Testosterone Replacement Therapy

Male hypogonadism (HG) can be defined according to its etiology as primary (pHG) when caused by any diseases affecting the testes, or as secondary (sHG) when due to a pituitary or hypothalamic dysfunction. Both fertility and testosterone (T) can be theoretically restored in sHG by removing the precipitating cause and/or by appropriate endocrine therapy. Conversely, only T treatment can be offered to patients with pHG. Symptoms and signs are quite similar independent of the underlying causes. Conversely, the phenotype of the hypogonadal patient is more often affected by the age of hypogonadism onset. Late-onset hypogonadism (LOH) that occurs in adulthood is probably the most common form of HG. In this chapter, the criteria defining LOH and the available T formulations along with their outcomes and main important side effects are analyzed in detail

Testosterone Therapy in Male Infertility

Normal spermatogenesis is dependent upon production of endogenous testosterone and elevated concentrations of intratesticular testosterone. Testosterone levels typically begin to decrease over time in men starting in their late 30s; however, as many as 12.4% of men below the age of 39 suffer the effects of low testosterone and seek treatment. This statistic suggests that a significant number of men seeking treatment for low testosterone are within their reproductive years, underscoring the importance of appropriate counseling for patients seeking testosterone therapy as it pertains to family planning. The standard treatment for men with low testosterone and symptoms of hypogonadism is administration of exogenous testosterone. The challenge for testosterone replacement among men who desire fertility is that exogenous testosterone is a known contraceptive. The key for treatment of low testosterone while preserving fertility is maintenance of high concentrations of intratesticular testosterone and promotion of endogenous testosterone production. Therapies that accomplish this goal include administration of gonadotropins like GnRH and hCG, selective estrogen receptor modulators like clomiphene citrate, and aromatase inhibitors like anastrozole. Experimental therapies include intranasal testosterone gels and Leydig stem cell transplantation