investigate the impact of the decreased loss of beta 2-adrenoceptor density on the good clinical experience with intermittent tocolysis.

the aim of this study was to evaluate the influence of serum leptin concentration on bone mass assessed by quantitative ultrasound (QUS) in a large sample of healthy pre and postmenopausal women.555 healthy pre and postmenopausal (n=261 and n=294) women (mean age, 49.5+/-17.2 years) not on hormone replacement therapy were recruited on the occasion of a routine gynecological visit. Before entry to the study, all women had answered a detailed questionnaire on important risk factors and gave written informed consent. Speed of sound (SOS), broadband ultrasound attenuation (BUA) and stiffness index (SI) of the os Calcis were measured using the Achilles ultrasonometer (GE/lunar). We systematically investigated the relation of menopause, BMI and leptin on bone mass by allocating women into the following groups: (a) premenopausal women BMI25 kg/m(2) (N=178); (b) premenopausal women BMI25 kg/m(2) (N=83); (c) postmenopausal women BMI25 kg/m(2) (N=125); and (d) postmenopausal women BMI25 kg/m(2) (N=169). Additionally we investigated the relation of serum leptin concentrations, age and BMI on ultrasonometry variables by performing a multiple linear regression analyses.in the initial analyses premenopausal women showed a significantly (P0.001) lower mean age, weight, BMI, follicle stimulating hormone (FSH) and leptin concentration, a higher mean height, serum estradiol and ultrasonometry variables in comparison to postmenopausal women. Irrespective of the menopausal status, women with a BMI25 kg/m(2) had significantly higher leptin concentrations (P0.001) and BUA (P0.05) whereas SOS and SI was not significant different, compared to women with a BMI25 kg/m(2). The multiple linear regression analyses showed that only BMI but not Leptin was related to higher ultrasonometry variables, whereas increasing age was associated with a decrease in ultrasonometry variables. Furthermore, the multiple linear regression analyses confirmed that age and BMI were the only statistically significant independent predictor for ultrasonometry variables. There was no significant influence of leptin on ultrasonometry variables even after controlling for BMI or age, or BMI and age.serum leptin concentrations are significantly higher in pre and postmenopausal obese women, compared with normal weight controls. Ultrasonometry variables are influenced by age and BMI but not by serum leptin concentrations.

Eighty percent of human ovarian and endometrial cancers express receptors for luteinizing hormone-releasing hormone (LHRH). These receptors might be used for targeted chemotherapy with cytotoxic LHRH analogs such as AN-152, in which doxorubicin is linked to agonist carrier [D-Lys6]LHRH. The antiproliferative effects of doxorubicin and AN-152 were assessed in LHRH receptor-positive ovarian (EFO-21, EFO-27) and endometrial (HEC-1A, Ishikawa) cancer cell lines as well as in LHRH receptor negative ovarian SKOV-3 and endometrial MFE-296 lines. The mechanism of action of AN-152 was investigated by a blockage of receptors using an excess of the LHRH agonist [D-Trp6]LHRH. In some cases, confocal laser-scanning microscopy was used to visualize the accumulation of AN-152 or doxorubicin within the cells. In 3 of 4 LHRH receptor-positive cell lines (EFO-21, HEC-1A, Ishikawa) AN-152 was more effective than doxorubicin in inhibiting cell proliferation. The effect of AN-152 was shown to be receptor-mediated because it could be reduced by competitive blockade of the LHRH receptors with [D-Trp6]LHRH. In contrast, AN-152 was less active than doxorubicin in LHRH receptor-negative lines. Confocal laser-scanning microscopy showed an intranuclear accumulation of AN-152 and competitive inhibition thereof by [D-Trp6]LHRH in LHRH receptor-positive cell lines, but no intracellular accumulation of AN-152 could be detected in the receptor-negative SKOV-3 line. These results suggest a selective receptor-mediated action of AN-152 in receptor-positive cell lines.

OBJECTIVE: The aim of this study was to evaluate the influence of menopausal status, serum estradiol and body mass index (BMI) on serum leptin concentration in a large sample of pre- and postmenopausal women. DESIGN: 434 healthy women (mean age +/-s.d., 52.2 +/- 10.3 years) were recruited at the University of Marburg on the occasion of a routine gynecological visit. Two hundred and eighteen (50.2%) women were premenopausal (mean age, 36.5 +/- 10.4 years) and not on oral contraceptives or hormone replacement therapy (HRT) and 216 (49.8%) women were postmenopausal (mean age 61.8 +/- 8.9 years) not on HRT. To evaluate the influence of menopausal status, estradiol level and BMI on serum leptin concentrations, women were allocated to one of the four groups: (a) premenopausal women BMI 25 kg/m(2) (n=81), (c) postmenopausal women BMI 25 kg/m(2) (n=122). RESULTS: Irrespective of the menopausal status, women with a BMI >25 kg/m(2) had significantly higher leptin concentrations in all age groups compared with women with a BMI

OBJECTIVE: To evaluate the impact of long-term, non-suppressive levothyroxine (L-T(4)) treatment on quantitative ultrasonometry in women. DESIGN: This was a case-control study. SUBJECTS AND METHODS: Altogether 667 women (mean age+/-s.d., 49.5+/-13.1 years) were studied. Of these, 156 (23%) had non-toxic goitre or hypothyroidism and had been taking L-T(4) (75-100 microg/day) for at least 5 years (mean+/-s.d., 12.5+/-7.5 years); the remaining 511 (77%) women were not receiving L-T(4). All women had completed a questionnaire on risk factors for thyroid dysfunction and osteoporosis, and those with diseases or treatments known to effect bone metabolism - other than thyroxine or hormone replacement therapy (HRT) - were excluded. Women underwent quantitative ultrasonometry (QUS) at the heel. Speed of sound (SOS), broadband ultrasound attenuation (BUA) and the stiffness index (SI) were compared, first, in all women taking L-T(4) and controls and, secondly, in women taking L-T(4) and controls pair-matched for age, weight, body mass index (BMI), menopausal status and HRT use. RESULTS: Even after matching for age, weight, BMI, menopausal and HRT status, women taking L-T(4) had significantly lower values for SOS and SI (P

This study assessed age changes in quantitative ultrasound sonometry (QUS) in a large sample of healthy German women. Speed of sound (SOS), broadband ultrasound attenuation (BUA), and stiffness index (SI) of the calcaneus were measured in 1333 women (mean age 50.5 +/- 11.5 years) using the Achilles ultrasonometer (Lunar Corp., Madison, WI, USA). The short-term precision in 31 adults was 0.2% for SOS, 1. 2% for BUA, and 1.3% for SI. There was an overall decline of 15% for BUA, 4% for SOS, and 31% for SI between late adolescence and old age. In premenopausal women, BUA decreased only slightly (-3%), whereas postmenopausal women showed a significantly increased decline (-12%). In contrast, SOS continuously decreased from the age of 15; there was a decline of 2% from adolescence to the menopause; postmenopausal women showed a slightly larger decline (-2.5%). The SI of premenopausal women decreased by 10%, but the postmenopausal decline of almost 22% was significantly greater. SI values for premenopausal German women were comparable to those observed in the American Achilles reference population, but postmenopausal German women had significantly higher SI values of 7% due to a lower rate of aging loss.

The expression of luteinizing hormone-releasing hormone (LHRH) and its receptors has been demonstrated in a number of human malignant tumors, including cancers of the breast, ovary, endometrium and prostate. These findings suggest the presence of an autocrine regulatory system based on LHRH. Recent studies in our laboratory have demonstrated that the function of LHRH produced by ovarian cancer cells is the inhibition of their proliferation. Dose-dependent antiproliferative effects of LHRH-agonists have been observed by several laboratories in cell lines derived from the above cancers. Interestingly, also LHRH-antagonists have marked antiproliferative activity in most of the ovarian, breast and endometrial cancer cell lines tested so far, indicating that the dichotomy of LHRH-agonists/LHRH-antagonists is not valid for the LHRH-system in cancer cells. In addition, our data suggest that the classical LHRH receptor signal transduction mechanisms known from the pituitary (phospholipase-C, protein kinase C, adenylyl cyclase) are not involved in the mediation of LHRH effects in cancer cells. Data obtained by several groups, including ours, rather suggest that LHRH analogs interfere with the signal transduction of growth-factor receptors and related oncogene products associated with tyrosine-kinase activity. The mechanism of action is probably an LHRH-induced activation of a phosphotyrosine phosphatase, counteracting the effects of receptor associated tyrosine kinase. In our hands, LHRH analogs virtually blocked the EGF-induced MAP-kinase activity of ovarian and endometrial cancer cells. The pharmacological exploitation of this mechanism might provide promising new therapies for these cancers.

Human endometrial carcinoma cell lines were established by using a new cell culture technique. The malignant endometrial tumors were grossly disaggregated by mechanical means and cultivated in suspension culture. Adhesion to the bottom of the culture flasks was prevented by first coating the flasks with a thin agarose layer. Four cell lines were derived from 17 samples by this new technique. The cell lines obtained in this way were fully characterized, including karyotyping, intermediate filament staining and transplantation to nude mice. This new technique of initial suspension culture may also be applicable to other human tumors that are equally difficult to cultivate in vitro.

Ortmann O, Ansari-Pirsarai B, Bloh P, Schulz K-D, Emons G. Modulatory actions of progesterone on gonadotropin-releasing hormone-induced arachidonic acid liberation from perifused rat pituitary cells. Eur J Endocrinol 1996;135:626–30. ISSN 0804–4643 The stimulatory action of gonadotropin-releasing hormone (GnRH) on gonadotropin secretion from cultured rat pituitary cells is modulated by estradiol and progesterone. Recent studies provided evidence that both steroids exert effects on different pathways of GnRH signal transduction, which might be responsible for their actions on luteinizing hormone (LH) release. Here we investigated whether the steroids are able to modulate GnRH-induced liberation of arachidonic acid, which is thought to be involved in GnRH signal transduction. Pituitary cells obtained from female rats were treated for 48 h with vehicle, 1 nmol/l estradiol or 1 nmol/l estradiol +100 nmol/l progesterone, 48 h with 1 nmol/l estradiol and 2 h with 100 nmol/l progesterone. In addition, these cells were prelabeled with [3H]arachidonic acid. Then the cells were transferred to a perifusion system and challenged with a 6-min pulse of 100 nmol/l GnRH. Estradiol treatment enhanced the LH secretory response while GnRH-induced [3H]arachidonic acid liberation remained unaffected. However, progesterone modulated both LH secretion and [3H]arachidonic acid release in response to the GnRH stimulus. The shortterm progesterone treatment paradigm enhanced the LH and arachidonic acid responses by up to 160 ±13 and 204 ±18%, respectively, while long-term treatment was inhibitory (59 ± 9 and 63 ± 4% vs control). Because arachidonic acid has been shown to be involved in GnRH signal transduction, it seems reasonable to speculate that the actions of progesterone described in the present study are related to its modulatory effect on GnRH-induced LH secretion. O Ortmann, Department of Obstetrics and Gynecology, Medical University of Lübeck, Ratzeburger Allee 160, D-23538 Lübeck, Germany

In addition to their antiprogestational activity, the antiprogestins RU486, ZK98.299 and ZK98.734 possess varying antiglucocorticoid as well as androgen-like or antiandrogen-like properties in human mammary cancer cells. The human mammary cancer cell line MFM-223, which contains only androgen receptors, was used as a model to investigate androgen receptor mediated effects of these antiprogestins. Proliferation of MFM-223 cells is inhibited by androgens and does not respond to oestrogens, progestins and glucocorticoids. As shown in proliferation assays, ZK98.734 was a strong inhibitor of cell proliferation. This effect was antagonised by the antiandrogen hydroxyflutamide. ZK98.734 was found to displace [3H]R1881 from the androgen receptor in MFM-223 cells, substantiating the involvement of the androgen receptor. The antiprogestin ZK98.299 failed to influence the proliferation of MFM-223 cells. ZK98.299 did not bind to the androgen receptor and was devoid of androgenic or antiandrogenic activity. RU486 bound to the androgen receptor. It was a weak inhibitor of MFM-223 cell proliferation, but the inhibition of proliferation by RU486 was not antagonised by hydroxyflutamide. This effect was probably not mediated by the androgen receptor. RU486 had antiandrogenic activity in this cell line, as it antagonised the inhibitory effect of dihydrotestosterone at a 100-molar excess. These results were confirmed by transfection experiments with an MMTV-CAT construct in the same cell line, demonstrating the biological function of the ZK98.734-androgen receptor complex. ZK98.299 and RU486 were not able to induce CAT activity. The different androgenic or antiandrogenic properties of the antiprogestins investigated should be considered when selecting antiprogestational properties of the antiprogestins investigated should be considered when selecting antiprogestational compounds for clinical applications, as a partial androgenic activity may be of benefit in breast cancer but can have undesired side-effects in other diseases.

Androgens are involved in many regulatory processes in mammary and endometrial epithelium, but their role in the development and progression of breast and endometrial carcinoma is poorly understood. Androgen receptors (AR) are found in normal epithelium as well as in more than 50% of specimen from both tumor types. The occurrence of AR is correlated with estrogen and progesterone receptors. Androgen receptor positive cell lines were established during the last few years in our laboratory from malignant mammary (MFM-223) and endometrial (MFE-296) tumors supplementing the small number of androgen-responsive cell lines published so far. In this paper some aspects of the role of androgens in these two types of hormone responsive female cancers are presented. The proliferation of ZR-75-1, MFM-223 and MFE-296 cells is inhibited by androgens. The progestin medroxyprogesterone acetate inhibits the proliferation of estrogen- and progesterone receptor negative MFM-223 cells via the androgen receptor. Some steroid metabolites with distinct estrogenic properties like androst-5-ene-3 beta,17 beta-diol possess androgenic properties in this model system. Androgens stimulate the in vitro secretion of gross cystic disease fluid proteins by human mammary cancer cells. These proteins are normally found in benign breast cysts in vivo. The occurrence of gross cystic disease is correlated with an increased risk of breast cancer. The AR is autoregulated in MFM-223 mammary cancer cells on the protein and mRNA level. In MFE-296 cells with endometrial origin AR protein was increased after incubation with androgens.

Recent results have shown that specific binding sites for luteinizing hormone-releasing hormone (LHRH) are present in biopsy samples of human endometrial cancer and in the human endometrial cancer cell lines Ishikawa and HEC-1A. The proliferation of these cell lines was retarded by LHRH analogs. The present study was undertaken to determine whether these endometrial tumor cells also produce LHRH or an LHRH-like peptide which could serve as natural ligand for the LHRH binding sites. Using a specific antibody, LHRH-immunoreactivity was detected in extracts of Ishikawa (426 +/- 84 fmol/10(6) cells) and HEC-1A (368 +/- 41 fmol/10(6) cells) cells. LHRH-like bioactivity of these samples was assessed in a rat pituitary cell culture system. The release of luteinizing hormone induced by endometrial cancer cell extracts corresponded to that obtained with comparable amounts of authentic LHRH. The expression of the mRNA for LHRH could be demonstrated by reverse transcriptase - polymerase chain reaction using specific primers according to the published sequence and by subsequent Southern blot analysis. The presence of immuno- and bioactive LHRH-like factors and the demonstration of expression of the mRNA for LHRH in two human endometrial cancer cell lines supports the concept of an autocrine regulatory system based on LHRH in endometrial cancer.

The ability of ovarian steroids to sensitize and desensitize the pituitary gonadotroph to hypothalamic gonadotrophin-releasing hormone (GnRH) is essential for their modulatory actions on gonadotrophin secretion. The time-dependent actions of progesterone on GnRH-stimulated gonadotrophin secretion from cultured pituitary cells obtained from female rats were examined. Progesterone induced an acute stimulatory effect on luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion in cell perifusion studies, from as early as 50 min after the onset of progesterone treatment. Long-term incubation (52 h) of pituitary cells in static culture reduced the responsiveness of the gonadotroph to GnRH. The antiprogestins RU486, ZK 98.299, and ZK 98.734 blocked both the acute facilitatory and the long-term inhibitory action of progesterone. In the absence of progesterone, the antiprogestins per se induced marked inhibitory and stimulatory effects on GnRH-stimulated LH secretion. In brief, short-term treatment of non-oestrogen-primed cells with antiprogestins was ineffective (ZK compounds) or reduced LH secretion (RU486), while long-term treatment was stimulatory. Oestrogen-primed cells exerted exclusively inhibitory effects on GnRH-induced LH secretion. In conclusion, antiprogestins are effective antagonists of progesterone actions in the gonadotroph. However, they exert diverse actions on gonadotrophin secretion in the absence of progesterone, which might interfere with their antagonistic properties.

MFE-296 endometrial cancer cells express androgen receptors in vitro. These cells, which are tumorigenic in nude mice, are derived from a moderately differentiated human endometrial adenocarcinoma. They express vimentin and the cytokeratins 7, 8, 18, and 19. Karyotyping revealed near-tetraploidy for most of the cells. No marker chromosomes were observed. DNA analyses confirmed the genetic identity of the cell line and the patient from whom the cell line was derived. Proliferation of MFE-296 cells was inhibited by the progestin R5020 and the androgen dihydrotestosterone (DHT). The inhibition of proliferation by DHT was antagonized by the antiandrogen Casodex, demonstrating the involvement of the androgen receptor. Androgen binding was determined at 22,000 binding sites per cell using a whole-cell assay (KD = 0.05 nM) and 30 fmol/mg protein with the dextran charcoal method; 7 fmol/mg protein of progesterone receptors were found, whereas estrogen receptors were below 5 fmol/mg protein. The androgen receptor was functionally intact, as demonstrated by transfection experiments with a reporter-gene construct, containing an androgen-responsive element. In MFE-296 cells the content of the androgen receptor was up-regulated by its own ligand.

Cells of the human ovarian carcinoma lines EFO-21, EFO-27, MFO-35 and MFO-36 secrete binding proteins for insulin-like growth factors (IGFBPs) into their culture media. By sodium dodecyl sulfate/polyacrylamide gel electrophoresis (SDS-PAGE) and ligand blotting, seven groups of IGFBPs with molecular masses of 25, 30 (doublet), 34, 37, 40, 45, and 50 kDa were observed, depending on the cell line under investigation. By Northern blot analyses using cDNAs or oligonucleotides specific for the six types of IGFBP (IGFBP-1 to IGFBP-6), mRNA for all IGFBPs tested except for IGFBP-1 could be detected in the ovarian carcinoma cell extracts. In detail, analysis of EFO-21 protein products by SDS-PAGE yielded IGFBPs of 25, 34, and 50 kDa; extracts of EFO-21 cells contained mRNAs for IGFBP-2, -3, -4, and -6. EFO-27 cells produced IGFBPs of 40 kDa and 45 kDa as determined by SDS-PAGE, and mRNAs for IGFBP-3, -4, and -6 were detected. In the conditioned medium of MFO-35 cells, IGFBPs of 25, 30 (doublet), 34, 37, 40, and 45 kDa were observed by SDS-PAGE, while mRNAs for the five proteins IGFBP-2 to IGFBP-6 were found. MFO-36 cells produced IGFBPs of 34 kDa and 50 kDa as determined by SDS-PAGE, and the cells expressed mRNAs for IGFBP-2, -3, -4, and -6. In relation to published molecular mass data of the known IGFBPs, the size of the secreted proteins could be correlated to the mRNA patterns expressed by the ovarian carcinoma cells. It is concluded that ovarian carcinoma cells frequently express IGFBP-3, -4, and -6 and, to a lesser extent, IGFBP-2; the expression of IGFBP-5 appears as a rather rare event, while IGFBP-1 was not found to be expressed in ovarian carcinoma cells.

It has been demonstrated that endothelins (ETs) induce LH secretory responses in cultured rat pituitary cells. Because estradiol and progesterone are known to be potent modulators of GnRH-induced gonadotropin secretion, we examined whether these steroids also influence the secretory responses of gonadotrophs to ETs. Cultured female rat pituitary cells were treated for 48 h with vehicle (0.2% ethanol), 1 nM estradiol alone, or a combination of 1 nM estradiol and 100 nM progesterone or for 48 h with 1 nM estradiol and a further 4 h with 100 nM progesterone and subsequently stimulated with 10 pM-100 nM ET-1 or ET-3. Forty-eight-hour estradiol treatment led to enhanced LH secretory responses to both ETs. This action was facilitated by short term progesterone treatment (3-fold vs. vehicle), while long term progesterone treatment was inhibitory. Perifusion experiments were performed to study the kinetics of individual and pulsatile LH secretory responses after steroid exposure of pituitary cells. ET-1 induced immediate biphasic LH responses that were augmented by long term estradiol treatment. Two-hour progesterone exposure led to marked increases in LH secretion, whereas 48-h progesterone treatment was inhibitory. Estradiol and progesterone were able to modulate both the initial spike and the secondary plateau phase of the secretory profile in response to ET-1, although these actions did not always reach statistical significance. The steroid treatment paradigms employed also induced inhibitory and stimulatory effects in cells that were stimulated with ET-3 in a pulsatile fashion. In these experiments it could be demonstrated that the facilitatory action of progesterone was present after 50 min of treatment and was maximum after 150 min (5-fold enhancement). The present data support the hypothesis that ETs are involved in the physiological regulation of gonadotropin secretion and demonstrate that ovarian steroids can act as potent modulators of ET-induced LH secretion.

Androst-5-ene-3 beta,17 beta-diol (ADIOL) and 5 alpha-androstane-3 beta,17 beta-diol (5 alpha A), which are metabolites of dehydroepiandrosterone and dihydrotestosterone, are known to have estrogenic properties. This study reevaluates the estrogenic effects of ADIOL and 5 alpha A in MCF-7 cells and demonstrates additionally androgen-like inhibitory properties of these compounds in human hormone-dependent mammary cancer cells. ADIOL and 5 alpha A (10-100 nM) stimulate the proliferation of estrogen-sensitive MCF-7 cells. Binding assays with the estrogen receptor and inhibition of stimulation with the antiestrogen tamoxifen support the involvement of the estrogen receptor. On the other hand, the mammary cancer cell line MFM-223 is strongly inhibited by ADIOL and 5 alpha A in the same concentration range. This cell line is androgen receptor positive and is inhibited by androgens, but unresponsive to estrogens and progestins. The inhibitory effects of ADIOL and 5 alpha A in MFM-223 cells are mediated by the androgen receptor as demonstrated by receptor studies and competition experiments with hormone antagonists. ADIOL and 5 alpha A thus possess estrogen- and androgen-like properties and can stimulate or inhibit proliferation of human mammary cancer cells. The reactions of mammary cancer cells to these steroids depend on the receptor content and the growth properties of the individual cell line.

Obwohl s-Mimetika derzeit die effektivsten Medikamente zur Unterdruckung vorzeitiger Wehen sind, ist der Nutzen der Therapie, sowie Dauer und Wahl des Zeitpunkts in der Schwangerschaft Gegenstand der Diskussion. Ziel unserer Studie war es, anhand objektivierbarer Kriterien eine optimale tokolytische Therapie unter gleichzeitiger Minimierung der mutterlichen Nebenwirkungen zu erreichen. Der Angriffspunkt der eingesetzten s-Mimetika ist der s-2-Rezeptor am Uterus. Dieser ist zwar in der Schwangerschaft nicht untersuchbar, jedoch steht uns mit den s-Rezeptoren auf Lymphozyten im peripheren Blut ein beobachtbares Modell zur Verfugung, das ausreichend Ruckschlusse auf die Vorgange am Uterus selbst erlaubt.

Die ovariellen Steroide Ostradiol (E) und Progesteron (P) sind potente Modulatoren der GnRH-induzierten Gonadotropinsekretion. Jungere Untersuchungen habengezeigt, das die Steriodeffekte uber einen Einflus auf das GnRH-Signaltransduktionssysthem vermittelt werden konnen. (1). Der Anstieg der intrazellularen Ca2+-Konzentration nach Agonist-Stimulation der gonadotropinen Zellen gilt als der zentrale Signaltransduktionsmechanismus (3). Wir gingen der FRagen anch, ob die modulatorischen Effekte von E und P uber eine Wirkung der Steriode auf den Ca2+-Influx durch Spannungsabhangige Ca2+-Kanale (VSCC) in die Hypophysenzelle vermittelt werden konnen.

Laboruntersuchungen sind fester diagnostischer Bestandteil bei der Uberwachung von Tumorpatienten (1, 2, 3). Die vorliegende Studie untersucht die Wertigkeit der etablierten biochemischen Laborparameter (Tumormarker, BSG, Leberenzyme, alk. Phosphatase) fur die Fruherkennung einer Metastasierung beim Mammakarzinom.

Die zunehmenden Anforderungen an Dokumentation, Statistik und Leistungserfassung ganz allgemein lassen in der Medizin den Einsatz der EDV primar sinnvoll erscheinen. Leider sind es oft unausgereifte Programme, die eher den Anforderungen der Verwaltung als den Notwendigkeiten des klinischen Alltags entsprechen, die zur groser Frustration beim Einsatz des Computer fuhren. Auf der Basis der seit vielen Jahren eingefuhrten EDV-Dokumentation im OP ensteht derzeit in Marburg ein Software-Paket, das die Routinearbeiten auf unseren operativen Stationen erleichtern soll.

Die operative Therapie des Mammakarzinoms hat sich in den letzten zehn Jahren entscheidend gewandelt. Die Ergebnisse internationaler und deutscher Therapiestudien (1, 2, 3) zeigten deutlich, das eingeschrankt operative Behandlungsverfahren unter Beachtung bestimmter operativer und patho-histologischer Kriterien radikal operativen Masnahmen im Bereich der weiblichen Brust nicht unterlegen sind. Sogenannte brusterhaltende Operationsverfahren stellen somit in Kombination mit einer unabdingbaren postoperativen Nachbestrahlung der Brust eine feste Grose im Rahmen der Mammachirurgie dar. Es ergeben sich jedoch in einer Vielzahl der Falle Kontraindikationen zur brusterhaltenden Behandlung und zwar nicht nur auf der Basis tumorbiologischer und patho-histologischer Befunde, sondern vielmehr existieren auch relevante Kontraindikationen aus rein kosmetischer Sicht. Bei einem Tumorsitz im oberen inneren oder unteren inneren Qudranten der Brust wird in vielen Fallen bei ausreichender Resektion des Tumors im Gesunden der Parenchymdefekt so gros, das es in Folge zur Deformation der Brust kommt. Im Falle einer ausgesprochenen Makromastie lassen sich zwar grose Substanzdefekte operativ ohne Probleme beseitigen, jedoch ruckt hier die strahlentherapeutische Problematik der homogenen Dosisverteilung bei grosem Brustvolumen in den Vordergrund. In der vorliegenden Studie wurde nun versucht durch besondere Schnittfiguren in den oben gennanten beiden Situationen ein brusterhaltendes Operationsverfahren moglich zu machen.

Wesentlicher Bestandteil prognostischer Aussagen und therapeutischer Entscheidungen in der gynakologischen Onkologie waren und sind die klinischen Befunde, sowie verschiedene makroskopische und mikroskopische Kriterien der untersuchten Tumoren. Sie stellen jedoch nur Momentaufnahmen eines sehr komplexen Krankheitsverlaufes dar. Momentaufnahmen konnen jedoch immer nur ein sehr grobes Raster fur die tatsachliche Einschatzung individuellen Tumorwachstums liefern. Therapeutische und prognostische Fehlentscheidungen ergeben sich zwangslaufig. Neue Wege resultieren aus der Erkenntnis, das proliferationskontrollierende Signale im gesunden Gewebe, aber auch in Malignomen einer Rezeptorvermittlung bedurfen. Inzwischen wissen wir, das auch andere humorale Einflusse, ebenso wie Zell-Zell-Interaktionen und von der Tumorzelle selbst gebildete Regulatoren nur uber entsprechende Rezeptoren wirksam werden konnen. Die routinemasige Bestimmung verschiedener Rezeptoren im Tumorgewebe wurde zum Hoffnungstrager fur eine therapie-relevante Definitionsmoglichkeit individueller Wachstumscharakteristika unterschiedlicher Krebsformen. Die nachfolgenden Ausfuhrungen sollen eine kritische Analyse dieses Konzeptes auf der Basis neuerer tumorbiologischer Erkenntnisse darstellen.

Kurzlich konnte unsere Arbeitsgruppe nachweisen, das operativ entfernte Endometri- umkarzinome in ca. 80% der Falle spezifische Bindungsstellen fur Luteinisierendes Hormon Releasing Hormon (LHRH)-Analoga besitzen (3,4). Wir prufen nun, ob diese Bindungsstellen direkte Effekte auf die Proliferation dieser Tumoren vermitteln konnten.

The regulation of the human androgen receptor (AR) by steroid hormones in human mammary cancer cells was investigated using immunocytochemical and ligand binding assays for its protein and Northern blot analyses for the corresponding mRNA. MFM-223 cells contain high levels of ARs and are growth-inhibited by dihydrotestosterone (DHT). The AR protein is down-regulated to 57% of the control by 10 nM DHT after 24 h, and the corresponding mRNA is also reduced. The nonsteroidal antiandrogen hydroxyflutamide had no effect on the AR level, whereas after incubation with 1 microM cyproterone acetate a slight down-regulation was observed. The AR level was restored completely after release from a 7 day treatment with DHT. However, only 60% of the control level was restored, if the cells wer grown in the presence of DHT for 6 weeks. In androgen-pretreated cells the proliferation rate remained decreased even after the withdrawal of DHT. Concomitantly the distinct growth inhibition was lost. Transfection experiments demonstrated a reduced activity of the residual androgen receptor in these pretreated cells. In addition to the AR, EFM-19 cells also contain significant amounts of estrogen and progesterone receptors. EFM-19 cells are not growth inhibited by physiological concentrations of DHT. Autoregulation of AR was also found in this cell line. Additionally, reduced levels of AR protein and mRNA were found in EFM-19 cells after treatment with the synthetic progestin R5020. The maximum effect of R5020 was observed at the high concentration of 1 microM. Estrogen treatment with 10 nM 17 beta-estradiol for 3 days reduced the AR level only by 25%.

Twenty-seven patients with uterine fibroids were treated for 3 months with the GnRH-agonist goserelin prior to surgical myomectomy. Ovarian function was suppressed reliably in all patients. After three applications, 15 fibroids were reduced in volume by more than 50%, and one complete remission was achieved. Seven patients showed a decrease of 10-50% in volume. However, in 5 cases there was no significant reduction. Analysing the time course of the fibroid reduction, the response can be predicted in most cases as early as four weeks after the first injection. Retrospective statistical analysis showed that a 50% reduction in fibroid size due to GnRH treatment is preceded by a 35% reduction after 4 weeks in 81% of cases, and after 8 weeks in all cases. Only 2 of 12 fibroids, which showed a smaller response (less than 50%) to GnRH therapy, were reduced by more than 35% after 4 and 8 weeks. In most cases it seems to be possible to estimate the individual response to GnRH-application after the first injection, so that it is possible to stop therapy in non-responding patients.

Ovarian carcinoma is one of the most common causes of cancer death in women. During the last decade there have been some advances in surgical, radiation, and cytotoxic chemotherapy of this malignancy. The overall results of these treatments, however, are still disappointing (MRC Gynecologic Cancer Working Party 1990; Averette and Donato 1990; Blackledge and Lawton 1989). Aggressive chemotherapy is burdened with severe acute side effects. In addition, chemotherapy in ovarian cancer is associated with a 4–12 times higher risk of developing leukemia (Kaldor et al. 1990). One trend in modern oncology has been to reduce at least therapy-induced morbidity, if the efficacy of therapy cannot be improved by increased aggressiveness. With breast and endometrial cancer this has been successfully achieved by the introduction of endocrine treatments, both ablative or additive, that take advantage of the sex-steroid dependence of some of these tumors, as reflected by the presence of estrogen and/or progestin receptors (Desombre et al. 1987). Also many ovarian cancers contain significant amounts of sex-steroid receptors. Therapeutic approaches, however, using either antiestrogens or progestins, have not been satisfying (for review, see Desombre et al. 1987; Rao and Slotman 1991).

The mortality risk in rupture of an aneurysm of the splenic artery is 69.4% for pregnant women and 90.8% for the foetus. 95% of all patients are asymptomatic up to this stage. If the aneurysm is diagnosed earlier, the maternal mortality rate can be reduced to 0.5% by prophylactic surgery. 25% of patients with symptoms display prodromes which, with accurate knowledge of the syndrome, make it possible to make an early diagnosis. Characteristics of the disorder, its risk factors, signs for early diagnosis and therapeutic measures, as well as an up-to-date review of the literature are presented here, illustrated by one of our own case studies.

Die Bestimmung von Tumormarkern als Erganzung zur klinischen und serologischen Diagnostik in der Verlaufskontrolle von Mammakarzinompatientinnen ist auf der Basis retrospektiver Untersuchungen etabliert. Unsere prospektive Studie untersucht die Validitat der CA 15.3 und CEA Bestimmung zur Fruherkennung einer Disseminierung beim Mammakarzinom im Rahmen der Nachsorge.

Antigestagene stellen eine neue Gruppe von Hormonantagonisten dar. Um die Einsatzmoglichkeiten dieser Substanzen in der Behandlung des Mammakarzinoms zu prufen, wurde die Wirkung der Progesteronantagonisten ZK 98.299 und ZK 98.734 auf humane MammakarzinomzeUen in vitro untersucht.

Die in einem gynakologischen oder auch sonstigen OP zu erfassenden Daten stellen fur den Computer, und insbesondere fur den Personal Computer (PC), ein ideales Einsatzgebiet dar. Unter der Vorstellung der Erfassung der Daten am Entstehungsort wurde an unserer Klinik ein Programm entwickelt, das die Routine-Aufgaben der Datenerfassung und Datenauswertung im OP schnell und bequem erledigt. Die Eingabe der Daten erfolgt durch die OP-Schwestern anstatt der Fuhrung des OP-Buches.

Noch vor wenigen Jahren wurde das Endometriumkarzinom als harmloser Tumor eingestuft, dessen Diagnose und Therapie im Vergleich zu Malignomen anderer primarer Organlokalisation unproblematisch erschien. Die bevorzugte Entstehung des Endometriumkarzinoms bei Frauen hoheren Lebensalters fuhrte zusatzlich zu einer Fehleinschatzung der gegenwartig erkannten Problematik. Unter Bezugnahme auf die verfugbaren Zahlen des Annual-Report hat sich wahrend der letzten Jahrzehnte eine enttauschend geringe Verbesserung der Heilungsergebnisse von etwa 10% herausgestellt. Dies wurde nicht durch eine Verbesserung der Therapie selbst, sondern lediglich durch eine bessere Nutzbarkeit langst etablierter Therapiemoglichkeiten erreicht. Diese Verdienste sind den modernen Entwicklungen in der Anasthesie und Intensivmedizin zuzuschreiben und nicht etwa Fortschritten in der onkologischen Forschung.

The failure of early studies to detect IgA on mucosal membranes and the lack of a reason to assume the presence of secretory antibody for many years preserved the dogma that mucosal membranes are without specific protection at the time of birth. In recent years secretory IgA (S-IgA) and IgM antibodies to Escherichia coli, to poliovirus type I and to milk proteins have been identified in the saliva of newborn infants1,2. S-IgA anti-β-lactoglobulin (BLG) and S-IgA anti-casein (Cas) were found independently of the mode of feeding, could be specifically blocked but were not blocked by preincubation with unrelated protein. In a subsequent study in which 158 infants were investigated, such antibodies were shown to be consistently present3; IgA accounted for the majority of specific binding. Comparison of infants with and without risk of allergy showed a significantly higher salivary S-IgA anti-Cas in infants at risk for allergy. In a follow-up of these 158 infants over 3 and 6 months of age, breast-fed infants had significantly lower antibody titers than formula-fed infants. This was unrelated to the amount of cow protein antigen received by the infants; breastfeeding of even 1–3 weeks duration resulted in suppression of S-IgA antibody formation4. The following paper will describe the relationship between elevated concentrations of anti-Cas antibodies at birth and the appearance of atopic disease during the first year of life. Data will also be shown from a second group of 108 infants whose secretory antibody response to respiratory syncytial virus (RSV) was determined at birth, 3 months, 6 months and 1 year of age.

Die Wachstumsfaktoren EGF, IGF-1 und IGF-2 sind mogliche Mediatorpeptide in einer autokrinen Wachstumsregulation von Mammakarzinomen. In vitro konnen Mammakarzinomzellen EGF- und IGF-ahnliche Peptide produzieren; auserdem wurde die Sekretion von Bindungsproteinen fur IGFs (IGFBPs) beobachtet. In der voruegenden Arbeit haben wir den Einflus von EGF, IGF-1 und IGF-2 auf die Proliferation der Ostrogen-sensitiven, menschlichen Mammakarzinom-Zelllinie EFM-19 (Simon et al. 1984) bestimmt, die membranstandigen Bindungsstellen der Zellen fur die Faktoren charakterisiert und die zellulare Sekretion von IGFBPs untersucht.

Considerable evidence exists that ovarian cancer might be gonadotrophin-dependent. Receptors for LH and FSH have been discovered in these tumors. Proliferation of ovarian cancer cells in vitro could be stimulated by gonadotrophins. Withdrawal of LH and FSH in animal models of ovarian cancer inhibited growth of these tumors. Phase-II clinical studies have shown that suppression of endogenous gonadotrophins by LHRH-agonists can be beneficial in women with advanced ovarian cancer. Respective controlled clinical trials are performed at present. Also direct effects of LHRH analogues on ovarian tumors have been reported. An LHRH like protein was found in human ovarian tissue. We discovered a specific LHRH binding site (mol. wt 63.2 kDa) in ovarian cancer tissue which is very similar to other human extrapituitary LHRH binding sites, of the low-affinity, high-capacity type, e.g. in breast cancer and the placenta. In the latter tissues, LHRH or a related substance has been proposed as an autocrine regulator of cellular function. If this was also the case in ovarian cancer, direct effects of LHRH analogs on the tumor cells could be used as additional therapeutical points of attack.

The study reports the C-reactive protein (CRP) plasma concentrations in 115 women with a presumed diagnosis of acute adnexitis. In addition to CRP, blood sedimentation rate, white blood cell count and the body temperature were evaluated and compared with the clinical findings. Diagnosis was confirmed or excluded by laparoscopy (n = 69) or laparotomy (n = 9). Clinical examinations and conventional laboratory examinations were of limited value in the diagnosis of acute adnexitis. In contrast, CRP was a highly sensitive indicator of inflammatory pelvic disease. Furthermore, the CRP determination was superior in assessing the efficacy of an antibiotic treatment.