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Although the normal range for serum testosterone might vary between different laboratories, the normal range for early morning total testosterone in healthy adult males is approximately 300 ng/dL to 1000 ng/dL.7,8 In males, serum testosterone levels show a circadian variation, with the highest levels in the morning and lowest levels in the late afternoon. Hypogonadism is a lack of testosterone in male patients and can be of central (hypothalamic or pituitary) or testicular origin, or a combination of both.
There are many suspected causes of osteoporosis, and the most frequent are corticosteroid use, Cushing’s syndrome, hypogonadism and excessive alcohol consumption. Hip fracture incidence is low until after 75 years, when the risk increases exponentially. Up to 13 million men are at increased risk because of low BMD and up to 2 million of these have osteoporosis (61,62). The mechanism underlying the insulin sensitising effects of testosterone needs to be elucidated. In addition, a small dose (50 mg/day) of testosterone gel improved both glycemic control and insulin sensitivity over and above the improvements because of diet and exercise (60). However, it seems likely that testosterone may suppress insulin resistance independently of its effects on adiposity. Leptin, released in response to increased adiposity, also inhibits the release of LH via its effect on the release of gonadotropin-releasing hormone
Large randomised trials using men with and without cardiovascular disease and with cardiovascular end-points are needed to better assess the consequences of testosterone treatment on cardiovascular risk (36). Human observational studies, however, have shown no associations between high testosterone levels and coronary artery disease, and testosterone has been shown to dilate the coronary arteries both in vitro and in vivo. In fact, the increased risk of cardiovascular disease in males compared with females has been taken to imply a role for testosterone (or oestrogen) in the disease. It is not yet understood whether the low testosterone levels are a consequence of the disease, are connected with the disease’s aetiology, or are one of the causes of the disease. As discussed below, a measurement of low testosterone in a patient should be reconfirmed at a later stage before considering treatment. A subject can have low testosterone levels, but can also have no clinically significant symptomatology.
It is recommended to perform a baseline digital rectal examinations (DRE) and a baseline PSA level measurement before starting testosterone therapy for any man, whatever his age (2,89). Although it is an effective oral androgen formulation, it is not recommended as a testosterone therapy for hypogonadism because of its hepatotoxic side effects and its association with long-term development of liver tumours. These are applied in the night and provide a good approximation of normal circadian plasma testosterone levels.




1 We recommend testosterone therapy in hypogonadal men to induce and maintain secondarysex characteristics and correct symptoms of testosterone deficiency. 1.3 In men who have hypogonadism, we recommend distinguishing between primary (testicular) and secondary (pituitary–hypothalamic) hypogonadism by measuring serum luteinizing hormone and follicle stimulating hormone concentrations. There are few absolute contraindications to testosterone replacement therapy other than prostate or breast cancer, a hematocrit of 55% or greater, or sensitivity to the testosterone formulation. Before initiation of testosterone replacement therapy, an examination of the prostate, including DRE, PSA assay, and assessment of prostate symptoms should be undertaken, and both the hematocrit and lipid profile should be measured. These include prostate cancer, which must be assessed by history and clinical examination. The usual treatment is initiation of therapy with small doses of testosterone (50–100 mg IM) every 3 to 4 weeks at the appropriate psychosocial stage in development.