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PubMed2004

Trends and regional differences in testosterone prescribing in Australia, 1991-2001.

OBJECTIVES: To analyse temporal trends and geographical variations in testosterone prescribing in Australia. DESIGN AND SETTING: An analysis of testosterone prescribing over the past 11 years according to products and region, determined by Pharmaceutical Benefits Scheme (PBS) expenditure in Australian states and territories. MAIN OUTCOME MEASURE: Patterns of monthly PBS expenditure on injectable, oral and implantable testosterone products from 1 January 1991 to 30 December 2001, classified by state or territory. RESULTS: There were two periods (1993-1994 and 1998-1999) of striking upsurge followed by declines in national total prescribing of testosterone. These changes were more prominent for oral than injectable testosterone products, and patterns were similar in all regions, apart from a disproportionately higher peak in Western Australia in 1998. On a per-capita basis, Western Australia showed a dramatic increase in prescribing of oral and implantable, but not injectable, testosterone coinciding with the opening of a franchised men's sexual health clinic in Perth. CONCLUSION: The two striking upsurges in testosterone prescribing despite no convincing new evidence to justify them appear to reflect promotional activity to prescribe testosterone for older men, rather than overcoming the underdiagnosis of androgen deficiency related to pituitary or testicular disease in younger men. The curtailments after the introduced restrictions to PBS prescribing for older men without overt androgen deficiency were partial and temporary, suggesting that such regulatory barriers are only partly successful in counteracting the commercial and populist pressure driving excessive testosterone prescribing. Professional and community education is needed for appropriate diagnosis of genuine androgen deficiency in younger men, while discouraging unproven testosterone treatment for ageing men.

Australia↗

PubMed2000

Is low serum free testosterone a marker for high grade prostate cancer?

PURPOSE: The association of free and total testosterone with prostate cancer is incompletely understood. We investigated the relationship of serum free and total testosterone to the clinical and pathological characteristics of prostate cancer. MATERIALS AND METHODS: We retrospectively reviewed the clinical records of 117 consecutive patients treated by 1 physician and diagnosed with prostate cancer at our medical center between 1994 and 1997. Low free and total testosterone levels were defined as 1.5 or less and 300 ng./dl., respectively. RESULTS: After evaluating all 117 patients we noted no correlation of free and total testosterone with prostate specific antigen, patient age, prostatic volume, percent of positive biopsies, biopsy Gleason score or clinical stage. However, in patients with low versus normal free testosterone there were an increased mean percent of biopsies that showed cancer (43% versus 22%, p = 0.013) and an increased incidence of a biopsy Gleason score of 8 or greater (7 of 64 versus 0 of 48, p = 0.025). Of the 117 patients 57 underwent radical retropubic prostatectomy. In those with low versus normal free testosterone an increased mean percent of biopsies demonstrated cancer (47% versus 28%, p = 0.018). Pathological evaluation revealed stage pT2ab, pT2c, pT3 and pT4 disease, respectively, in 31%, 64%, 8% and 0% of patients with low and in 40%, 40.6%, 12.5% and 6.2% in those with normal free testosterone (p>0.05). CONCLUSIONS: In our study patients with prostate cancer and low free testosterone had more extensive disease. In addition, all men with a biopsy Gleason score of 8 or greater had low serum free testosterone. This finding suggests that low serum free testosterone may be a marker for more aggressive disease.

Aged↗

PubMed2002

What happens to testosterone after prostate radiation monotherapy and does it matter?

PURPOSE: There is uncertainty in the literature regarding the extent and relevance of temporary decreases in testosterone levels which occur after external radiation therapy for prostate cancer. We describe the phenomenon in detail and assess the impact on biochemical control and prostate specific antigen (PSA) doubling time in patients with relapse. MATERIALS AND METHODS: A total of 666 men were followed after external beam radiation without neoadjuvant or adjuvant androgen ablation. Serial testosterone and PSA were measured before and at 3 to 6-month intervals after therapy. RESULTS: At a median nadir time of 6 months testosterone decreased to an average of 83% of baseline. Of the patients 7.5% experienced a decrease greater than 50%. All but 3% of those with normal initial testosterone levels experienced recovery to at least normal levels but only 60% had recovery to their individual pretreatment level. Multivariate analysis showed that patients with a low pre-intervention testosterone level, and those treated with larger radiation volumes had a lower testosterone nadir. In regard to biochemical control rates, initial testosterone level, degree of decrease, and absolute testosterone nadir had no effect in either univariate or multivariate analysis. PSA doubling times in patients with relapse were no different than in those with a small or larger testosterone decrease. CONCLUSIONS: Temporary testosterone decrease after radiation therapy to the prostate is a real phenomenon with no impact on subsequent tumor outcomes.

Adult↗

PubMed2003

Delivery of testosterone replacement therapy.

Optimal testosterone replacement therapy remains a considerable challenge for the estimated five out of 1000 men in the general community with androgen deficiency. Oral delivery is not possible due to rapid first pass metabolism and short half-life. Testosterone derivatives have been developed to enhance intrinsic androgenic potency, prolong duration of action, or improve oral bioavailability of synthetic androgens. Structural modification of testosterone include 17 beta-esterification, 17 alpha-alkylation, 1-methylation, addition of a 19-normethyl group, and 7 alpha-methylation. Currently, oral (testosterone undecanoate), transcutaneous (Andropatch, Virormone, Testoderm (ALZA Corp), Testogel), sublingual (testosterone cyclodextrin), intramuscular (Sustanon, Primoteston Depot), and fused crystalline testosterone pellet preparations are available for clinical use. Transbuccal testosterone systems have also been developed for clinical use and require twice daily application. Suspensions of biodegradable microspheres consisting of a polyglycolide-lactide matrix laden with testosterone can deliver stable, physiological levels of testosterone for 2 to 3 months. Micronized testosterone has low oral bioavailability requiring high daily doses. 7 alpha-Methyl 19-nortestosterone, a potent, synthetic androgen free of hepatotoxicity, has tissue-specific selectivity, being susceptible to aromatization but not 5 alpha-reduction, thereby potentially avoiding intraprostatic androgen amplification.

Administration, Cutaneous↗

PubMed2005

Testosterone and aggressiveness.

Aggressiveness is an ancestral behavior common to all animal species. Its neurophysiological mechanisms are similar in all vertebrates. Males are generally more aggressive than females. In this review, aggressive behavior in rodents, monkeys, and man and the role of testosterone and brain serotonin levels have been considered. Interspecific aggressiveness in rats has been studied considering the mouse-killing behavior; the neonatal androgenization of females increases adult mouse-killing as does the administration of testosterone in adults. Intraspecific aggressiveness was studied by putting two or more male rats (or mice) in the same cage; the condition of subjection or dominance is influenced by testosterone. In monkeys, testosterone is related to aggressiveness and dominance and, during the mating season, increases in testosterone levels and aggressive attitude are observed. In men, higher testosterone levels were obtained in perpetrators of violent crimes, in men from the army with antisocial behaviors, in subjects with impulsive behaviors, alcoholics and suicidals, in athletes using steroids, and during competitions. Aggressive and dominant behavior are distinguished. Testosterone influences both of these, even if man is usually inclined to affirm his power without causing physical damage. Testosterone receptors are mainly in some hypothalamic neurons, where it is aromatized into estrogens, which determine the increase in aggressiveness. A relation between testosterone levels and diencephalic serotonin has been shown: in fact, the lack of serotonin increases aggressive behaviors both in animals and man. Testosterone also increases ADH levels in the medial amygdala, lateral hypothalamus, and preoptical medial area, involved in aggressive behaviors.

Adult↗

PubMed2006

Gender-dependent differences in sensation seeking and social interaction are correlated with saliva testosterone titre in adolescents.

OBJECTIVES: In the present study, we tested the hypothesis that gender - dependent differences in novelty seeking, leadership, and sympathy might correlate with testosterone titre. Since several studies report that the impact of testosterone on personality traits is more visible under emotional challenging situations, we harvested saliva testosterone upon an anticipated stressor (academic examination) and under basal conditions. SETTING AND DESIGN: 19 female and 23 male adolescents (17 to 19 years of age) completed standardized questionnaires on sensation seeking, anxiety, and social interaction. Two weeks later, they had to write an anticipated, rigorous examination in mathematics in their school. Before and after the examination, saliva had been harvested from each subject and testosterone titre has been estimated. METHODS: Saliva testosterone was quantified using a luminescence immunoassay (LIA). Each subject completed questionnaires on sensations seeking according to Zuckerman (SSS - V), anxiety (STAI), and social interactions. RESULTS: Both genders showed an increase in their testosterone titre shortly after examination or announcement of test scores. A Spearman correlation coefficient indicated a significant correlation between testosterone titre and sensation seeking subscales in female but not in male subjects. Analysis of social interactions revealed that peers regarded male subjects, who had high testosterone titres, as leaders but not as likeable individuals, whereas they regarded female subjects, who had high testosterone titres, not as leaders but as highly likeable individuals. CONCLUSION: Theses findings strongly suggest that testosterone has gender specific effects on novelty seeking, dominance, and sympathy.

Adolescent↗

PubMed2006

Testosterone levels and discounting delayed monetary gains and losses in male humans.

OBJECTIVES: Although impulsivity has been associated with androgens (e.g., testosterone), little is known regarding the relationship between testosterone levels and impulsivity in intertemporal choice (delay discounting). This study was aimed to examine the relationship between delay discounting of gains and losses and testosterone levels, which is of interest in neuroendocrinology and neuroeconomics. METHODS: We assessed degrees to which delayed monetary gains and losses were discounted (hyperbolic discounting rate) in healty male students (age: 22.4+/-2.67). Participants' salivary testosterone levels were also assessed by utilizing liquid chromatography/mass spectroscopy (LC/MS) method. RESULTS: Non-linear curve fitting analysis showed an inverted-U relationship between delay discounting of gains and salivary testosterone levels; while no relationship between salivary testosterone levels and delay discounting of losses was observed. CONCLUSIONS: The results indicate that (i) testosterone may enhance delay discounting rate of gains in non-impulsive subjects, (ii) testosterone may have an opposite (reducing) effect on delay discounting rate of gains in impulsive subjects, and (iii) testosterone is unrelated to subject's sensitivity to future bad outcomes. Implications for evaluating the effects of testosterone treatment and anti-androgenic therapy on impulsive behavior often observed in psychiatrics (e.g., pathological gambling, credit card debt, substance misuse, and needle-sharing) are discussed.

Adult↗

PubMed1988

Testosterone and alcoholic cirrhosis. Epidemiologic, pathophysiologic and therapeutic studies in men.

The present review summarizes the pathogenic mechanisms leading to variation of plasma testosterone concentrations, consequences of hypoandrogenization and hyperoestrogenization, and effects of oral testosterone treatment in men with alcoholic cirrhosis. These patients have normal median plasma testosterone concentrations, but 20% have values above and 20% have values below the normal limits. The majority of patients have raised sex hormone binding globulin (SHBG) concentrations. This increase accounts for the supranormal plasma testosterone concentrations. With decreasing liver function, plasma testosterone concentrations decrease significantly. The combination of increased SHBG levels and decreasing liver function leads to low or subnormal plasma concentrations of non-protein bound and non-SHBG bound testosterone. This decrease, together with raised oestrogen concentrations, may explain the increased prevalence of gynecomastia and testicular atrophy which raises with decreasing liver function. Oral testosterone treatment of alcoholic cirrhotic men produces an increase in the plasma concentrations of testosterone, androstenedione and dihydrotestosterone, but oestrogen concentrations increase as well. Oral testosterone treatment significantly reduces the prevalence of gynecomastia, but is without significant effects on liver biochemistry, morphology, haemodynamics, and function, general well being, sexual dysfunction and survival of alcoholic cirrhotic men. A pooled estimate of the mortality risk of cirrhotic patients treated with anabolic-androgenic steroids does not disclose any significant difference compared with placebo treatment (relative risk 0.98; 95% confidence limits 0.77-1.22). Seldom, but serious, side-effects of oral testosterone treatment can not be excluded.

Administration, Oral↗

PubMed1988

Hormonal consequences of orchidectomy for carcinoma of the prostate. With special reference to the measurement of free testosterone in saliva and prostatic dihydrotestosterone levels.

22 patients with metastatic carcinoma of the prostate were treated by subcapsular orchidectomy and followed by regular determinations of plasma testosterone, dihydrotestosterone, delta 4-androstenedione, dehydroepiandrosterone sulfate and testosterone estradiol-binding globulin as well as salivary testosterone, which reflects free plasma testosterone. Subcapsular orchidectomy constantly induced a dramatic and stable decrease in testicular androgens without modification of adrenal androgens or testosterone estradiol-binding globulin. Free testosterone levels vary widely for a given value of plasma testosterone, probably due to individual variations of testosterone estradiol-binding globulin. Salivary testosterone is preferable to plasma testosterone for monitoring hormonal therapy for metastatic carcinoma of the prostate. In another group of orchidectomized stage-D2 patients, obstructive symptoms motivated transurethral resection of the prostate allowing the assay of intraprostatic dihydrotestosterone which was constantly below the dihydrotestosterone level of androgen-independent tissues (below 2.5 ng/g).

Aged↗

PubMed1997

The induction of benign epithelial neoplasms of the ovaries of guinea pigs by testosterone stimulation: a potential animal model.

We studied the effects of different hormones on the epithelial cells of the ovaries of 11 guinea pigs. Three received testosterone, two received estrone, three megestrol, and three chorionic gonadotropin. Three control guinea pigs received sterile water. Benign epithelial cysts larger than 1.5 mm were found in six guinea pigs, three who received testosterone, one who received megestrol, and two who received chorionic gonadotropin. In one of the three guinea pigs who received testosterone, 2.5-cm bilateral cysts were grossly identified. Papillary excrescences were found on the ovarian surface in four guinea pigs, three who received testosterone and one who received megestrol. The proliferating epithelial cells also formed benign glands in the ovarian stroma in two guinea pigs who received testosterone, the most exuberant epithelial proliferations, including large bilateral cystadenomas, papillary excrescence that formed a small papillary neoplasm, and glands in the ovarian stroma that formed adenomatous areas, were seen in the guinea pig who received an intermediate dose of testosterone for the longest time. By radioimmunoassay, the serum level of testosterone was 22 ng/dL in one of the controls and 10,000, 12,000, and 15,000 ng/dL in the three guinea pigs who received testosterone. In the guinea pig with the most exuberant epithelial proliferation, the level of testosterone in the uterus was similar to that in the serum (13,860 ng/mg), but in the wall of the ovarian epithelial cyst, it was three times higher than it was in the serum (44,000 ng/mg). Our study shows that testosterone stimulates the growth of epithelial cells in the ovaries of guinea pigs, resulting in benign cysts, small adenomas in the ovarian parenchyma, and papillomas on the ovarian surface. The study also shows that guinea pigs can be used as an animal model for epithelial tumors of the human ovary.

Animals↗

PubMed1976

Acute reductions in serum testosterone levels by narcotics in the male rat: stereospecificity, blockade by naloxone and tolerance.

The effects of a single injection of morphine (20 mg/kg) on serum testosterone levels were examined in the male rat. Within 2 hours after the morphine injection, testosterone levels were significantly lower than control levels. The decline in testosterone levels reached a maximum 4 hours after the administration of morphine, at which time testosterone levels were reduced by more than 85% with respect to controls. The ability of a large number of narcotics to depress serum testosterone levels, 4 hours after their administration, was also examined. All narcotics depressed testosterone levels significantly and their potency relative to morphine was comparable to that observed in several other preparations, such as the guinea-pig ileum and mouse vas deferens. The testosterone-depleting effects of the narcotics appear to represent specific narcotic effects since the (-)-isomers of the narcotics were considerably more potent than the (+)-isomers, naloxone competitively inhibited the effects of morphine on testosterone levels and tolerance developed to the testosterone-depleting effects of these drugs. Acute treatment with morphine also lowered serum luteinizing hormone levels, and this reduction preceded the fall in testosterone levels by 1 to 2 hours.

Animals↗

PubMed1998

Blockade of the in vitro effects of testosterone and erythropoietin on Cfu-E and Bfu-E proliferation by pretreatment of the donor rats with cyproterone and flutamide.

Erythropoietin is obligatory to support the terminal proliferation and differentiation of erythroid cells but it is not the only agent in modulating red cell production. Previously, we have shown that Testosterone enhances erythropoiesis, at least in part, by increasing renal erythropoietin production. Testosterone may also influence directly the behavior of the erythroid progenitor cells increasing erythroid stem cell proliferation. To gain further insight into the role of testosterone in regulation of erythropoiesis and its interactions with erythropoietin, we studied the effect of testosterone and erythropoietin, using clonal cultures of erythropietic progenitors, to observe CFU-E and late and early BFU-E colonies proliferation from bone marrow cells of donor rats pretreated for 2 days with the androgen antagonists cyproterone (10 mg/kg/day) and flutamide (160 mg/kg/day). Specific nuclear receptors for testosterone were demonstrated in marrow erythroid cells. Then, erythroid progenitors may come with their androgen receptors blocked by pretreatment. Cultures were prepared using the methylcellulose technique containing a standard dose of erythropoietin (250 mU/ml) or testosterone (10(-7)M). Results obtained demonstrate that testosterone produced a significant stimulation on CFU-E and BFU-E colony formation. A dose effect correlation was apparent. Testosterone enhances proliferation of late BFU-E more than CFU-E and produce only a slight augmentation of early BFU-E. As expected, erythropoietin markedly stimulate all erythroid colony growth, mainly CFU-E. The effects of testosterone were completely abolished in cultures from bone marrow cells of rats pretreated with cyproterone and flutamide. Activation of the specific androgen nuclear receptors in erythroid cells appears to be necessary for testosterone to develop the erythropoietic effect. Surprisingly, the effects of erythropoietin on erythroid colonies proliferation were also completely blocked by pretreatment with flutamide and partially blocked by pretreatment with cyproterone. Right now, we do not have a satisfactory explanation regarding inhibition of the effects of erythropoietin by pretreatment to marrow donor rats with the androgen antagonists. In conclusion, we postulate triggering late BFU-E cells, a marrow erythropoietin responsive cell population, into active cell cycle, as well as by increasing blood erythropoietin concentration.

Androgen Antagonists↗

PubMed1997

Enzyme immunoassay for testosterone and androstenedione in culture medium from rabbit oocytes matured in vitro.

Two enzyme immunoassays (EIAs) were validated to determine testosterone and androstenedione levels in culture medium (Brackett's medium with or without the addition of IGF-I, hormone and serum-free), without previous extraction, from rabbit oocytes matured in vitro. Polyclonal testosterone (C917), and androstenedione (C9111) antibodies were raised in rabbits using testosterone 3-carboxymethyloxime:BSA, and androstenedione 3-carboxymethyloxime:BSA. Horseradish peroxidase was used as label, conjugated to testosterone 3-carboxymethyloxime, and to androstenedione 6-hemisuccinate. Standard dose response curves covered a range between 0 and 1 ng/well. The low detection limits of the technique were 11.43 pg/ml for testosterone, and 2.32 pg/ml for androstenedione. Intra- and inter-assay coefficient of variation percentages were < 6.4 and < 7.1 for testosterone, and < 5.1 and < 6.3 for androstenedione, respectively (n= 10). The recovery rate of known testosterone or androstenedione concentrations added to pools of culture maturation medium samples averaged 97.58 +/- 2.11%, and 95.73 +/- 1.59%, respectively. Compared with RIA, EIA values were in close agreement for testosterone (n= 15, r= 0.96, P< 0.001), and androstenedione (n= 15, r= 0.94, P< 0.001). Culture medium samples were obtained at the end of oocyte in vitro maturation (14-16 h). Mean +/- SE culture maturation medium concentrations (ng/ml) were 1.80 +/- 0.09 and 0.52 +/- 0.01 for testosterone, and 1.70 +/- 0.04 and 0.24 +/- 0.01 for androstenedione in both the oocytes with and without cumulus cells, respectively. We concluded that our EIA is a highly sensitive and specific assay that provides a rapid, simple, inexpensive and nonradiometric alternative to RIA for determining testosterone and androstenedione concentrations in oocyte maturation culture medium.

Journal Article↗

PubMed2005

Testosterone as a predictor of pathological stage in clinically localized prostate cancer.

PURPOSE: Substantial controversy exists in the literature regarding the association between pretreatment testosterone and disease outcome in patients with prostate cancer. We explored the relationship between preoperative total testosterone, and pathological stage and progression in patients with clinically localized prostate cancer treated with radical prostatectomy. MATERIALS AND METHODS: We retrospectively reviewed the records of consecutive patients with clinically localized prostate cancer treated with radical prostatectomy between January 1990 and June 2003. A total of 326 patients with pretreatment testosterone levels available were eligible for this analysis. Biochemical progression (BCR) was defined by postoperative prostate specific antigen (PSA) greater than 0.4 ng/ml with a confirmatory increase and it occurred in 41 men. No men received adjuvant therapy. Univariate and multivariate logistic regression analyses were done to examine whether pretreatment testosterone was associated with pathological stage. Cox regression was used to assess the association of testosterone and BCR. RESULTS: Median PSA was 6.01 ng/ml (range 0.13 to 86), testosterone was 385 ng/dl (range 133 to 998) and followup was 36 months (range 4 to 136). In 245 patients (75%) disease was organ confined. Lower testosterone correlated with adverse pathological stage on multivariate analysis (p = 0.01), as did clinical stage, biopsy grade and PSA. However, we found no relationship between testosterone and BCR after adjusting for covariates. Furthermore, we found no evidence of an interaction between PSA and testosterone (p = 0.4). CONCLUSIONS: On multivariate analysis low preoperative total testosterone was associated with advanced pathological stage but not with BCR. Future studies are warranted with data on more patients who have progressed.

Biomarkers, Tumor↗

PubMed1997

Dietary testosterone suppresses protective responsiveness to Plasmodium chabaudi malaria.

This study investigates the effect of orally administered testosterone on serum testosterone levels and immune responses including outcome of Plasmodium chabaudi malaria. Female C57BL/10 mice were fed on a diet impregnated with 17 alpha-methyl-testosterone for 3 weeks. This raised the circulating testosterone levels from 0.28 ng/ml to 2.69 ng/ml on the average. In these mice, blood-stage infections of P. chabaudi resulted in a lethal outcome, whereas protective immunity developed in about 80% of mice fed on control diet without testosterone. Dietary 17 alpha-methyl-testosterone reduced the capacity of peritoneal cells to generate reactive oxygen intermediates after stimulation with C3b-coated zymosan and phorbol-myristate-acetate. Also, mice fed on dietary 17 alpha-methyl-testosterone responded to heat-killed Salmonella typhimurium with a higher increase in serum TNF, whereas the induced increase in the production of IL-10 by spleen cells was largely suppressed and no effect was found with respect to the production of IFN-gamma and IL-4. Our data indicate that the method of oral administration of 17 alpha-methyl-testosterone raises circulating testosterone to levels that impair protective immune responses to P. chabaudi malaria.

Animals↗

PubMed2006

Low testosterone levels and the risk of anemia in older men and women.

BACKGROUND: Anemia is a frequent feature of male hypogonadism and anti-androgenic treatment. We hypothesized that the presence of low testosterone levels in older persons is a risk factor for anemia. METHODS: Testosterone and hemoglobin levels were measured in a representative sample of 905 persons 65 years or older without cancer, renal insufficiency, or anti-androgenic treatments. Hemoglobin levels were reassessed after 3 years. RESULTS: At baseline, 31 men and 57 women had anemia. Adjusting for confounders, we found that total and bioavailable testosterone levels were associated with hemoglobin levels in women (P = .001 and P = .02, respectively) and in men (P<.001 and P = .03, respectively). Men and women in the lowest quartile of total and bioavailable testosterone were more likely than those in the highest to have anemia (men, 14/99 vs 3/100; odds ratio [OR], 5.4; 95% confidence interval [CI], 1.4-21.8 for total and 16/99 vs 1/99; OR, 13.1; 95% CI, 1.5-116.9 for bioavailable testosterone; women, 21/129 vs 12/127; OR, 2.1; 95% CI, 0.9-5.0 for total and 24/127 vs 6/127; OR, 3.4; 95% CI, 1.2-9.4 for bioavailable testosterone). Among nonanemic participants and independent of confounders, men and women with low vs normal total and bioavailable testosterone levels had a significantly higher risk of developing anemia at 3-year follow-up (21/167 vs 28/444; relative risk, 2.1; 95% CI, 1.1-4.1 for total and 26/143 vs 23/468; relative risk, 3.9; 95% CI, 1.9-7.8 for bioavailable testosterone). CONCLUSION: Older men and women with low testosterone levels have a higher risk of anemia.

Aged↗

PubMed2006

Effect of testosterone replacement therapy on prostate tissue in men with late-onset hypogonadism: a randomized controlled trial.

CONTEXT: Prostate safety is a primary concern when aging men receive testosterone replacement therapy (TRT), but little information is available regarding the effects of TRT on prostate tissue in men. OBJECTIVE: To determine the effects of TRT on prostate tissue of aging men with low serum testosterone levels. DESIGN, SETTING, AND PARTICIPANTS: Randomized, double-blind, placebo-controlled trial of 44 men, aged 44 to 78 years, with screening serum testosterone levels lower than 300 ng/dL (<10.4 nmol/L) and related symptoms, conducted at a US community-based research center between February 2003 and November 2004. INTERVENTION: Participants were randomly assigned to receive 150 mg of testosterone enanthate or matching placebo intramuscularly every 2 weeks for 6 months. MAIN OUTCOME MEASURES: The primary outcome measure was the 6-month change in prostate tissue androgen levels (testosterone and dihydrotestosterone). Secondary outcome measures included 6-month changes in prostate-related clinical features, histology, biomarkers, and epithelial cell gene expression. RESULTS: Of the 44 men randomized, 40 had prostate biopsies performed both at baseline and at 6 months and qualified for per-protocol analysis (TRT, n = 21; placebo, n = 19). Testosterone replacement therapy increased serum testosterone levels to the mid-normal range (median at baseline, 282 ng/dL [9.8 nmol/L]; median at 6 months, 640 ng/dL [22.2 nmol/L]) with no significant change in serum testosterone levels in matched, placebo-treated men. However, median prostate tissue levels of testosterone (0.91 ng/g) and dihydrotestosterone (6.79 ng/g) did not change significantly in the TRT group. No treatment-related change was observed in prostate histology, tissue biomarkers (androgen receptor, Ki-67, CD34), gene expression (including AR, PSA, PAP2A, VEGF, NXK3, CLU [Clusterin]), or cancer incidence or severity. Treatment-related changes in prostate volume, serum prostate-specific antigen, voiding symptoms, and urinary flow were minor. CONCLUSIONS: These preliminary data suggest that in aging men with late-onset hypogonadism, 6 months of TRT normalizes serum androgen levels but appears to have little effect on prostate tissue androgen levels and cellular functions. Establishment of prostate safety for large populations of older men undergoing longer duration of TRT requires further study. Trial Registration clinicaltrials.gov Identifier: NCT00161304.

Adult↗

PubMed2005

Testosterone for peri- and postmenopausal women.

BACKGROUND: : The value of adding testosterone to hormone therapy (HT) for the management of peri- and postmenopausal women is controversial and has not been systematically reviewed. OBJECTIVES: : To determine the benefits and risks of testosterone therapy for peri- and postmenopausal women taking hormone therapy. SEARCH STRATEGY: : We searched the Cochrane Menstrual Disorders and Subfertility Group Trials Register (1st November 2003), The Cochrane Library (Issue 2, 2003), MEDLINE (1966 to 1st November 2003), EMBASE (1980 to 1st November 2003), Biological Abstracts (1969 to 2002), PsycINFO (1972 to 1st November 2003), CINAHL (1982 to 1st November 2003), and reference lists of articles. We also contacted pharmaceutical companies and researchers in the field. SELECTION CRITERIA: : Studies that were randomized comparisons of testosterone plus hormone therapy versus hormone therapy alone in peri- or postmenopausal women. DATA COLLECTION AND ANALYSIS: : Two review authors assessed the quality of the trials and extracted data independently. Where it was necessary, the corresponding authors of eligible trials were contacted for additional information. For dichotomous outcomes Peto odds ratios and 95% confidence intervals were calculated. For continuous outcomes non-skewed data from valid scales were synthesized using a weighted mean difference or standardized mean difference. If statistical heterogeneity was found, a random-effects model was used and reasons for the heterogeneity were explored and discussed. MAIN RESULTS: : Twenty-three trials with 1957 participants were included in the review. The median study duration was 6 months (range 1.5 to 24 months). Most of the trials were of adequate quality with regard to randomization and concealment of allocation sequence. The major methodological limitations were attrition bias and lack of a washout period in the cross-over studies. The pooled estimate from the studies suggested that the addition of testosterone to HT regimens improved sexual function scores for postmenopausal women. A significant adverse effect was a decrease in high-density lipoprotein (HDL) cholesterol levels. The discontinuation rate was not significantly greater with testosterone therapy (Peto odds ratio 1.01, 95% confidence interval 0.76 to 1.33) than with HT alone. There was insufficient evidence of a treatment effect for perimenopausal women or for other outcomes. AUTHORS' CONCLUSIONS: : Only a limited number of studies could be pooled in the meta-analyses. This limited the power of the meta-analysis to provide conclusions about efficacy and safety. However, there is evidence that adding testosterone to HT has a beneficial effect on sexual function in postmenopausal women. There was a reduction in HDL cholesterol associated with the addition of testosterone to the HT regimens. The meta-analysis combined studies using different testosterone regimens. It is, therefore, difficult to estimate the effect of testosterone on sexual function in association with any individual hormone treatment regimen.

Androgens↗