Association of serum testosterone levels and testicular volume in adult patients

Andrologia ◽  
2017 ◽  
Vol 50 (3) ◽  
pp. e12933 ◽  
Author(s):  
S. F. Ruiz-Olvera ◽  
O. Rajmil ◽  
J.-R. Sanchez-Curbelo ◽  
J. Vinay ◽  
J. Rodriguez-Espinosa ◽  
...  
Keyword(s):  
Serum Testosterone ◽  
Adult Patients ◽  
Testicular Volume ◽  
Testosterone Levels

Why Do We Need New Markers for Male Hypogonadism and How Seminal Proteomics Might Solve the Problem?

2020 ◽  
Vol 27 (12) ◽  
pp. 1186-1191
Author(s):  
Giuseppe Grande ◽  
Domenico Milardi ◽  
Silvia Baroni ◽  
Andrea Urbani ◽  
Alfredo Pontecorvi
Keyword(s):  
Serum Testosterone ◽  
Clinical Syndrome ◽  
Testosterone Replacement ◽  
Total Testosterone ◽  
Male Hypogonadism ◽  
Grey Zone ◽  
Testosterone Levels ◽  
Normal Number ◽  
Replacement Treatment

Male hypogonadism is “a clinical syndrome that results from failure of the testis to produce physiological concentrations of testosterone and/or a normal number of spermatozoa due to pathology at one or more levels of the hypothalamic– pituitary–testicular axis”. The diagnostic protocol of male hypogonadism includes accurate medical history, physical exam, as well as hormone assays and instrumental evaluation. Basal hormonal evaluation of serum testosterone, LH, and FSH is important in the evaluation of diseases of the hypothalamus-pituitary-testis axis. Total testosterone levels < 8 nmol/l profoundly suggest the diagnosis of hypogonadism. An inadequate androgen status is moreover possible if the total testosterone levels are 8-12 nmol/L. In this “grey zone” the diagnosis of hypogonadism is debated and the appropriateness for treating these patients with testosterone should be fostered by symptoms, although often non-specific. Up to now, no markers of androgen tissue action can be used in clinical practice. The identification of markers of androgens action might be useful in supporting diagnosis, Testosterone Replacement Treatment (TRT) and clinical follow-up. The aim of this review is to analyze the main findings of recent studies in the field of discovering putative diagnostic markers of male hypogonadism in seminal plasma by proteomic techniques. The identified proteins might represent a “molecular androtest” useful as a seminal fingerprint of male hypogonadism, for the diagnosis of patients with moderate grades of testosterone reduction and in the follow-up of testosterone replacement treatment.

scholarly journals Testosterone in Female Depression: A Meta-Analysis and Mendelian Randomization Study

Biomolecules ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 409
Author(s):  
Dhruba Tara Maharjan ◽  
Ali Alamdar Shah Syed ◽  
Guan Ning Lin ◽  
Weihai Ying
Keyword(s):  
Mendelian Randomization ◽  
Meta Analysis ◽  
Menopausal Status ◽  
Serum Testosterone ◽  
Serum Levels ◽  
Testosterone Levels ◽  
Mendelian Randomization Analysis ◽  
The Difference ◽  
Diagnostic Capabilities ◽  
Randomization Analysis

Testosterone’s role in female depression is not well understood, with studies reporting conflicting results. Here, we use meta-analytical and Mendelian randomization techniques to determine whether serum testosterone levels differ between depressed and healthy women and whether such a relationship is casual. Our meta-analysis shows a significant association between absolute serum testosterone levels and female depression, which remains true for the premenopausal group while achieving borderline significance in the postmenopausal group. The results from our Mendelian randomization analysis failed to show any causal relationship between testosterone and depression. Our results show that women with depression do indeed display significantly different serum levels of testosterone. However, the directions of the effect of this relationship are conflicting and may be due to menopausal status. Since our Mendelian randomization analysis was insignificant, the difference in testosterone levels between healthy and depressed women is most likely a manifestation of the disease itself. Further studies could be carried out to leverage this newfound insight into better diagnostic capabilities culminating in early intervention in female depression.

Short-term adverse effects of testosterone used for priming in prepubertal boys before growth hormone stimulation test

2018 ◽  
Vol 31 (1) ◽  
pp. 21-24 ◽  
Author(s):  
Andrea Albrecht ◽  
Theresa Penger ◽  
Michaela Marx ◽  
Karin Hirsch ◽  
Helmuth G. Dörr
Keyword(s):  
Growth Hormone ◽  
Side Effects ◽  
Adverse Effects ◽  
Side Effect ◽  
Serum Testosterone ◽  
Low Flow ◽  
Effect Rate ◽  
Testosterone Levels ◽  
Testicular Pain ◽  
Prepubertal Boys

AbstractBackground:Despite the fact that priming with sex steroids in prepubertal children before growth hormone (GH) provocative tests is recommended, there is an ongoing controversial discussion about the appropriate age of the children, the drug used for priming, the dose and the period between priming and the GH test. Interestingly, there is no discussion on the safety of this procedure. To date, only little data have been available on the possible side effects of priming with testosterone.Methods:We analyzed the outcome in 188 short-statured prepubertal boys who had been primed with testosterone enanthate (n=136: 50 mg; n=51: 125 mg, and accidentally one boy with 250 mg) 7 days prior to the GH test. Serum testosterone levels were measured on the day of the GH test in 99 boys.Results:Overall, only five boys developed adverse side effects. Two boys (dose 125 mg) showed severe low-flow priapism and had to undergo decompression of the corpora cavernosa. One boy suffered from self-limiting priapism and testicular pain (dose 50 mg). Two patients reported testicular pain (each dose 50 mg). The single patient with 250 mg testosterone did not show any adverse effects. The total side effect rate was 2.7%. The serum testosterone levels of the boys with side effects were not different from the testosterone levels of the boys without any side effects.Conclusions:Parents and patients should be informed about the possible side effects of priming with testosterone such as priapism and testicular pain. However, the overall side effect rate is low. We found no correlation between the outcome and the testosterone dose used and/or the level of serum testosterone.

Low serum testosterone levels are predictive of prostate cancer

2011 ◽  
Vol 31 (2) ◽  
pp. 247-252 ◽  
Author(s):  
Luigi Mearini ◽  
Alessandro Zucchi ◽  
Elisabetta Nunzi ◽  
Tommaso Villirillo ◽  
Vittorio Bini ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Serum Testosterone ◽  
Testosterone Levels ◽  
Low Serum

Serum Testosterone Levels in Males with Alzheimer's Disease

2004 ◽  
Vol 16 (2) ◽  
pp. 95-98 ◽  
Author(s):  
C. Pennanen ◽  
M. P. Laakso ◽  
M. Kivipelto ◽  
J. Ramberg ◽  
H. Soininen
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Serum Testosterone ◽  
Testosterone Levels

scholarly journals Mice lacking β-carotene-15,15’-dioxygenase exhibit reduced serum testosterone, prostatic androgen receptor signaling, and prostatic cellular proliferation

2016 ◽  
Vol 311 (6) ◽  
pp. R1135-R1148 ◽  
Author(s):  
Joshua W. Smith ◽  
Nikki A. Ford ◽  
Jennifer M. Thomas-Ahner ◽  
Nancy E. Moran ◽  
Eric C. Bolton ◽  
...  
Keyword(s):  
Androgen Receptor ◽  
Cellular Proliferation ◽  
Serum Testosterone ◽  
Cell Number ◽  
Immunofluorescent Staining ◽  
Receptor Signaling ◽  
Ki 67 ◽  
Androgen Receptor Signaling ◽  
Testosterone Levels ◽  
Β Carotene

β-Carotene-15,15’-dioxygenase (BCO1) cleaves dietary carotenoids at the central 15,15’ double bond, most notably acting on β-carotene to yield retinal. However, Bco1 disruption also impacts diverse physiological end points independent of dietary carotenoid feeding, including expression of genes controlling androgen metabolism. Using the Bco1−/− mouse model, we sought to probe the effects of Bco1 disruption on testicular steroidogenesis, prostatic androgen signaling, and prostatic proliferation. Male wild-type (WT) and Bco1−/− mice were raised on carotenoid-free AIN-93G diets before euthanasia between 10 and 14 wk of age. Weights of the prostate and seminal vesicles were significantly lower in Bco1−/− than in WT mice (−18% and −29%, respectively). Serum testosterone levels in Bco1−/− mice were significantly reduced by 73%. Bco1 disruption significantly reduced Leydig cell number and decreased testicular mRNA expression of Hsd17b3, suggesting inhibition of testicular testosterone synthesis. Immunofluorescent staining of the androgen receptor (AR) in the dorsolateral prostate lobes of Bco1−/− mice revealed a decrease in AR nuclear localization. Analysis of prostatic morphology suggested decreases in gland size and secretion. These findings were supported by reduced expression of the proliferation marker Ki-67 in Bco1−/− prostates. Expression analysis of 200 prostate cancer- and androgen-related genes suggested that Bco1 loss significantly disrupted prostatic androgen receptor signaling, cell cycle progression, and proliferation. This is the first demonstration that Bco1 disruption lowers murine circulating testosterone levels and thereby reduces prostatic androgen receptor signaling and prostatic cellular proliferation, further supporting the role of this protein in processes more diverse than carotenoid cleavage.

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