Testosterone replacement therapy to improve secondary sexual characteristics and body composition without adverse behavioral problems in adult male patients with Prader-Willi syndrome: An observational study

2013 ◽  
Vol 161 (9) ◽  
pp. 2167-2173 ◽  
Author(s):  
Yasuhiro Kido ◽  
Satoru Sakazume ◽  
Yoshiko Abe ◽  
Yuji Oto ◽  
Hisashi Itabashi ◽  
...  
2005 ◽  
Vol 00 (01) ◽  
pp. 75
Author(s):  
Adrian S Dobs

Male hypogonadism affects an estimated four to five million men in the US. It is defined as failure of the testes to produce an adequate amount of testosterone and/or conduct normal spermatogenesis. The production of adequate amounts of testosterone is necessary for development of external genitalia and development of secondary sexual characteristics in children and adolescents. In adults, androgen production is necessary for maintenance of lean body mass (LBM), bone mass, libido, sexual function, and spermatogenesis.


2009 ◽  
Vol 53 (8) ◽  
pp. 996-1004 ◽  
Author(s):  
Edésio Seara de Andrade Júnior ◽  
Ruth Clapauch ◽  
Salo Buksman

OBJECTIVE: To assess the efficacy and safety of testosterone replacement in males with late-onset hypogonadism compared to hypogonadal men without replacement, and controls, during six months. METHODS: We assessed, through ADAM, AMS, IIEF-5 and SF-36 questionnaires, and through clinical and laboratorial examinations, 62 patients divided into three groups: 17 hypogonadal males (HR) used intramuscular testosterone every three weeks; 14 hypogonadal males (HV) and 31 non-hypogonadal males (CV) used oral vitamins daily. RESULTS: When compared to others, HR group obtained libido improvement assessed by ADAM 1 (p = 0.004), and borderline sexual potency improvement assessed by IIEF-5 (p = 0.053), besides a decrease in waist circumference after eight weeks (p = 0.018). The remaining parameters did not differ between the groups. PSA and hematocrit remained stable in those using testosterone. CONCLUSION: Six months of testosterone replacement improved sexuality and body composition, with prostatic and hematological safety.


2005 ◽  
Vol 13 (12) ◽  
pp. 2195-2201 ◽  
Author(s):  
William H. Hoffman ◽  
Paule Barbeau ◽  
Mark S. Litaker ◽  
Maribeth H. Johnson ◽  
Cheryl A. Howe ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Jaco Botha ◽  
Line Velling Magnussen ◽  
Morten Hjuler Nielsen ◽  
Tine Bo Nielsen ◽  
Kurt Højlund ◽  
...  

Aims. To investigate how circulating microvesicle phenotypes correlate with insulin sensitivity, body composition, plasma lipids, and hepatic fat accumulation. We hypothesized that changes elicited by testosterone replacement therapy are reflected in levels of microvesicles. Methods. Thirty-nine type 2 diabetic males with lowered testosterone levels were assigned to either testosterone replacement therapy or placebo and evaluated at baseline and after 24 weeks. Microvesicles were analysed by flow cytometry and defined as lactadherin-binding particles within the 0.1–1.0 μm gate. Microvesicles of platelet, monocyte, and endothelial cell origin were identified by cell-specific markers and their expression of CD36 was investigated. Results. Triglycerides correlated positively with all investigated microvesicle phenotypes in this study (p<0.05), and indicators of hepatic fat accumulation, alanine aminotransferase, and gamma glutamyltransferase correlated with platelet and endothelial microvesicles and CD36-expressing microvesicles from platelets and monocytes (p<0.05). BMI, waist circumference, and fat percentage correlated with CD36-expressing monocyte microvesicles (p<0.05), while insulin sensitivity did not correlate with any microvesicle phenotypes. Microvesicle levels were unaffected by testosterone therapy. Conclusions. Metabolic syndrome components and hepatic fat accumulation correlated with microvesicle phenotypes, supporting the involvement of especially CD36 on monocytes in metabolic syndrome pathogenesis. Although testosterone therapy improved body composition measures, microvesicle phenotype levels were unaffected. This trial was registered at ClinicalTrials.gov (NCT01560546).


2014 ◽  
Vol 32 (4_suppl) ◽  
pp. 229-229
Author(s):  
Aksam Yassin ◽  
Dany-Jan Yassin ◽  
Peter Hammerer

229 Background: There is controversy over whether testosterone replacement therapy is a risk factor for prostate cancer. Herein, we evaluate whether testosterone deficiency (TD), testosterone replacement therapy (TRT) or 5-alpha reductase inhibitor (5-ARI) therapy affect the risk of prostate cancer. Methods: Data were collected from 224 male patients who had an indication for prostate biopsy: Prostate specific antigen (PSA) greater than 4, PSA-Velocity >=0.75 in a year, hypogonadism with PSA >=1.5, positive digital rectal exam (DRE) and/or positive Transrectal Ultrasonography (TRUS) finding. Each patient was then subjected to a TRUS-guided 10 core prostate biopsy. Results: 25% (3 out of 12) of the patients on TRT were found to have prostate cancer via biopsy and 32.1% (68 out of 212) of patients who did not receive TRT were found to have prostate cancer; insignificant with p = 0.757. Seventeen our of 76 (22.4%) of the patients on 5-ARI treatment were found to have prostate cancer and 36.5% (54 out of 148) of the patients who did not receive 5-ARI were found to have prostate cancer; significant with p = 0.03. There was no significant statistical difference in Gleason grades among patients who were on TRT, no TRT, on 5-ARI and no 5-ARI. Conclusions: Our data suggest that TRT is not associated with increased risk of prevalence or Gleason grade of prostate cancer. 5-ARI therapy is associated with lower prevalence of prostate cancer but with no relationship to Gleason grade.


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