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Open access

Farid Saad, Antonio Aversa, Andrea M Isidori, Livia Zafalon, Michael Zitzmann, and Louis Gooren

Objective

Testosterone has a spectrum of effects on the male organism. This review attempts to determine, from published studies, the time-course of the effects induced by testosterone replacement therapy from their first manifestation until maximum effects are attained.

Design

Literature data on testosterone replacement.

Results

Effects on sexual interest appear after 3 weeks plateauing at 6 weeks, with no further increments expected beyond. Changes in erections/ejaculations may require up to 6 months. Effects on quality of life manifest within 3–4 weeks, but maximum benefits take longer. Effects on depressive mood become detectable after 3–6 weeks with a maximum after 18–30 weeks. Effects on erythropoiesis are evident at 3 months, peaking at 9–12 months. Prostate-specific antigen and volume rise, marginally, plateauing at 12 months; further increase should be related to aging rather than therapy. Effects on lipids appear after 4 weeks, maximal after 6–12 months. Insulin sensitivity may improve within few days, but effects on glycemic control become evident only after 3–12 months. Changes in fat mass, lean body mass, and muscle strength occur within 12–16 weeks, stabilize at 6–12 months, but can marginally continue over years. Effects on inflammation occur within 3–12 weeks. Effects on bone are detectable already after 6 months while continuing at least for 3 years.

Conclusion

The time-course of the spectrum of effects of testosterone shows considerable variation, probably related to pharmacodynamics of the testosterone preparation. Genomic and non-genomic effects, androgen receptor polymorphism and intracellular steroid metabolism further contribute to such diversity.

Free access

Julia Rohayem, Frank Tüttelmann, Con Mallidis, Eberhard Nieschlag, Sabine Kliesch, and Michael Zitzmann

Context

Classical congenital adrenal hyperplasia (CAH), a genetic disorder characterized by 21-hydroxylase deficiency, impairs male fertility, if insufficiently treated.

Patient

A 30-year-old male was referred to our clinic for endocrine and fertility assessment after undergoing unilateral orchiectomy for a suspected testicular tumor. Histopathological evaluation of the removed testis revealed atrophy and testicular adrenal rest tumors (TARTs) and raised the suspicion of underlying CAH. The remaining testis was also atrophic (5 ml) with minor TARTs. Serum 17-hydroxyprogesterone levels were elevated, cortisol levels were at the lower limit of normal range, and gonadotropins at prepubertal levels, but serum testosterone levels were within the normal adult range. Semen analysis revealed azoospermia. CAH was confirmed by a homozygous mutation g.655A/C>G (IVS2-13A/C>G) in CYP21A2. Hydrocortisone (24 mg/m2) administered to suppress ACTH and adrenal androgen overproduction unmasked deficient testicular testosterone production. As azoospermia persisted due to sustained hypogonadotropic hypogonadism, a combined s.c. gonadotropin replacement with human chorionic gonadotropin (hCG) (1500 IU twice weekly) and FSH (human menopausal gondadotropin (hMG) 150 IU three times weekly) was initiated.

Results

Normalization of testosterone levels and a stable low sperm concentration (0.5 mill/ml) with good sperm motility (85% A+B progressive) were achieved within 21 months of treatment. Despite persisting TARTs, while receiving treatment, the patient successfully impregnated his wife twice, the latter impregnation leading to the birth of a healthy girl.

Conclusions

TARTs in unrecognized (simple virilizing) CAH may lead to unnecessary orchiectomy. In hypogonadotropic, azoospermic CAH, a combined treatment with oral corticosteroids and subcutaneously administered hCG and FSH can successfully restore testicular testosterone production and fertility, even if only one hypoplastic and atrophic testis with adrenal rest tumors is present.

Free access

Giovanni Corona, Vito A Giagulli, Elisa Maseroli, Linda Vignozzi, Antonio Aversa, Michael Zitzmann, Farid Saad, Edoardo Mannucci, and Mario Maggi

Objective

The role of testosterone (T) in regulating body composition is conflicting. Thus, our goal is to meta-analyse the effects of T supplementation (TS) on body composition and metabolic outcomes.

Methods

All randomized controlled trials (RCTs) comparing the effect of TS on different endpoints were considered.

Results

Overall, 59 trials were included in the study enrolling 3029 and 2049 patients in TS and control groups respectively. TS was associated with any significant modification in body weight, waist circumference and BMI. Conversely, TS was associated with a significant reduction in fat and with an increase in lean mass as well as with a reduction of fasting glycaemia and insulin resistance. The effect on fasting glycaemia was even higher in younger individuals and in those with metabolic diseases. When only RCTs enrolling hypogonadal (total T <12 mol/l) subjects were considered, a reduction of total cholesterol as well as triglyceride (TGs) levels were also detected. Conversely, an improvement in HDL cholesterol levels as well as in both systolic and diastolic blood pressure was not observed.

Conclusion

Our data suggest that TS is able to improve body composition and glycometabolic profile particularly in younger subjects and in those with metabolic disturbances. Specifically designed studies are urgently needed to confirm this point.

Restricted access

Julia Rohayem, Lena Maria Bäumer, Michael Zitzmann, Susanne Fricke-Otto, Klaus Mohnike, Bettina Gohlke, Felix Reschke, Claus Jourdan, Hermann L Müller, Désirée Dunstheimer, Johannes Weigel, Norbert Jorch, Elke Müller-Roßberg, Erwin Lankes, Imke Gätjen, Annette Richter-Unruh, Berthold P Hauffa, Sabine Kliesch, Aniko Krumbholz, and Jurgen Bramswig

Objective: To study the impact of the quality of therapeutic control on fertility and on the prevalence of testicular adrenal rest tumors (TARTs) in young males with congenital adrenal hyperplasia (CAH).

Design: Combined cross-sectional and retrospective clinical study.

Methods: Twenty-nine patients and age-matched controls underwent clinical investigation, including semen analysis, testicular and adrenal ultrasound imaging, and serum and hair steroid analysis. The quality of therapeutic control was categorized as “poor”, “moderate” or “medium”. Evaluation of current control was based on concentrations of 17-hydroxy-progesterone and androstenedione in serum and 3 cm hair; previous control was categorized based on serum 17-hydroxy-progesterone concentrations during childhood and puberty, anthropometric and puberty data, bone age data and adrenal sizes.

Results: Semen quality was similar in males with CAH and controls (p = 0.066), however patients with “poor” past control and large TARTs, or with “poor” current CAH control, had low sperm counts. Follicle-stimulating hormone was decreased, if current CAH control was “poor” (1.8 ± 0.9 U/L; “good”: 3.9 ± 2.2 U/L); p = 0.015); luteinizing hormone was decreased if it was “poor” (1.8 ± 0.9 U/L; p = 0.041) or “moderate” (1.9 ± 0.6 U/L; “good”: 3.0 ± 1.3 U/L; p = 0.025). None of the males with “good” past CAH control, 50% of those with “moderate” past control and 80% with “poor” past control had bilateral TARTs. The prevalence of TARTs in males with severe (class null or A) CYP21A2 mutations was 53%, and 25% and 0% in those with milder class B and C mutations, respectively.

Conclusions: TART development is favoured by inadequate long-term hormonal control in CAH. Reduced semen quality may be associated with large TARTs. Gonadotropin suppression by adrenal androgen excess during the latest spermatogenic cycle may contribute to impairment of spermatogenesis.