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At least 127 records · Page 7Linked to original sources
PubMed1997

Comparative effect of the calcium antagonist verapamil and the synthetic steroids gestrinone and danazol on human monocyte phagocytosis in vitro.

Recent evidence suggested that periovulatory treatment with an immunomodulatory agent such as verapamil might be an effective alternative to conventional treatment for endometriosis-associated subfertility. In particular, it has been reported that the drug might reduce the accentuated macrophage peritoneal activation demonstrated in patients with endometriosis. In this study, we compared the effect of the calcium antagonist verapamil with those of gestrinone, danazol and testosterone on human monocyte phagocytosis in an attempt to evaluate any significant differences in their ability to influence a parameter of cell inflammatory activation. Peripheral blood monocytes were isolated from 37 healthy women. Monocyte function was determined by phagocytosis of fluorescent microspheres after an overnight incubation in the presence or absence of the various agents. This study indicates that verapamil at the pharmacological concentration of 0.4 micrograms/ml, the systemic level in patients taking 40-80 mg/8 h p.o., significantly inhibits monocyte function. A lower immunosuppressive but still significant effect was achieved in this assay system with gestrinone at a concentration of 3 x 10(-8) M). The pharmacological concentration of danazol (10(-6) M) and the physiologic concentration of testosterone (10(-8) M) did not significantly affect this immunologic test system. These results provide evidence that verapamil is able to exert a slightly greater immunosuppressive effect than steroidal drugs on monocyte phagocytosis. However, due to the small differences observed, further studies on the biological mechanism of the drug seem to be necessary to completely elucidate its potential role in endometriosis-associated subfertility.

Adult↗
PubMed1998

[Hormonal therapy of constitutionally tall children].

Children of constitutionally tall stature may experience serious problems related to their height. Treatment with high dose sex steroids may be considered in order to limit final adult height. Prediction of adult height plays a central part in the management of children of tall stature. Various aspects of height prediction in children of tall stature are discussed. The height reducing effect varies between studies from 2 to 10 cm. Recently, in a large Dutch study the mean effects of therapy were 0.7 and 2.4 cm for boys and girls respectively. The effect depended on the bone age at start of treatment. Beyond a critical bone age of about 14 years treatment had no effect. Minimal age for intervention is 9.5-10 year for boys and 9.0-9.5 year for girls. Recommended treatment for boys is 250 mg testosterone esters i.m. per week and for girls ethinyloestradiol orally 200 micrograms per day in combination with medroxyprogesterone or dydrogesterone (both 5-10 mg per day) during the first 12-14 days of the cycle. Treatment has to be continued until complete closure of the epiphyses. While side effects during hormonal therapy are frequent, they are mostly temporary and mild and seldom lead to cessation of therapy. So far there have been no indications of adverse effects on, for instance, gonadal function.

Administration, Oral↗
PubMed1996

Pharmacodynamic effects of depot-medroxyprogesterone acetate (DMPA) administered to lactating women on their male infants.

Normal postpartum women, who had a spontaneous vaginal delivery of one full-term male infant, free of congenital abnormalities and other diseases, were recruited for this study. Thirteen women received 150 mg depot-medroxy-progesterone acetate (DMPA), intramuscularly on days 42 + 1 and 126 + 1 postpartum. Infants of nine mothers, who did not receive DMPA, served as controls. Blood samples were collected from treated mothers on days 44, 47, 74, 124, 128, and 130 postpartum for medroxyprogesterone acetate (MPA) measurements. Four-hour urine collections were obtained from all 22 infants in the morning on days 38, 40, 42, 44, 46, 53, 60, 67, 74, 88, 102, 116, 122, 124, 126, 128, 130, and 137. Urinary follicle stimulating hormone (FSH), luteinizing hormone (LH), unconjugated testosterone, and unconjugated cortisol were measured by radioimmunoassay, and serum MPA and urinary MPA metabolites were measured by gas chromatography-mass spectrometry (GC-MS). No MPA metabolites could be detected in the urine of the infants from the DMPA-receiving mothers. Hormonal profiles in the urine samples were not suppressed in comparison with those of the control infants. The present study demonstrates that DMPA, administered to the mother, does not influence the hormonal regulation of the breast-fed normal male infant.

Breast Feeding↗
PubMed1992

[Primary amenorrhea revealing micropolycystic ovary syndrome].

Nine patients with polycystic ovary syndrome revealed by primary amenorrhea were studied clinically, biochemically and ultrasonographically. One of them had excess weight, four had hirsutism and five acne. Testosterone and delta 4-androstenedione levels were high in all patients. Luteinizing hormone (LH) basal levels were increased in five patients. Basal values of follicle-stimulating hormone (FSH) remained within normal range. The LH to FSH ratio was elevated (over 2) in six patients. The LSH response to gonadotropin-releasing hormone (GnRH) was explosive in all patients. Ultrasonography showed that three out of five patients had enlarged ovaries with multiple follicles not exceeding 8 mm. Following treatment, two patients had children after ovulation was induced with clomiphene citrate, one patient became pregnant spontaneously but thereafter opted for voluntary interruption; two patients are still on ovulation-inducing therapy; four patients still have contraception. These results indicate the clinical heterogeneity and the diagnostic problems that surround this uncommon form of a frequently observed disease.

Adolescent↗
PubMed2006

The effect of progesterone, testosterone and synthetic progestogens on growth factor- and estradiol-treated human cancerous and benign breast cells.

OBJECTIVE: The effects of progesterone (P), testosterone (T), chlormadinone acetate (CMA), medroxyprogesterone acetate (MPA), norethisterone (NET), levonorgestrel (LNG), dienogest (DNG), gestodene (GSD) and 3-ketodesogestrel (KDG) were investigated in normal human breast epithelial MCF10A cells. In addition, the effects of these steroids were tested in estrogen and progesterone receptor positive HCC1500 human primary breast cancer cells. STUDY DESIGN: MCF10A cells were incubated with each progestogen at 1 microM and 100 nM for 7 days with growth factors epidermal growth factor (EGF), fibroblast growth factor (FGF) and insulin-like growth factor (IGF-I) (GFs, each 1 pM), and HCC1500 cells with GFs and/or estradiol (E2) 100 pM. Cell proliferation rate was measured by ATP-assay and cell death by photometric enzyme immunoassay. Ratios of cell death:proliferation were calculated. RESULTS: MPA and CMA with GFs induced proliferation of MCF10A cells. P, T, NET, LNG, DNG, GSD and KDG had no significant effect. In HCC1500 cells, MPA and CMA with GFs had an inhibitory effect compared to GFs alone. NET, LNG, DNG, GSD, KDG and T enhanced the proliferative effect of GFs. P had no significant effect. No progestogen could further enhance the stimulatory effect of E2 on HCC1500 cells; all but KDG inhibited it. MPA, GSD, T, CMA and NET had an anti-proliferative effect on the mitotic GF and E2 combination. P, LNG, DNG and KDG had no significant effect. CONCLUSIONS: Estrogens and mitogenic growth factors from stromal breast tissue are significant in growth-regulation of breast cells and may alter responses to progestogens. Certain progestogens are able to induce proliferation of or inhibit growth of benign or malignant human breast epithelial cells independently of the effects of growth factors and E2; therefore, choice of progestogen for hormone therapy may be important in terms of influencing possible breast cancer risk.

Breast↗
PubMed1997

Trends in anabolic-androgenic steroid use among adolescents.

OBJECTIVE: To examine the trends in anabolic steroid use among adolescents in the United States between 1988 and 1996. DESIGN: Computerized and manual literature searches were performed, and the resultant local, state, and national cross-sectional surveys of illicit anabolic steroid use by adolescents were reviewed. Trends in steroid use were evaluated using state and national studies administered in multiple periods. Various sampling procedures were employed, and all surveys used anonymous questionnaires. The national studies used for this analysis included the Monitoring the Future (MTF) study, the national component of the Youth Risk and Behavior Surveillance System, and the National Household Survey on Drug Abuse. SETTING: Most of the surveys described were self-administered in school classrooms. The National Household Survey on Drug Abuse was administered in the respondent's home. PARTICIPANTS: Most survey respondents were junior high an high school male and female students aged 12 to 18 years. RESULTS: Individual state studies (ie, a single point in time) provide evidence of continued steroid use throughout the United States despite educational and legal interventions. The findings of multiyear state-level studies show a decrease in lifetime steroid use rates between 1988 and 1994 for male and female adolescents, although no tests of statistical significance were conducted. At the national level, a significant decline (P < .01) in lifetime steroid use has taken place from 1989 to 1996 for male and female students (MTF data). However, since 1991, lifetime steroid use by male students, as measured by 2 of the 3 national surveys, has been generally stable. The third survey, MTF, shows a significant decrease (P < .05) in use from 1991 to 1996. Likewise, from 1991-1996 use of anabolic steroids during the past year (MTF data) was stable for 10th and 12th grade males; use among eighth grade males decreased significantly (P < .01). Since 1991, data from the 3 national surveys indicate an increase in lifetime anabolic steroid use among adolescent females, although only 1 of these increases is statistically significant. Furthermore, past year use of steroids (MTF data) increased for females in the 8th (P < .05), 10th (P < .05), and 12th (ns) grades. CONCLUSIONS: A long-term comparison of anabolic steroid use (from 1989-1996) indicates that use among adolescent males and females has decreased significantly (P < .05). However, for females the low point in lifetime steroid use was reached in 1991, with subsequent significant (P < .05) increases in use being reported in several national data sets. For adolescent males, after declining sharply between 1989 and 1991, steroid use has generally been stable since 1991. Moreover, based on the 1995 estimates of high school students and Youth Risk and Behavior Surveillance System data, approximately 375,000 adolescent males and 175,000 adolescent females in public and private schools in the United States used anabolic steroids at least once in their lives. These results suggest that prevention, intervention, and regulatory efforts to reduce steroid use at the local, state, and national levels should be reassessed, especially those efforts that focus on adolescent female steroid use.

Adolescent↗
PubMed1997

Synergistic activation of androgen receptor by androgen and luteinizing hormone-releasing hormone in prostatic carcinoma cells.

BACKGROUND: We investigated modulation of androgen receptor (AR) activity in prostatic tumor cells by luteinizing hormone-releasing hormone (LHRH)-induced increase of the intracellular cyclic adenosine monophosphate (cAMP) level. METHODS: AR transactivation activity was assessed in transiently transfected DU-145 and in LNCaP cells. RESULTS: LHRH and cAMP derivative, respectively, induced reporter gene activity to about 15% of the maximal level in DU-145 cells transfected with an AR expression vector and an androgen-inducible reporter gene. LHRH or the cAMP analogue acted synergistically in combination with low concentrations of androgen thus lowering the androgen concentration required for maximal AR activation by a factor of 100. A similar activation of the AR by cAMP analogue was observed in LNCaP cells when enhancement of androgen-induced secretion of prostate-specific antigen was determined. The two nonsteroidal antiandrogens hydroxyflutamide and Casodex(R) inhibited reporter gene activity. CONCLUSIONS: The AR is synergistically activated by low doses of androgen and LHRH or the second messenger cAMP. This may have implications for the treatment of advanced prostate cancer.

Androgen Antagonists↗
PubMed1998

Structure-function analysis of Lymantria testis ecdysiotropin: a search for the active core.

A structure-function study was performed on the synthetic 21 residue neuropeptide, Lymantria testis ecdysiotropin (LTE), originally isolated from brains of Lymantria dispar pupae. The peptide induces ecdysteroid synthesis by testis sheaths of various lepidopteran species. LTE, as well as synthetic LTE 1-11, 11-21, and 11-15, stimulated synthesis in larval and pupal testes of Lymantria dispar at concentrations of 10(-9) to 10(-15) M; LTE 16-21 was weakly active, and an elongated LEU-LTE was inhibitory to synthesis at all but extremely low concentrations (10(-15) M). Since the sequence and polarity of residues in LTE 1-11, 11-15, and 11-21 are quite different, several parts of the molecule must activate receptors which initiate the cascade, resulting in ecdysiogenesis in Lepidopteran testes.

Amino Acid Sequence↗
PubMed2000

Phenotypic characterization of immortalized normal and primary tumor-derived human prostate epithelial cell cultures.

BACKGROUND: Cell lines can provide powerful model systems for the study of human tumorigenesis. However, the human prostate cancer cell lines studied most intensively by investigators (PC3, DU145, and LNCaP) were established from metastatic lesions, and it is unlikely that they accurately recapitulate the genetic composition or biological behavior of primary prostate tumors. Cell lines more appropriate for the study of human prostate primary tumors would be those derived from spontaneously immortalized cells; unfortunately, explanted prostate cells survive only short-term in culture, and rarely immortalize spontaneously. Therefore, we examined whether cell lines developed through viral gene-mediated immortalization of human normal or primary tumor prostate epithelium express aspects of the normal or malignant phenotypes, and could serve as appropriate models for normal or transformed human prostatic epithelium. METHODS: To accomplish these goals, we assessed the phenotypic expression of cell cultures established through the immortalization of normal (1532N, 1535N, 1542N, and PrEC-T) or malignant (1532T, 1535T, and 1542T) human prostate epithelium with the E6 and E7 genes of HPV-16, or the large T antigen gene of SV40. RESULTS: Examination of these cell lines for their proliferative rates and their abilities to grow with or without serum or androgen stimulation, to form colonies in soft agar, or to form tumors in vivo, suggests that they may serve as valid, useful tools for the elucidation of prostate tumorigenesis. Moreover, the observation of structural alterations involving chromosome 8, including gain of 8q in 3 of the 4 cell lines expressing aspects of the malignant phenotype, implies that these cell lines accurately recapitulate the genetic composition of primary prostate tumors. CONCLUSIONS: Taken together, these data suggest that cell lines generated from immortalized normal or primary tumor epithelium may be useful for the elucidation of early transforming events in the prostate.

Animals↗
PubMed2000

Different proportions of various prostate-specific antigen (PSA) and human kallikrein 2 (hK2) forms are present in noninduced and androgen-induced LNCaP cells.

BACKGROUND: Human prostate-specific antigen (PSA) and human kallikrein 2 (hK2) are expressed primarily by prostate epithelial cells. PSA and hK2 both exist as free protein and complexed with protease inhibitors (e.g., alpha1-antichymotrypsin, ACT) in serum. The expression of PSA and hK2 in LNCaP cells is upregulated by androgen. METHODS: LNCaP, a prostate cancer cell line that secretes both PSA and hK2, was used as a model to study the biosynthesis and processing of PSA and hK2 upon androgen induction. RESULTS: Precursor (zymogen or pro) forms of both PSA and hK2 were detected in spent media of induced and noninduced LNCaP cells, indicating that PSA and hK2 are secreted as proPSA (pPSA) and prohK2 (phK2), respectively, and are converted to the mature forms extracellularly. A 3-fold higher ratio of mature to pPSA was detected in the spent media of mibolerone-induced LNCaP cells compared to noninduced cells. In addition to the inactive proform of PSA, more than half of the mature unclipped PSA present in the spent media did not complex with exogenously added ACT. Spent media of mibolerone-induced LNCaP cells contained nearly 100% mature hK2, whereas the spent media of noninduced cells contained mostly phK2. CONCLUSIONS: These results indicate that androgens not only upregulate the expression of these kallikreins, but also have a significant effect on the processing of PSA and hK2. These results also show that LNCaP cells express a heterogeneous mixture of inactive PSA and hK2 forms that may serve as a model for the genesis of these forms in physiological fluids. These findings may also provide insights into the forms and ratios of PSA and hK2 in normal and malignant breast tissues.

Antibodies, Monoclonal↗
PubMed1977

Cancer induction by exogenous hormones: possible androgen-induced cancer.

Since 1973, there has been an increase in the reported number of cases of liver tumors (both benign and malignant), associated with the intake of male hormones as anabolic steroids and oral contraceptives. Because these tumors are very rare in the younger age groups, and because there are approximately 50 million women taking oral contraceptives at the present time, there is a definite need for a large-scale epidemiological investigation to clarify this possible association.

Adult↗
PubMed1979

Refractory anemia with excess of blast cells: prognostic factors and effect of treatment with androgens or cytosine arabinoside. Results of a prospective trial in 58 patients. Cooperative Group for the Study of Aplastic and Refractory Anemias.

The results of a prospective study of 58 patients with refractory anemia and partial blastic infiltration of the bone marrow lead to the following conclusions. The median survival (12 months from diagnosis) is shorter and the rate of acute leukemia as cause of death (60%) higher than in other retrospective series. This group of patients, however, appears to be a "continuum" of preleukemic states with more or less rapid evolution, so that the exclusion of the most severe cases appears unjustified. Based on the degree of bone marrow blastosis, and also on the degree of blood cytopenias, the anomalies of 59 Fe incorporation kinetics and the bone marrow stem-cell cultures, it is possible to derive a plausible prognosis for individual patients, which could aid the choice of therapy. Androgen therapy does not accelerate leukemic evolution, but does not improve the bone marrow insufficiency. Cytosine-arabinoside at low dosage exhibited no toxicity, but did not delay the appearance of overt leukemia.

Acute Disease↗
PubMed1979

Erythroleukemia following drug induced hypoplastic anemia.

Three patients with drug-induced hypoplastic anemia terminating 2 to 6 years after presentation with erythroleukemia are described. All were treated for prolonged periods with androgen and corticosteroid and two of the patients showed apparent dependence on this therapy for optimal hematologic status. The leukemic phase was heralded by loss of this dependence and development of sideroblastic dyserythropoiesis with progression to bizarre erythroid hyperplasia and fatal cytopenia. The exact relationship between androgen and corticosteroid therapy and the erythroleukemia remains speculative.

Adrenal Cortex Hormones↗
PubMed1986

A randomized comparison of maintenance treatment with androgens, immunotherapy, and chemotherapy in adult acute myelogenous leukemia. A Leukemia-Lymphoma Group Trial of the EORTC.

Twenty-three European centers participated in a randomized clinical trial (AML-5) to study the effect of androgens and immunotherapy during maintenance in adult acute myelogenous leukemia. Induction treatment consisted of Adriamycin (doxorubicin) 50 mg/m2 day 1, vincristine VCR 1 mg/m2 day 2, and cytosine arabinoside 80 mg/m2 every 12 hours by push injection days 3-9. Patients in complete remission were randomized into four groups: (1) 6-mercaptopurine 70 mg/m2 days 1-14, methotrexate 15 mg/m2 twice weekly days 15-28, and reinduction with daunorubicin 35 mg/m2 and vincristine 1 mg/m2 day 29; (2) chemotherapy as in group 1 plus stanozolol 0.15 mg/kg/day; (3) 6-thioguanine 70 mg/m2 orally on 4 consecutive days and cytosine arabinoside 80 mg/m2 subcutaneously day 5 every week; and (4) chemotherapy as in Group 3 plus irradiated blast cells treated with neuraminidase. Three hundred forty-eight patients were eligible and 295 were evaluable. The median age was 45 yrs. A complete remission was achieved in 64% of the patients, with 158 complete remissions randomized. Patients not randomized and patients receiving bone marrow transplantation (BMT) were analyzed separately. There was no difference in disease-free survival (DFS) or survival in the four maintenance arms. For patients reaching complete remission, the median DFS was 40 weeks, and median survival was 22 months with 30% surviving at 4 years. The overall survival was 18% at 4 years. There was no beneficial effect for DFS or survival by adding either immunotherapy or androgens to chemotherapy during maintenance. However, patients receiving immunotherapy seemed to have a higher rate of responses to reinduction after relapse than those in the other treatment arms.

Adolescent↗
PubMed1987

Partial androgen resistance due to a distinctive qualitative defect of the androgen receptor.

Using whole genital skin fibroblasts, we have characterized a novel androgen receptor mutation in a family with partial androgen resistance. The proposita was born with bilateral labioscrotal folds and a single perineal urogenital orifice. Her similarly affected maternal aunt was raised as a female with the support of gonadectomy and vaginoplasty. The mutant androgen receptor has a normal maximum binding capacity (Bmax), but an increased apparent equilibrium dissociation constant (Kd) with 5 alpha-dihydrotestosterone (DHT) and 2 synthetic androgens, methyltrienolone (MT) and mibolerone (MB). Preformed mutant DHT-receptor complexes dissociate (k) at a near-normal rate, but their MT and MB counterparts dissociate twice as quickly as normal. The native free mutant receptor is not more thermolabile than normal, but its recently dissociated counterpart is. Prolonged incubation of the cells with each of the 3 androgens causes the mutant receptor to acquire a normal increment of increased androgen-receptor activity. This androgen-sensitive pattern of misbehavior of the present mutant receptor distinguishes it from those responsible for 3 other families with partial androgen resistance studied previously. These differences will help to identify structure-function domains on the androgen receptor protein, particularly in conjunction with the use of DNA probes to analyze mutations at the X-linked androgen receptor locus.

Androgen-Insensitivity Syndrome↗