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PubMedDate not supplied

Regulation of gonadotropin response in testicular feminization syndrome.

The effects of hormonal manipulation on gonadotropin, androgen, and estrogen concentrations in a patient with testicular feminization syndrome (TFS) were studied to clarify the feedback regulation of gonadotropins. Baseline serum LH concentrations were normal to high and FSH concentrations were normal despite markedly elevated plasma testosterone concentrations, implying the lack of a reciprocal control relationship, and fluoxymesterone administration failed to alter gonadotropin or androgenic steroid levels. Clomiphene administration resulted in a rise in both LH and androgen levels, while moderate doses of exogenous estrogens effected a diminution in testosterone but did not significantly alter the levels of gonadotropins. Following gonadectomy, these same doses of estrogens produced a dramatic fall in the very high postoperative levels of gonadotropins. These results suggest that gonadotropin regulation is mediated by estrogens and not directly by androgens in TFS.

Adult↗
PubMed1999

Rat liver lysosomal and mitochondrial activities are modified by anabolic-androgenic steroids.

PURPOSE: The aim of this study was to examine the separate and combined effects of an 8-wk treatment with high doses of 17alpha-alkylated anabolic-androgenic steroids (AAS) and exercise training on selected lysosomal and mitochondrial enzyme activities in rat liver. METHODS: Sedentary and treadmill-trained (25 m x min(-1), 45 min x d(-1), 5 d x wk(-1)) male rats were treated with fluoxymesterone, methylandrostanolone, or stanozolol (2 mg x kg body weight(-1), 5 d x wk(-1)) for 8 wk. RESULTS: Acid phosphatase, arylsulfatase, beta-glucuronidase, and beta-galactosidase activities were increased in liver homogenates of sedentary and trained AAS-treated rats. The mitochondrial respiratory chain activities rotenone-sensitive NADH-cytochrome c reductase (NCCR), succinate cytochrome c reductase (SCCR), and cytochrome oxidase (COX) showed a significant decrease in steroid-administered rats, whereas citrate synthase (CS), a matrix enzyme, exhibited no changes in activity, pointing to a selective effect of AAS on mitochondrial membrane complexes. In vitro studies in mitochondrial fractions isolated from the liver of control rats showed that COX and CS activities were insensitive to the AAS, whereas NCCR and SCCR activities were partly inhibited. On the other hand, the mean values of serum parameters related to hepatic function were within normal ranges in all the experimental groups of animals. CONCLUSIONS: The present data show that 8-wk ingestion of three different anabolic-androgenic steroids, either with or without concurrent exercise training, affects lysosomal hydrolases and mitochondrial respiratory chain electron transport in rat liver without modifying classical serum indicators of hepatic function.

Anabolic Agents↗
PubMed1994

Androgen therapy in myelodysplastic syndromes with thrombocytopenia: a report on 20 cases.

Twenty patients with myelodysplastic syndromes (MDS) and (i) platelets < 50 x 10(9)/l and (ii) bone marrow blasts < or = 10% were treated with androgen therapy (fluoxymesterone at 1 mg/kg/d: seven patients; danazol at 600 mg/d: 13 patients) for at least 3 months. 11 of them (55%) had an increase in platelet counts by at least 30 x 10(9)/l and a disappearance of bleeding symptoms was seen in 6/6 patients with initial bleeding. A response with neutrophil counts (six cases) or haemoglobin levels (five cases) was less often seen. Treatment was continued for 3+ to 27 months in responders (the dose being reduced by 50% after 6 months). Seven patients on maintenance treatment were still responding. Another patient died while he was still responding, and the remaining three patients relapsed after discontinuation (two cases) and dose reduction to 50% (one case) of the androgen used. Side-effects of treatment were moderate. In our experience, androgen therapy can be useful in patients with 'low risks' MDS (i.e. with marrow blasts < or = 10%) and severe thrombocytopenia, especially because no growth factor regularly active on platelets is currently available.

Adult↗
PubMed1988

Effects of human chorionic gonadotropin, androgens, adrenocorticotropin hormone, dexamethasone and hyperprolactinemia on plasma sex steroid-binding protein.

This presentation reports the effects of androgens, glucocorticoids and some pituitary hormones on plasma sex steroid-binding protein (SBP). The latter was measured by a solid phase method after desteroidation of the plasma. An hCG test (1500 I.U. every other day X 7) was given to 60 boys. In the children with a normal testosterone (T) rise, plasma SBP decreased (% of basal values) either significantly (38.3 +/- 9.3%, group A; n = 29), or moderately (13.4 +/- 4.4%, group B; n = 9) or did not change (-1.6 +/- 6.4%, group C; n = 10). In the 3 infants tested at an age when SBP normally rise sharply, hCG partially prevented this rise. The administration of either fluoxymesterone (10 mg/m2 for 10 days) or depot-T (4 I.M. injections of 100 mg/m2 every 2 weeks) induced a significant drop (about 2-fold) in plasma SBP in a control group of infants or children, but did not change SBP in 3 infants with the androgen insensitivity syndrome. A single injection of 0.25 mg of ACTH did not significantly alter SBP levels. In contrast, at the end of a 3-day ACTH test (0.5 mg/m2 12 hourly X 6) SBP levels had significantly decreased (mean 35% fall) with no age or sex differences, and with no correlation with the cortisol levels reached. However, the lowering effect of ACTH on SBP levels is likely mediated by glucocorticoids, since its effect was reproduced by high doses (8 mg/day for 3 days) of dexamethasone given at once or after 3 days of treatment at lower dose (20 micrograms/kg BW). It would appear that the depressive effect of ACTH and/or dexamethasone is observed for a threshold dose of glucocorticoids (greater than 5-fold physiological levels) and a certain time (greater than or equal to 3 days) of exposure. The mechanism by which androgens and glucocorticoids lower SBP levels in vivo is not yet understood. From recent experiments, showing that both stimulate the secretion of SBP in hepatoma cells in vitro, it would appear that both hormones may alter SBP metabolism. In a selected population of hyperprolactinemic women, with normal weight and no hirsutism, plasma SBP levels were found in the normal female range. The discrepancy with previous studies in the literature may be explained by differences in the degree of hyperprolactinemia and/or associated hyperandrogenim. This study further documents the multifactorial and intricated hormonal influences involved in the regulation of plasma SBP in vivo.

Adrenocorticotropic Hormone↗
PubMed1975

Interaction of anabolic steroids with glucocorticoid receptor sites in rat muscle cytosol.

While glucocorticoid hormones act catabolically on skeletal muscle through their binding to glucocorticoid-specific receptors in the cytosol, androgens exert anabolic responses but no androgen-specific binding proteins could be detected in this responsive tissue. However, various nonradioactive androgens were effective in displacing labeled dexamethasone or cortisol from their respective cytoplasmic receptors in muscle, both in vitro and in vivo. The inhibition of glucocorticoid binding by androgens is competitive, and could be observed following a single or repeated administration of the androgens to adrenalectomized-castrated animals. The synthetic androgen fluoxymesterone and the hormone testosterone displayed Ki values of 7.5 X 10(-6) M and 1 X 10(-5) M, respectively, for the inhibition of [3H]dexamethasone binding in muscle cytosol. On the basis of competition experiments it is postulated that interaction of androgens with glucocorticoid receptors prevents the binding of glucocorticoids and might be responsible in part for the anabolic effects of pharmacologic doses of androgens in muscle.

Anabolic Agents↗
PubMed1980

Effect of a long-acting fluorinated androgen on implantation in 'delayed' mice.

The effect of fluoxymesterone (FMA), a fluorinated androgen, on ovum implantation has been studied using ovariectomized, progesterone-treated pregnant ('delayed') mice. 500 micrograms FMA, given either continuously from day 4 to 9 or singly on day 8, was able to induce implantation but at the same time caused total resorption of implanted embryos in the case of prolonged treatment with the drug. This anti-estrogenic activity of FMA could be reversed by supplementation of 0.25 micrograms estradiol-17 beta given on day 8. Testosterone also induced implantations in 'delayed' mice. FMA and testosterone given to long-term ovariectomized, progesterone-primed mice showed characteristic changes in uterine epithelial cell morphology similar to the attachment found in normal pregnancy. The possible mechanism of action of FMA in early pregnancy will be discussed.

Animals↗
PubMed1986

Stimulatory effects of androgens on normal children's bone marrow in culture: effects on BFU-E, CFU-E, and uroporphyrinogen I synthase activity.

We studied the effect of natural and synthetic androgens on children's erythropoietic precursor cells in culture. Cultures of normal marrow were carried out according to a miniaturized methylcellulose method in the presence of erythropoietin. We then evaluated the effects of testosterone, nortestosterone, fluoxymesterone and etiocholanolone (10(-9)-10(-6) M) on erythroid colony-forming units (CFU-E) and burst-forming units (BFU-E). Androgen-induced growth of erythroid progenitors was quantified by directly scoring colonies and by a biochemical determination of the uroporphyrinogen I synthase activity (UROS). We observed a significant increase (p less than or equal to 0.05) in the number of CFU-E and BFU-E and in the UROS activity of derived colonies in the presence of androgens (10(-8) or 10(-7)M). This microculture assay could be useful not only to study the effect of androgens on erythroid progenitor cells in culture, but also to predict the best androgenic treatment of anemia in children and adults.

Ammonia-Lyases↗
PubMed1993

Effect of conventional dose growth hormone therapy for two years on height velocity and height prognosis in girls with Turner syndrome.

The aims of this national multicentre study in Finland were to evaluate whether the height velocity of patients with Turner syndrome would increase with the conventional human growth hormone (GH) therapy regimen normally given to GH-deficient children and whether girls with Turner syndrome actually show GH neurosecretory dysfunction. Finally, the study should show whether GH therapy improves height prognosis and, eventually, final height. Twenty-five girls with Turner syndrome, aged 7.5-14.4 years, entered the study. Their ability to secrete GH was determined and, surprisingly, several would have been classified as having GH deficiency. All girls received GH, 0.1 IU/kg/day (maximum dose 4 IU/day) s.c., and once over 12.5 years old, they also received oestradiol valerate and fluoxymesterone. They showed a convincing increase in height velocity, and rapid growth continued during the second year of therapy. The effect of GH therapy on final height is still unknown. The therapy was remarkably free of side-effects.

Adolescent↗
PubMed1978

The treatment of depressed geriatric patients.

Biological changes more frequently associated with late onset depressions, such as cerebral arteriosclerosis, increased urinary MHPG concentrations, decreased gonadal functions, and increased MAO activity were reviewed and the therapeutic implications of these biological changes considered. The rationale for the use of Hydergine, amitriptyline, Gerovitol H3, fluoxymesterone, doxepin, and trazodone in geropsychiatric patients was discussed.

Age Factors↗
PubMed1994

Adult height in girls with Turner syndrome treated with low-dose estrogens and androgens.

OBJECTIVE: To determine if low dosages of estrogens and androgens administered to girls with Turner syndrome adversely affected their adult height. DESIGN: A nonrandomized control trial of nine girls. SETTING: The endocrine clinic at Texas Children's Hospital in Houston, Texas, an academic referral center. PARTICIPANTS: Participants had chromosomal defects consistent with Turner syndrome. Informed consent was obtained in accordance with institutional review board procedures. Eligibility criteria included an absence of previous hormone treatment. No one withdrew from this study because of adverse effects. INTERVENTIONS: Hormonal replacement therapy was initiated with conjugated estrogen 0.15 mg and fluoxymesterone 1 mg administered daily. MAIN OUTCOME MEASURES: Outcome measurements were a comparison of the final heights following treatment versus the predicted adult heights prior to treatment. RESULTS: The predicted adult height in these children prior to treatment was 140.0 +/- 4.4 cm (mean +/- SD); the actual adult height was 139.63 +/- 4.1 cm. The difference was 0.37 +/- 3.54 cm, which was not statistically significant by Wilcoxon signed-rank test (p = 0.23). The 95% confidence interval on this difference ranged from -3.1 to 2.3 cm, which indicates a true mean height loss of no more than 3.1 cm or a true mean gain of no more than 2.3 cm. CONCLUSIONS: Our results indicate that hormone replacement therapy with low dosages of conjugated estrogens and androgens starting at 10-11 years of age in children with Turner syndrome does not adversely affect actual adult height.

Adolescent↗
PubMed1986

Prospective evaluation of carcinoembryonic antigen levels and alternating chemotherapeutic regimens in metastatic breast cancer.

Ninety-seven eligible and evaluable women with metastatic breast cancer were placed on a prospective clinical protocol to evaluate the use of continuous cyclic therapy with dibromodulcitol, doxorubicin, vincristine, tamoxifen, and fluoxymesterone (DAVTH) v DAVTH alternating with cyclophosphamide, methotrexate, 5-fluorouracil, and prednisone (CMFP); and the use of pretreatment and serial carcinoembryonic antigen (CEA) levels in these patients. Continuous DAVTH and DAVTH/CMFP were equivalent therapies with respect to response rates, time to treatment failure (TTF), and survival. Pretreatment CEA levels were elevated (greater than 5 ng/mL) in 42/97 patients and less than 5 ng/mL in the remaining patients. Patients with elevated pretreatment CEA levels were more likely to be estrogen receptor (ER) positive (P = .006), to have prolonged disease-free intervals (P = .017), to have hepatic (P = .004) and/or osseous (P = .01) metastases, and to have multiple sites of metastatic disease (P = .004). Pretreatment CEA levels did not significantly predict for overall response rates, TTF, or survival; nonetheless, those patients with low pretreatment CEA levels had more complete responses (CRs) (16/55 v 4/42; P = .02). Serial CEA levels during therapy revealed a number of interesting patterns. During the first 4 months of treatment, serial CEA levels in responding patients either (1) progressively declined (15/29 women with elevated pretreatment CEA levels), or (2) initially rose significantly (mean, 243% of pretreatment value) and then declined (14/29 women with elevated pretreatment CEA levels). Peak CEA levels in the latter patients were seen 27 to 135 days following initiation of cytotoxic therapy. In some patients the initial increase in the CEA level was incorrectly interpreted as evidence of impending disease progression. CEA levels frequently increased around the time of clinical disease progression. However, rising CEA levels rarely provided a clinically meaningful lead time before the appearance of other clinical evidence of disease progression. These data suggest that routine pretreatment and monthly serial CEA levels in metastatic breast cancer patients have minimal use in clinical practice. Two further noteworthy findings were observed in this prospective study. First, patients with an unknown ER status had a prolonged median survival when compared with patients with ER positive or negative tumors; this appeared to be related to prolonged disease-free intervals in ER unknown patients. Second, two case of secondary acute leukemia were seen in patients treated with continuous DAVTH therapy.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1991

Factors predicting for response, time to treatment failure, and survival in women with metastatic breast cancer treated with DAVTH: a prospective Eastern Cooperative Oncology Group study.

Six hundred twenty-four women with metastatic breast cancer were entered on Eastern Cooperative Oncology Group (ECOG) study EST 2181. Patients were treated with mitolactol, doxorubicin, vincristine (DAV), tamoxifen, and fluoxymesterone (DAVTH). Nine patients were canceled, and 114 were ineligible (half because of concomitant diseases). Among the 501 eligible patients, the overall response rate was 54% (14% complete response and 5% not assessable). The median time to treatment failure (TTF) was 9.0 months, and the median survival was 20.9 months. Multivariate models were fit on a randomly chosen half of the eligible cases and then verified on the other half. About half of the variables that were significant in the models remained significant in the verification data set. In the verification data set the variables that remained significantly associated with lower probability of response were three or more organ sites of disease and lack of nodal metastases; the variables associated with a significantly shorter TTF were liver metastases, estrogen receptor (ER)-negativity, and prior adjuvant therapy. The variables associated with significantly shorter survival were liver metastases, ER negativity, three or more organ sites of disease, and prior adjuvant chemotherapy. None of the variables in the data set had a significant influence on toxicity. The 125 patients aged over 65 years did not have worse toxicity or worse prognosis than younger patients. Ineligible patients had significantly less response but virtually identical TTF curves, survival curves, and toxicities. Therefore, patient discriminants are of paramount importance in predicting the outcome of treatment. Many of the current criteria for eligibility for entry on study may not be justified.

Adenocarcinoma↗
PubMed1994

Reinduction with the same cytostatic treatment in patients with metastatic breast cancer: an Eastern Cooperative Oncology Group study.

PURPOSE: To investigate the therapeutic value of reinduction with the same cytostatic treatment that had been used in induction treatment for women with metastatic breast cancer. MATERIALS AND METHODS: One hundred six women with metastatic breast cancer were given dibromodulcitol (mitolactol), doxorubicin, vincristine, tamoxifen, and fluoxymesterone (DAVTH) for 6 months of induction treatment, then randomized to receive one of two chemotherapy regimens if they had obtained an induction partial response (PR) or no change (NC), or to receive observation versus chemotherapy if they had obtained an induction complete response (CR). Patients were then retreated with DAVTH reinduction after relapse. RESULTS: Seventy-four patients were eligible or had minor reasons for ineligibility. Severe or life-threatening toxicity was documented in 46%, and lethal toxicity in 4%. Eighteen percent had a response on reinduction (zero of 16 induction nonresponders, 15% induction PR, 44% induction CR). The median time to treatment failure (TTF) from reinduction was 3 months, and the median survival duration from reinduction was 14 months. In a logistic model, factors associated with more reinduction responses were observation after induction CR (P = .002) and age greater than 55 years (P = .04). Time since induction was not significant. CONCLUSION: Reinduction of response after treatment failure remains a therapeutic problem. The need for better salvage treatment underlines the importance of developing new regimens.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2000

Comparison of chemotherapy with chemohormonal therapy as first-line therapy for metastatic, hormone-sensitive breast cancer: An Eastern Cooperative Oncology Group study.

PURPOSE: Although hormonal therapy represents standard therapy for metastatic hormone-sensitive disease, many patients receive initial chemotherapy because of the location, bulk, or aggressiveness of their disease. It is uncertain whether simultaneous hormonal therapy provides additional benefit compared with chemotherapy alone. Eastern Cooperative Oncology Group trial E3186 was initiated to explore this question. PATIENTS AND METHODS: Between January 1988 and December 1992, 231 patients with estrogen receptor (ER)-positive or ER-unknown metastatic breast cancer were randomized to receive either chemotherapy (cyclophosphamide, doxorubicin, and fluorouracil ¿CAF) or chemohormonal therapy (CAF plus tamoxifen and Halotestin ¿fluoxymesterone; Pharmacia-Upjohn, Kalamazoo, MI ¿CAFTH) as front-line therapy for metastatic breast cancer. Patients who experienced a complete response to induction therapy either received or did not receive maintenance cyclophosphamide, methotrexate, fluorouracil, prednisone, and TH as a secondary randomization. RESULTS: The response rates (complete response and partial response) of patients who received CAF and CAFTH were similar (69.2% v 68.9%, respectively; P =.99). Time to treatment failure (TTF) was slightly longer for patients who received chemohormonal therapy compared with chemotherapy alone patients (13.4 months v 10.3 months, respectively; P =.087), and TTF was significantly longer in ER-positive compared with ER-negative patients (17.4 months v 10.3 months, respectively; P =.048). However, ER status had no effect on overall survival (30.0 months for CAF v 29.3 months for CAFTH). CONCLUSION: In patients with potentially hormone-sensitive metastatic breast cancer, chemohormonal therapy prolongs TTF for ER-positive patients without improving overall survival.

Adult↗
PubMed2006

An orally active selective androgen receptor modulator is efficacious on bone, muscle, and sex function with reduced impact on prostate.

A number of conditions, including osteoporosis, frailty, and sexual dysfunction in both men and women have been improved using androgens. However, androgens are not widely used for these indications because of the side effects associated with these drugs. We describe an androgen receptor (AR) ligand that maintains expected anabolic activities with substantially diminished activity in the prostate. LGD2226 is a nonsteroidal, nonaromatizable, highly selective ligand for the AR, exhibiting virtually no affinity for the other intracellular receptors. We determined that AR bound to LGD2226 exhibits a unique pattern of protein-protein interactions compared with testosterone, fluoxymesterone (an orally available steroidal androgen), and other steroids, suggesting that LGD2226 alters the conformation of the ligand-binding domain. We demonstrated that LGD2226 is fully active in cell-based models of bone and muscle. LGD2226 exhibited anabolic activity on muscle and bone with reduced impact on prostate growth in rodent models. Biomechanical testing of bones from animals treated with LGD2226 showed strong enhancement of bone strength above sham levels. LGD2226 was also efficacious in a sex-behavior model in male rats measuring mounts, intromissions, ejaculations, and copulation efficiency. These results with an orally available, nonaromatizable androgen demonstrate the important role of the AR and androgens in mediating a number of beneficial effects in bone, muscle, and sexual function independent from the conversion of androgens into estrogenic ligands. Taken together, these results suggest that orally active, nonsteroidal selective androgen receptor modulators may be useful therapeutics for enhancing muscle, bone, and sexual function.

Administration, Oral↗
PubMed1989

Androgens directly stimulate proliferation of bone cells in vitro.

This report describes the first observation of a direct mitogenic effect of androgens on isolated osteoblastic cells in serum-free culture. [3H]thymidine incorporation into DNA and cell counts were used as measures of cell proliferation. The percentage of cells that stained for alkaline phosphatase was used as a measure of differentiation. Dihydrotestosterone (DHT) enhanced mouse osteoblastic cell proliferation in a dose dependent manner over a wide range of doses (10(-8) to 10(-11) molar), and was maximally active at 10(-9) M. DHT also stimulated proliferation in human osteoblast cell cultures and in cultures of the human osteosarcoma cell line, TE89. Testosterone, fluoxymesterone (a synthetic androgenic steroid) and methenolone (an anabolic steroid) were also mitogenic in the mouse bone cell system. The mitogenic effect of DHT on bone cells was inhibited by antiandrogens (hydroxyflutamide and cyproterone acetate) which compete for binding to the androgen receptor. In addition to effects on cell proliferation, DHT increased the percentage of alkaline phosphatase (ALP) positive cells in all three bone cell systems tested, and this effect was inhibited by antiandrogens. We conclude that androgens can stimulate human and murine osteoblastic cell proliferation in vitro, and induce expression of the osteoblast-line differentiation marker ALP, presumably by an androgen receptor mediated mechanism.

Alkaline Phosphatase↗
PubMed1976

Unconjugated dehydroepiandrosterone plasma levels in normal subjects from birth to adolescence in human: the use of a sensitive radioimmunoassay.

A specific and sensitive radioimmunoassay for measuring unconjugated plasma dehydroepiandrosterone (DHA) has been developed and the results expressed in ng/100 ml. Mean values +/-1 SD were in mixed cord blood 593.3 +/- 186.5 in 21 females and 712.7 +/- 190.9 in 18 males. During the first day of life the peripheral plasma concentration of DHA was 917.6 +/- 317.8 in 22 female and 922.65 +/- 290 in 17 male neonates. During the first month of age, DHA levels decreased significantly and then more progressively throughout the first year of life. Mean levels observed between the first and 6th month of life were 147.1 +/- 53.6 in 15 girls and 151.6 +/- 62.7 in 28 boys. Between 6 and 12 months of age mean DHA levels were 90.9 +/- 43.3 and 68.14 +/- 30.9 in 11 girls and 24 boys, respectively. In 250 normal children, plasma DHA levels were very low between 1 to 6 years of age, but rising progressively thereafter without any sex difference long before any clinical sign of puberty. A circadian rhythm parallel to that of cortisol was observed as early as 5 years of age. Acute and chronic stimulation of ACTH confirmed the adrenal origin of DHA, while the results of hCG stimulation test and fluoxymesterone suppression test assessed the testicular participation to the DHA production.

Adolescent↗
PubMed1980

17 beta-hydroxysteroid dehydrogenase deficiency in malignant interstitial cell carcinoma of the testis.

A partial defect in testosterone (T) secretion due to a 17 beta-hydroxysteroid dehydrogenase deficiency has been documented in a patient with advanced metastatic interstitial cell carcinoma of the testis. Basal serum T was decreased (83 ng/ml), whereas androstenedione was markedly elevated (847 ng/ml). Dehydroepiandrosterone sulfate and estrone were moderately increased, while LH, FSH, and estradiol were minimally increased. After hCG administration, androstenedione rose to much greater degree than T. Fluoxymesterone failed to suppress circulating androgens and estrogens to below basal values, although LH and FSH were suppressed to immeasurable levels. These data support a partial enzyme deficiency within the tumor. They also suggest that although the tumor was autonomous, it still was capable of being stimulated by exogenous gonadotropins.

17-Hydroxysteroid Dehydrogenases↗