Male hypogonadism is a clinical condition that results from the body’s inability to produce physiological concentrations of testosterone and/or normal amounts of sperm. Roughly, it is estimated that approximately 6% of Americans have androgen deficiency and that 1 in 500,000 people per year can be diagnosed with androgen deficiency. Over the past two decades, there have been important advances in the diagnosis and treatment of male hypogonadism, including the identification of new genetic factors for hypogonadism, the development of sensitive testosterone assays, and the development of testosterone replacement therapy that can be easily administered and maintained at physiologic concentrations. Basaria summarized the relevant literature between 1970 and 2012 as follows: Male hypogonadism is a clinical condition resulting from disruption at any level of the hypothalamic-pituitary-gonadal axis. In primary hypogonadism, testicular lesions result in lower serum testosterone concentrations, impaired spermatogenesis, and elevated gonadotropin levels. Secondary hypogonadism has reduced serum testosterone concentrations, decreased spermatogenesis, and decreased gonadotropin levels. Many congenital or acquired disorders can lead to primary or secondary hypogonadism. The diagnosis of hypogonadism in men is based on a reliable assessment of signs and symptoms, low serum testosterone concentrations in the morning (at least twice, using a reliable assessment method. It is important to note that the diagnosis of hypogonadism should be avoided following acute illness, systemic disease, eating disorders, medication misuse, and excessive exercise in patients. The initial evaluation of disease should screen for total testosterone concentration in the morning blood sample and, if the concentration of sex hormone-binding globulin is abnormal, for free testosterone (balanced dialysis is recommended) or bioavailable testosterone (the gold standard is ammonium sulfate precipitation). If the male is infertile, a semen analysis should also be performed. Further evaluation should include a gonadotropin test and genetic analysis to rule out Klinefelter’s syndrome. If gonadotropins are below normal, secondary hypogonadism may be considered. Prolactin and other pituitary hormones, iron ions should also be checked and Cushing’s syndrome should be ruled out. If hyperprolactinemia is associated with more symptoms, an MRI of the pterygoid saddle should be performed to rule out diabetes mellitus and metabolic syndrome (both without pterygoid saddle damage). In addition, the diagnosis of male hypogonadism should also exclude other conditions that can affect serum testosterone concentrations, such as the use of opiates, glucocorticoids, ketoconazole, etc. Testosterone replacement therapy should only be used to treat patients with confirmed hypogonadism, with the aim of establishing and maintaining secondary sexual characteristics, sexual function, somatic structure and quality of life. This treatment is contraindicated in some patients, such as prostate and breast cancers. There are different preparations and dosing regimens for testosterone replacement therapy, and the pros and cons of each are shown in the table below (Table 4). Clinicians should select treatment options based on patient preference, ability to pay, availability, and composition characteristics. Side effects of testosterone replacement therapy include erythrocytosis, elevated prostate characteristic antigen (and resulting prostate biopsy), unknown cardiovascular and lipid effects, and sleep apnea. Both treatment effects and adverse effects should be monitored during treatment for this reason. Monitoring plan for testosterone replacement therapy In young adults with organic hypogonadism, the benefits of testosterone replacement therapy outweigh the drawbacks. However, the efficacy and risks of long-term treatment with testosterone replacement therapy are unclear, especially in older men older than 60 years with pathological hypogonadism, and the effects of testosterone replacement therapy on their prostate and cardiovascular systems are unknown. These will pose challenges over the next 10 years, and large randomized controlled clinical trials will help address these types of questions.