Effects of testosterone replacement therapy on bone metabolism in male post-surgical hypogonadotropic hypogonadism: focus on the role of androgen receptor CAG polymorphism

2014 ◽  
Vol 37 (4) ◽  
pp. 393-400 ◽  
Author(s):  
G. Tirabassi ◽  
N. delli Muti ◽  
A. Gioia ◽  
A. Biagioli ◽  
A. Lenzi ◽  
...  
Keyword(s):  
Androgen Receptor ◽  
Replacement Therapy ◽  
Bone Metabolism ◽  
Hypogonadotropic Hypogonadism ◽  
Testosterone Replacement ◽  
Testosterone Replacement Therapy ◽  
Cag Polymorphism

scholarly journals Androgen Receptor Gene CAG Repeat Polymorphism Regulates the Metabolic Effects of Testosterone Replacement Therapy in Male Postsurgical Hypogonadotropic Hypogonadism

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Giacomo Tirabassi ◽  
Nicola delli Muti ◽  
Giovanni Corona ◽  
Mario Maggi ◽  
Giancarlo Balercia
Keyword(s):  
Androgen Receptor ◽  
Replacement Therapy ◽  
Receptor Gene ◽  
Hypogonadotropic Hypogonadism ◽  
Cag Repeat ◽  
Pituitary Function ◽  
Metabolic Effects ◽  
Testosterone Replacement ◽  
Testosterone Replacement Therapy ◽  
Repeat Polymorphism

Aim. To evaluate the independent role of androgen receptor (AR) gene CAG repeat polymorphism on metabolic effects of testosterone replacement therapy (TRT) in male postsurgical hypogonadotropic hypogonadism, a condition frequently associated with hypopituitarism and in which the TRT-related metabolic effects are combined with those deriving from concomitant administration of metabolically active pituitary-function replacement therapies.Methods. 15 men affected by postsurgical hypogonadotropic hypogonadism were evaluated before and after TRT. Cardiovascular risk factors (CVRFs), pituitary-dependent hormones, and AR gene CAG repeat polymorphism were considered.Results. Testosterone, insulin-like growth factor 1 (IGF-1), and estradiol were the only hormones, which varied significantly between the two phases. All CVRFs significantly improved after TRT. The number of CAG triplets was positively and significantly correlated with all the variations (Δ-) of CVRFs (except for a significant negative correlation with Δ-high-density lipoprotein); the opposite occurred between the latter and Δ-testosterone. No correlation between Δ-IGF-1 or estradiol and Δ-CVRFs was found. At multiple linear regression, after correction for Δ-testosterone, nearly all the associations between the number of CAG triplets and Δ-CVRFs were confirmed.Conclusions. In male postsurgical hypogonadotropic hypogonadism, shorter AR gene CAG tract length seems to yield greater metabolic improvement after TRT, independently of the effects of concomitant pituitary-function replacement therapies.

Testosterone Replacement Therapy in Males With Erectile Dysfunction

2011 ◽  
Vol 24 (3) ◽  
pp. 298-306 ◽  
Author(s):  
Bobby C. Jacob
Keyword(s):  
Erectile Dysfunction ◽  
Replacement Therapy ◽  
Common Factor ◽  
Serum Testosterone ◽  
Testosterone Replacement ◽  
Testosterone Replacement Therapy ◽  
Testosterone Deficiency ◽  
Global Estimates ◽  
The Relationship

Erectile dysfunction (ED) is defined as the inability to achieve or maintain an erection sufficient for satisfactory sexual performance. Endogenous testosterone is critical for normal libido; however, studies have also demonstrated a potentially important role with respect to the erectile process. The prevalence of testosterone deficiency ranges from 1.7% to 35% in patients with ED, and age is a common factor linking ED and testosterone deficiency. By 2025, global estimates are that there will be 356 million men >65 years. Age-associated testosterone deficiency is characterized by symptoms such as ED, and low serum testosterone. Randomized, placebo controlled studies have established the utility of testosterone replacement therapy (TRT) for the restoration of serum testosterone levels to the normal range in hypogonadal males; however, well designed studies are limited with respect to specific evaluation of the role of TRT as monotherapy in improving erectile function. In addition, recent literature suggests a possible role for TRT in combination with phosphodiesterase-5 (PDE-5) inhibitors for men with ED. The following review describes the potential roles of testosterone in erectile physiology, examines the relationship between testosterone deficiency and ED, and reviews published literature evaluating the use of TRT in hypogonadal males with a diagnosis of ED.

scholarly journals Switch to restoration therapy in a testosterone treated central hypogonadism with erythrocytosis

2017 ◽  
Vol 2017 ◽  
Author(s):  
B Cangiano ◽  
C Cacciatore ◽  
L Persani ◽  
M Bonomi
Keyword(s):  
Side Effects ◽  
Replacement Therapy ◽  
Late Onset ◽  
Clomiphene Citrate ◽  
Hypogonadotropic Hypogonadism ◽  
Vitamin D Supplementation ◽  
Testicular Volume ◽  
Testosterone Replacement ◽  
Testosterone Replacement Therapy ◽  
List Type

We describe a case of severe erythrocytosis caused by testosterone replacement therapy in a 66-year-old man affected with hypogonadotropic hypogonadism (HH) determining osteoporosis, resolved by switching to restoration therapy with clomiphene citrate. The patient complained fatigue, loss of libido and defective erections and a spontaneous vertebral fracture despite bisphosphonate therapy and vitamin D supplementation. The examinations proved isolated HH and he was therefore treated with testosterone gel with regression of specific manifestations but elevated hemoglobin and hematocrit values. Therefore, it was decided to switch to a restoration therapy with clomiphene citrate 25 mg/die, which resulted in the resolution of symptoms without evident side effects. In a couple of months, the patient showed normalization of testosterone levels and increment of testicular volume. Since secondary hypogonadism is the consequence of an insufficient stimulation of the gonads by hypothalamic–pituitary axis, therapeutic approaches aimed to restore endogenous testosterone production should be considered in alternative to testosterone replacement, particularly if side effects intervene. Among these strategies, clomiphene citrate seems to have a high efficacy and safety profile also in the elderly with isolated HH and no evident pituitary lesion. Learning points: Hypogonadism should always be assessed in patients with severe loss in BMD and undergo appropriate medical treatment. In hypogonadotropic hypogonadism, more approaches are available other than testosterone replacement therapy alone. In patients with severe late-onset central hypogonadism presenting with erythrocytosis even at low doses of replacement therapy, restoration therapy with clomiphene could prove to be an effective solution, particularly in patients with a reversible disruption of GNRH/gonadotropin functions. Clomiphene citrate increases gonadotropin levels and testicular volume and should therefore be considered in hypogonadal men who wish to remain fertile.

scholarly journals A Case of Male Osteoporosis: A 37-Year-Old Man with Multiple Vertebral Compression Fractures

2017 ◽  
Vol 2017 ◽  
pp. 1-7
Author(s):  
Suhaib Radi ◽  
Andrew C. Karaplis
Keyword(s):  
Bone Mass ◽  
Replacement Therapy ◽  
Fragility Fractures ◽  
Testosterone Replacement ◽  
Vertebral Compression Fractures ◽  
Testosterone Replacement Therapy ◽  
Male Hypogonadism ◽  
Mineral Density ◽  
Compression Fractures

While the contributing role of testosterone to bone health is rather modest compared to other factors such as estradiol levels, male hypogonadism is associated with low bone mass and fragility fractures. Along with stimulating physical puberty by achieving virilization and a normal muscle mass and improving psychosocial wellbeing, the goals of testosterone replacement therapy in male hypogonadism also include attainment of age-specific bone mineral density. We report on a 37-year-old man who presented with multiple vertebral compression fractures several years following termination of testosterone replacement therapy for presumed constitutional delay in growth and puberty. Here, we discuss the management of congenital hypogonadotropic hypogonadism with hyposmia (Kallmann syndrome), with which the patient was ultimately diagnosed, the role of androgens in the acquisition of bone mass during puberty and its maintenance thereafter, and outline specific management strategies for patients with hypogonadism and high risk for fragility fractures.

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