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Biomedical subjects

U Goebelsmann

Publications and source records attributed to U Goebelsmann.

At least 37 records · Page 2Linked to original sources
PubMed1982

The modulating role of obesity and 17 beta-estradiol (E2) on bound and unbound E2 and adrenal androgens in oophorectomized women.

17 beta-Estradiol (E2) pellet replacement therapy for oophorectomized women has been shown to be safe and effective. Some investigators have advocated the addition of testosterone (T) pellets for oophorectomized women. This study was carried out to measure the level of androgens in oophorectomized women with and without E2 pellets. The possible modulating role of E2 upon adrenal androgens was investigated as well as the effects of obesity on bound and unbound serum levels of E2 and T. Seven obese patients and eight nonobese normal patients with E2 pellets were compared to nine oophorectomized age- and weight-matched control women not receiving estrogen. Obese patients had higher levels of androstenediol (Adiol) and androstenedione (A) than nonobese patients, yet compared to oophorectomized controls, nonobese patients had higher levels of dehydroepiandrosterone sulfate (DHEA-S) and Adiol. As a group, patients with E2 pellets had higher levels of DHEA-S, Adiol A, and unbound T compared to oophorectomized controls, and their Adiol and total and unbound T levels were similar to those of premenopausal females. Obese patients had lower levels of total E2, yet a higher percentage of unbound E2, resulting in unbound E2 levels which were similar to those of the nonobese women. Unbound T was higher in obese patients compared to the nonobese women and oophorectomized controls. In conclusion, these data suggest that 1) there may be a modulating role of E2 on adrenal androgens exemplified by an increased serum level of delta 5-3 beta-ol androgens in women with E2 pellets, 2) supplemental T implants for oophorectomized women may not be necessary, and 3) obese women with pellets have higher levels of Adiol, A, and unbound T then nonobese women and therefore have a higher ratio of androgen to estrogen.

Adult↗
PubMed1982

Clinical and laboratory predictors of clomiphene response.

A prospective study was carried out on 158 anovulatory women for the purpose of finding parameters that might predict the clomiphene dose at which ovulation would occur. Both body weight and obesity were positively correlated with the dose required to achieve ovulation (P less than 0.05). Once ovulation occurred, obesity did not affect the ability to conceive. Fifty-eight women who ovulated with various doses of clomiphene, including six women who failed to ovulate, had hormonal measurements performed prior to treatment. Compared with normally ovulating controls, serum luteinizing hormone (LH), the ratio of LH to follicle-stimulating hormone (FSH), serum androgens, unbound testosterone, and unbound estradiol were elevated and sex hormone binding globulin-binding capacity (SHBG-BC) significantly lower in women receiving clomiphene. Although the ovulatory dose of clomiphene was positively correlated with both weight and obesity, neither weight nor any laboratory parameter could accurately predict the clomiphene response.

Androgens↗
PubMed1981

Antepartum fetal surveillance in diabetic pregnant patients.

The antepartum fetal surveillance (biochemical and biophysical) data of 140 pregnant diabetic patients were evaluated. We determined how often intervention occurred on the basis of abnormal tests and correlated each test with neonatal outcome. Fifteen of the total 140 patients had their pregnancies terminated because of abnormal biochemical and/or biophysical tests. An abnormal estriol (E3) value preceded the abnormal antepartum fetal heart rate testing in eight of 10 instances. We conclude that the major benefit of the antepartum fetal surveillance techniques, in this group of patients and under the present scheme, is in determining when not to intervene, thus allowing safe prolongation of pregnancy.

Estriol↗
PubMed1981

Detection of estrogen receptor in breast and endometrial carcinoma by the immunoperoxidase technique.

Paraffin-embedded tissues from 15 women with breast or endometrial carcinomas were analyzed in a study designed to explore the possible value and validity of an immunoperoxidase method for the detection of estrogen receptor in formalin-fixed paraffin-embedded tissue. Results were compared with biochemical assays for estrogen receptor performed on cytosols of fresh tissue from the same patients. There was complete correlation in nine of 15 (60%) of the tumors analyzed. Four cases (26.7%) were judged positive for estrogen binding sites by immunoperoxidase but were negative for estrogen receptor by biochemical assays; in two cases the converse was observed. The immunohistologic technique is relatively rapid and utilizes fixed paraffin sections of the same tissue that is used for standard histologic diagnosis. The provision of a permanent record that can be kept for future reference provides an advantage over immunofluorescence methods that have been advanced for the detection of estrogen receptors. The excellent morphology achieved permits an assessment of the staining of individual cells in relation to the usual histologic criteria employed in the diagnosis of breast and endometrial cancer. This stands in contrast to biochemical cytosol-based assays that take no account of variations in receptor expression by the tumor cells or variations in the proportion of the assayed material that is in fact neoplastic as distinct from supporting stroma and connective tissue.

Adenocarcinoma↗
PubMed1981

Hypergonadotropic hypogonadism in female patients with galactosemia.

We evaluated gonadal function in 18 female and eight male patients with galactosemia due to transferase deficiency; it was normal in the males, but 12 females had signs of hypergonadotropic hypogonadism. All female patients had a 46,XX karyotype, normal levels of thyroid hormone and prolactin, and no anti-ovarian antibodies. The biologic activity of urinary gonadotropins was normal. Ultrasonography of the pelvis revealed that ovarian tissue was diminished or absent. Total estrogens increased in one of two patients after administration of human menopausal gonadotropin. The frequency of hypergonadotropic hypogonadism was higher in females in whom dietary treatment for galactosemia was delayed. Clinical course and mean erythrocyte galactose-1-phosphate and urinary galactitol levels did not correlate with ovarian function. We conclude that female patients with galactosemia have a high incidence of ovarian failure due to acquired ovarian atrophy. Galactose or its metabolites may be toxic to the ovarian parenchyma, particularly during the immediate neonatal period.

Adolescent↗
PubMed1981

Estriol in pregnancy. VII. Unconjugated plasma estriol in prolonged gestation.

This study was undertaken to determine the course of unconjugated plasma estriol (E3) concentrations after 40 weeks' gestation and to assess whether the latter may be used as a first-line test in the management of term pregnancies with poor dates and prolonged gestation. Plasma E3 was measured twice weekly in 134 women with well-dated pregnancies of 40 weeks or more and in 213 women with pregnancies of unverified age but believed to be in excess of 40 weeks from the last menstrual period. The obstetric management was based upon twice weekly determinations of urinary E3 and antepartum heart rate testing, but not all patients complied. Plasma E3 levels were not availabe for management of the patients. The results indicate that unconjugated plasma E3 levels are highest at 40 weeks' gestation and decline thereafter by 12% each week. Because of this slow decline, biweekly assays suffice. Increasing and plateauing serial plasma E3 levels reveal that a patient approaches term or has reached 39 to 41 weeks' gestation, respectively, whereas decreasing E3 concentrations indicate that the patient is well beyond 40 weeks, and that her fetus may be about to or has become postmature. Only seven of the 347 patients studied were delivered of a postmature infant. Their last plasma E3 levels ranged from 3.8 to 8.0 ng/ml, i.e., were below the 95% confidence limits established for normal term pregnancies. It was found that 73% of the 347 patients had plasma E3 levels of 12 ng/ml or more, and that all their pregnancies ended normally, except for three instances of presumed intrapartum fetal distress. However, in 19 (20%) of the other 27% of the 347 patients who had plasma E2 levels of less than 12 ng/ml, abnormal outcome was encountered: postmaturity (seven), fetal death (four), intrauterine growth retardation (three), malformations (two), or intrapartum fetal distress (three). These results allow the conclusion that twice weekly assays of unconjugated plasma E2 may be used as a first-line test in the management of prolonged gestation.

Congenital Abnormalities↗
PubMed1981

Elevations in unbound serum estradiol as a possible mechanism for inappropriate gonadotropin secretion in women with PCO.

Twenty-three women considered to have polycystic ovarian disease (PCO) were studied in an effort to better understand the mechanism of inappropriate secretion (IGS) which is so characteristic of these women. Criteria for PCO included oligomenorrhea, infertility, an obesity index (ponderal index, PI) < 12, and an LH:FSH ratio > 3. The mean +/- SE weight and PI for this group were 175 +/- 7.5 lbs. and 11.2 +/- 0.2 respectively. Weight was not correlated with steroid levels in PCO or control women. The mean (+/- SE) of serum androgen concentrations (DHEA-S: 2.9 +/- 0.5 micrograms/ml; androstenedione: 2.6 +/- 0.3 ng/ml; and testosterone: 47 +/- 5 ng%) were all significantly higher than those in control women (p < .05). Total serum estradiol (E2) was comparable to those of controls in the follicular phase, while estrone (E1): E2 ratios averaged 2:1. Serum sex hormone binding globulin-binding capacity (SHBG-BC) averaged 56.8 +/- 4.2 nM which was significantly lower than that of controls (p < .05). The percent unbound E2 was significantly elevated in PCO (62% vs 37%). The mass of unbound E2 was also significantly higher in PCO women (40 +/- 3 pg/ml) than in controls (17 +/- 2 pg/ml) (p < .005). Serum LH:FSH ratios had a positive correlation with the relative and absolute concentration of unbound E2. In control women, unbound E2 correlated significantly with LH levels. This suggests that IGS characteristically found in PCO patients and exemplified by elevated LH;FSH ratios, is the result of the feedback response to elevated levels of unbound (i.e., biologically active) E2.

Adolescent↗
PubMed1981

Evidence for reduced 3 beta-ol-hydroxysteroid dehydrogenase activity in some hirsute women thought to have polycystic ovary syndrome.

Congenital adrenal hyperplasia due to 3 beta-ol-hydroxysteroid dehydrogenase (3 beta-ol) deficiency is usually lethal. A partial deficiency in 3 beta-ol has been suggested in some women presenting with androgen excess. In this study, 24 women were investigated who had hirsutism and oligomenorrhea and high serum delta 5 androgens compared to delta 4 androgens. Of these women, 9 had significantly elevated 17-hydroxypregnenolone (17 Preg) to 17-hydroxyprogesterone (17 Prog) ratios when compared to controls under basal conditions. On further testing of 9 women with ACTH, 4 had significantly elevated 17 Preg to 17 Prog ratios. Eight women had elevated ratios of dehydroepiandrosterone sulfate to androstenedione, 4 had elevations of androstenediol (Adiol) to testosterone (T), and 4 had abnormal 17 Preg to cortisol ratios. Only 3 women out of the original 24 selected for study had elevated ratios for all 4 different steroid pairs measured. 17 Prog was normal in these women with 3 beta-ol deficiency in contradistinction to the high levels normally observed in women with congenital adrenal hyperplasia due to 21- or 11-hydroxylase deficiency. It is suggested that the cause of androgen excess in these women is high circulating levels of Adiol and, in part, the slightly elevated unbound T levels in these women. In conclusion, a subtle, incomplete form of 3 beta-ol deficiency may exist in adult women and is manifest by high delta 5 androgens such as dehydroepiandrosterone sulfate and Adiol and normal delta 4 androgens such as androstenedione and T.

17-alpha-Hydroxypregnenolone↗
PubMed1981

Serum levels of DHEAS in gynecologic endocrinopathy and infertility.

Serum dehydroepiandrosterone sulfate (DHEAS) was measured in 32 infertility patients who were found to be ovulatory, in 37 women with oligomenorrhea, and in 52 hirsute patients under basal conditions. It was also measured in conjunction with adrenocorticotropic hormone (ACTH) stimulation and dexamethasone suppression in 10 of the hirsute women. Serum DHEAS levels were elevated in only 19% of the infertile women with regular ovulation, in 34% of the oligomenorrheic patients, and in 60% of the hirsute women. Of the C-19 steroids (androgens) measured in the 52 hirsute women, ie, total and unbound serum testosterone (T), androstenedione (A), and DHEAS, unbound serum T was most frequently elevated. Eighty-two percent of the hirsute women had either an elevated serum DHEAS level or an increased unbound T level, suggesting 1) that elevations in unbound serum T may be associated with or result from increased serum DHEAS levels and 2) that only a minority of women with so-called idiopathic hirsutism do not have demonstrable androgen excess. Three of 10 hirsute women with elevated serum DHEAS levels had an increased ACTH-induced rise in DHEAS. Dexamethasone given as a single daily dose of 0.5 mg at bedtime resulted in a marked decrease in serum DHEAS in all of the 10 hirsute patients tested within 2 weeks of therapy. Thus, serum DHEAS is a clinically useful indication of adrenal C-19 steroid secretion. When combined with clinical and other hormonal evaluations, its measurement adds an important dimension to the study of gynecologic endocrinology and infertility.

17-Ketosteroids↗
PubMed1981

Dehydroepiandrosterone sulfate as an indicator of adrenal androgen function.

This study was undertaken to determine whether serum dehydroepiandrosterone sulfate (DHEA-S) assays could be used in lieu of urinary 17-ketosteroid (17-KS) determinations. To delineate normal values, serum DHEA-S levels were measured in 41 normal women (controls). These averaged 1.78 +/- 0.1 (SE) micrograms/ml and ranged from 0.3 to 2.8 micrograms/ml. Serum DHEA-S and urinary 17-KS and creatinine were measured in 71 patients with and without signs of androgen excess who were attending the Reproductive Endocrinology/Infertility Clinic. Serum DHEA-S levels did not correlate with body weight, surface area, or ponderal index, and were not elevated in obese women without androgen excess. Both normal and elevated serum DHEA-S concentrations correlated well with total urinary 17-KS when corrected for creatinine (P < .0005). In another group of 26 patients, the 2 urinary 17-KS fractions androsterone (A) and dehydroepiandrosterone (DHEA) correlated well with serum DHEA-S levels, but the third urinary 17-KS fraction, etiocholanolone (E), did not correlate. Eleven of the 26 patients who had elevated serum DHEA-S concentrations excreted increased amounts of urinary A and DHEA but not E. It is concluded that serum DHEA-S levels are much more conveniently measured than urinary 17-KS and should replace the latter because DHEA-S is a better indicator of adrenal "androgen" secretion.

Adrenal Glands↗
PubMed1981

Feedback effects of estradiol and progesterone upon gonadotropin and prolactin release.

The relationship between estradiol- and progesterone-mediated gonadotropin release and steroid-induced changes in prolactin levels was investigated in an improved human experimental model. Three women who had undergone bilateral ovariectomy were studied after they had received a subcutaneous implant of one 25-mg estradiol (E2) pellet. Serum E2 levels remained between 60 and 125 pg/ml, and serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) concentrations were within the normal or slightly elevated range. Serum prolactin (PRL) levels were normal. Each woman received intramuscular injections of gradually increasing doses of estradiol benzoate (E2B) alone and in combination with progesterone (P) in 7 different experiments. An E2B-induced rise in E2 levels comparable to that observed at midcycle elicited a clearly defined LH surge but no change in FSH and PRL. Rising E2 concentrations followed by increasing P levels caused LH and FSH release but no change in PRL. When only P was administered or when serum P levels rose concomitantly with E2 levels, PRL and gonadotropin levels remained unchanged. These data indicate that a surge of E2 similar to that observed at midcycle triggers an acute release of LH only. Moreover, P levels commensurate with those found at mid-cycle facilitate an E2-mediated LH release and induce a concomitant peak in FSH. The lack of a significant increase in PRL levels suggests that different mechanisms are responsible for the pituitary release of PRL and gonadotropins.

Adult↗
PubMed1981

Urinary estradiol-17-beta-glucuronide assay for gonadotropin therapy.

To investigate the possibility of using urinary estradiol-17 beta-glucuronide (E2-17G) measured by direct radioimmunoassay to monitor ovulation induction with human menopausal gonadotropin (hMG), serum estrogen and urinary E2-17G levels were determined daily by 21 women treated with hMG for a total of 32 treatment cycles. Urinary E2-17G was measured in 24-hour and overnight specimens. A significant correlation was found between serum estrogens (primarily estradiol) measured by radioimmunoassay without preceding chromatography and urinary E2-17G excretion measured at 24 hours and overnight. The correlation was not significantly improved by correcting the 24-hour and overnight urinary E2-17G excretion levels with creatinine measurements. Although there was significant correlation between serum estrogens and urinary E2-17G measured by direct radioimmunoassay, the urinary E2-17G concentrations observed when serum estrogens levels indicated preovulatory follicle maturation (ie, at serum estrogens levels between 500 and 1000 pg/ml) varied so much that a clinical decision to trigger or not to trigger ovulation with human chorionic gonadotropin could not be reached in each case. These data indicate that significant correlation is not the only prerequisite for a new method to replace a proved procedure. Further studies are required to determine the reliability of monitoring hMG therapy with direct E2-17G radioimmunoassays in overnight urine collections.

Adult↗
PubMed1980

Prolactin modulation of dehydroepiandrosterone sulfate secretion.

To clarify the controversy about the effect of prolactin (PRL) on dehydroepiandrosterone sulfate (DHEA-S), this study was undertaken to investigate the effects of alterations in plasma PRL on plasma DHEA-S concentrations in hyperprolactinemic women, as well as in normal male subjects. DHEA-S was measured in a group of 21 women with hyperprolactinemia, galactorrhea, and amenorrhea (PRL:257 +/- 89 ng/ml; mean +/- SEM). In these women, mean plasma concentrations of DHEA-S (2.54 +/- 0.2 microgram/ml) were significantly higher (p < 0.005) than those in 41 normal control women (1.78 z microgram/ml) and those in a group of 11 amenorrheic patients (1.77 +/- 0.2 microgram/ml). Eight women with hyperprolactinemia were given 5 mg of bromocriptine each day for 4 consecutive weeks. Within 1 week of medication, PRL levels fell by 60% (p < 0.05). To test whether lowering normal plasma levels of PRL would affect plasma concentrations of DHEA-S, five normal male subjects received a 48-hour infusion of dopamine at an average rate of 6 microgram/kg/min. Plasma levels of PRL fell by 60% (p < 0.01) after 8 hours of infusion, and DHEA-S decreased by 27% by 16 hours (p < 0.05). These data suggest that PRL modulates the secretion of DHEA-S: an increase in plasma levels of PRL is correlated with elevated concentrations of DHEA-S, whereas a decrease in PRL is followed by a fall in DHEA-S.

Adult↗
PubMed1980

Adult manifestation of congenital adrenal hyperplasia due to incomplete 21-hydroxylase deficiency mimicking polycystic ovarian disease.

This study was carried out to document the postpubertal presentation of congenital adrenal hyperplasia (CAH), to elaborate the diagnostic criteria for it, and to investigate family members of CAH patients. Serum 17-hydroxyprogesterone (17OHP) was measured in normal women and 25 hirsute oligomenorrheic patients, five of whom were shown to have CAH. These five CAH patients, as a group, had significantly elevated levels of 17OHP when compared to normal and hirsute women, although the other 20 hirsute oligomenorrheic women also had higher levels of 17OHP than the follicular phase control subjects. A single intravenous bolus of 0.25 mg of adrenocorticotropic hormone (ACTH) caused much larger increased in 17OHP in all five CAH patients than in the control and hirsute women. The five CAH patients had decreased cortisol but normal 11-deoxycortisol responses to ACTH, thus indicating 21-hydroxylase deficiency (21HD). Clinically, they were indistinguishable from women with polycystic ovarian disease (PCO) and had basal serum levels of androgens and urinary 17-ketosteroids which were similar to those found in 47 other women presenting with the complaint of hirsutism. However, the androstenedione levels and androstenedione/cortisol ratios in response to ACTH were significantly higher in the five CAH patients than in both the normal and hirsute women. Of seven family members tested, two fathers and one mother had an intermediate 17OHP response to ACTH, thus suggesting heterozygosity. Human lymphocyte antigen (HLA) typing on family members indicated that the inheritance of the disorder may be linked to B antigens. Two siblings of one of the CAH patients had normal 17OHP responses to ACTH and also had a different HLA-B complement. These data document the existence of adult manifestation of CAH, due to 21 HD. This disorder presents with androgen excess and oligomenorrhea or amenorrhea and mimicks PCO. The diagnosis of it hinges upon the post-ACTH rise in 17OHP, whereas the levels of serum androgens and urinary 17-ketosteroids may be inconclusive.

Adolescent↗
PubMed1980

Subdermal estradiol pellets following hysterectomy and oophorectomy. Effect upon serum estrone, estradiol, luteinizing hormone, follicle-stimulating hormone, corticosteroid binding globulin-binding capacity, testosterone-estradiol binding globulin-binding capacity, lipids, and hot flushes.

Subderman estradiol (E2) pellets (25 mg) were inserted immediately after hysterectomy and oophorectomy in 22 menstruating women, ages 29 to 50 years. Serum samples were obtained daily for 7 days, weekly for 4 weeks, and at monthly intervals for 6 months. Although there was significant variation between patients, E2 levels remained within the follicular phase range, averaging 50 to 70 pg/ml for 3 months, and then slowly declining to a mean of 37 pg/ml at 6 months, when new pellets were inserted. Over the entire study period, the E2:estrone (E1) ratio was greater than unity. Subdermal E2 pellets limited the rise in luteinzing hormone (LH) and follicle-stimulating hormone (FSH) after gonadectomy and the levels of LH and FSH 6 months after the insertion of E2 pellets were significantly lower (p < 0.01) than in 20 postmenopausal women who had undergone oophorectomy and whose serum E2 levels were less than 20 pg/ml. Serum corticosteroid binding globulin-binding capacity (CBG-BC) and serum testosterone-estradiol binding globulin-binding capacity (TeBG-BC) remained unchanged with E2 pellets. Although high-density lipoprotein-cholesterol increased significantly (p < 0.05), low-density lipoprotein-cholesterol, total cholesterol, and triglycerides were unaffected, except for a rise in triglycerides in three older women with diabetes mellitus and hypertension. There were no complaints of severe hot flushes. Women who had vasomotor symptaoms had mild or moderate flushes that occurred at 5 or 6 months after replacements of the pellets. Thus, E2 pellets are an effective form of parenteral estrogen replacement therapy and offer both practical and theorteical advantages over other forms of estrogen.

Adult↗