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M Zwirner

Publications and source records attributed to M Zwirner.

22 records · Page 2Linked to original sources

CA125 in ovarian cancer: European Group on Tumor Markers guidelines for clinical use.

CA125 is currently the most widely used tumor marker for ovarian epithelial cancer. The aim of this article is to provide guidelines for the routine clinical use of CA125 in patients with ovarian cancer. Due to lack of sensitivity for stage I disease and lack of specificity, CA125 is of little value in the detection of early ovarian cancer. At present, therefore, CA125, either alone or in combination with other modalities, cannot be recommended for screening for ovarian cancer in asymptomatic women outside the context of a randomized controlled trial. Preoperative levels in postmenopausal women, however, may aid the differentiation of benign and malignant pelvic masses. Serial levels during chemotherapy for ovarian cancer are useful for assessing response to treatment. Although serial monitoring following initial chemotherapy can lead to the early detection of recurrent disease, the clinical value of this lead-time is unclear. CA125 is the ovarian cancer marker against which new markers for this malignancy should be judged.

Biomarkers, Tumor↗

Androgen response in polycystic ovarian syndrome to FSH treatment after LHRH agonist suppression.

Anovulatory patients with clomiphene-resistant polycystic ovarian syndrome were treated by two different stimulation protocols. Follicular maturation was induced in 14 women with hMG; 12 of them received pure FSH in a later series after previous pituitary desensitization with the LHRH agonist D-Trp-6-LHRH (Decapeptyl). Both basal and stimulated serum androstenedione, testosterone, and free testosterone were elevated in the hMG-treated group compared with controls. However, only androstenedione exhibited a significant increase between early and late follicular levels. Marked suppression of these androgens has been observed after two weeks of LHRH agonist pretreatment, but nearly the same concentrations were obtained with pure FSH on the day of hCG administration. Again, only the increase of androstenedione levels proved to be significant. Polycystic follicular maturation, hyperstimulation, and peak estradiol levels were comparable with the two protocols. Nevertheless, more pregnancies were achieved using the LHRH agonist+FSH combination (4 vs. 1). It is suggested that 2 weeks' suppression of ovarian androgens with LHRH agonist is not sufficient to neutralize the unfavourable intraovarian mechanisms interfering with normal folliculogenesis. More data are required to confirm the superiority of LHRH agonist pretreatment in the management of polycystic ovarian syndrome.

Androgens↗

An international proficiency study with the tumor marker CA 125.

A strict and adequate quality assurance program is the only real guarantee of the reliability of laboratory test results. Such proficiency testing was carried out for the CA 125 test system in five university laboratories over a period of three years (1984-1987) using five different reference materials (BIOREF, FRG). A concentration-dependent performance profile could thus be established evaluating a total of 301 assays. Intra-assay precision of the test ranged between 4.8 and 11.5%, and interassay precision between 13.6 and 19.1%. Laboratory specific average values of the individual reference materials ranged between 26 and 32 U/ml for reference 1, 51 and 59 U/ml for reference 2, 109 and 121 U/ml and 193 to 240 U/ml for references 3 and 4, respectively. Mean values for reference 5 ranged between 401 and 458 U/ml. There was no significant difference between mean values for the laboratories. Considerable batch-dependent variations of values became evident during the study but these were not indicated by the kit control supplied by the manufacturer. During the whole investigation period no systematic drift in values could be observed using trend analysis, indicating excellent stability of the reference material if stored frozen (-20 degrees C).

Antigens, Tumor-Associated, Carbohydrate↗

Estradiol concentrations in premenopausal women with coronary heart disease.

BACKGROUND: Because of the beneficial effects of estrogen, premenopausal women are normally protected against coronary heart disease (CHD) and are at lower risk for myocardial infarction; consequently, CHD occurs very rarely in menstrually active women. Given this background, the aim of the present study was to test the hypothesis that decreased concentrations of estrogen are associated with CHD in premenopausal women. METHODS: Fourteen premenopausal women with CHD were investigated and compared with a healthy control group comparable for age and cardiovascular risk factors. Relevant characteristics of patients and controls were assessed: age, blood pressure, body mass index, total cholesterol and high-density lipoprotein cholesterol, triglycerides, former pregnancies, ovariectomy and related surgical interventions, smoking history and former use of oral contraceptives. To ensure the premenopausal status of the participants, the regularity of the menstrual cycle and the follicle-stimulating hormone concentrations were also assessed. Plasma estradiol and progesterone and urine estrone concentrations (24 h urine collection) were measured at day 6 after estimated ovulation to assess the relative increase in plasma estradiol and progesterone during the second half of the menstrual cycle. RESULTS: Compared with the control group, premenopausal women with CHD had significantly lower concentrations of plasma estradiol (408.9 +/- 141 pmol/l and 287.8 +/- 109 pmol/l respectively; P = 0.0228) and total estrogen (2061 +/- 693 pg/mumol creatinine and 1607 +/- 448 pg/mumol creatinine respectively; P = 0.025) in the urine. However, the progesterone concentrations were not significantly different between the groups. These findings might be explained by a partial ovarian dysfunction, as the patient group had a significantly higher number of tubal sterilizations (eight compared with one). CONCLUSION: Our data provide support for the hypothesis that decreased concentrations of estradiol might be an additional pathogenetic factor for the development of CHD in menstrually active premenopausal women.

Adult↗