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There is no relation between the degree of hyperglycaemia and testosterone concentration (40,43). In the HIM study, a diabetic man was approximately twice as likely to be hypogonadal compared with a non-diabetic man (18). Projections based on data from the National Health and Nutrition Examination Surveys (NHANES) show that by 2021 there are anticipated to be approximately 33 million people with diabetes in the United States, representing 13.5% of the population (39). In 2007, it was estimated that 23.6 million people, or 7.8% of the US population, had diabetes (38). The relationship between testosterone and HDL is confounded by the fact that both HDL and testosterone are inversely related to BMI. Vascular tissue (including endothelium and vascular smooth muscle cells) contains androgen receptors, so it is to be expected that testosterone (or its metabolite, oestrogen) is likely to affect the cardiovascular system. There appears to be no consistent evidence that the prevalence of hypogonadism differs between racial and ethnic groups (24–26).
An age-related guideline for referral if PSA levels exceed 2.5 ng/ml in males under 60 years or 4 ng/ml in men over 60 years is often used (97). Bone mineral density measurement should also be carried out at baseline because hypogonadism is an important cause of male osteoporosis. Elevated haematocrit values above 54% require action – usually therapy should be stopped until the values decrease to a safe level. Any significant increase in PSA deserves a referral to a urologist and treatment should be discontinued until evaluated. AEs, adverse events; BMD, bone mineral density; DRE, digital rectal examination; PSA, prostate-specific antigen.
The estradiol produced by aromatisation also provides negative feedback on the HPG axis, further reducing testosterone. Thus, the degree of hypogonadism is positively correlated to the degree of obesity in obese men (51,52). Such patients have also been shown to have mild anaemia, low bone mineral density (BMD) in the arms and ribs, and increased adiposity when compared with eugonadal type 2 diabetics (44,45).
In addition, research has uncovered that enclomiphene increases total and free testosterone levels without increasing dihydrotestosterone disproportionately, suggesting that it \"normalizes endogenous testosterone production pathways and restores normal testosterone levels in men with secondary hypogonadism.\" They wrote that while testosterone replacement therapy often resulted in side effects such as transference risk, supranormal testosterone levels, suppressed spermatogenesis, suppressed testicular function, and testicular atrophy, none of these risks are present in enclomiphene. Men with secondary hypogonadotropic hypogonadism have abnormally low testosterone levels due to low-normal levels of luteinizing hormone (LH) and follicular stimulating hormone (FSH).
It is therefore important that physicians are aware of the major symptoms of the condition and of the treatment options currently available. There is, however, no established consensus about what constitutes a significant rise in PSA levels or when urological referral should occur for men with normal PSA levels at baseline. It is not yet known if the normal PSA reference ranges should be lowered for men with type 2 diabetes. However, recent analysis has shown that, although there are case studies of occult conversions, these represent a very small number of the 200,000 cases of prostate cancer diagnosed in the United States and there is no evidence of causality. In addition, 5 alpha-reductase inhibitors, such as finasteride and dutasteride, reduce prostate volume and PSA levels. Case reports of occult cancers apparently stimulated to become clinically relevant cancers by testosterone treatment added to the concern. The origins of this concern date back to papers published in 1941 that reported that androgens stimulated prostate cancer, whereas oestrogen or castration reduced them (91).
Primary hypogonadism requires no further investigation into the cause, although some clinicians do a karyotype to definitively diagnose or exclude Klinefelter syndrome. Klinefelter syndrome should be considered in adolescent males in whom puberty is delayed, young men with hypogonadism, and all adult men with very small testes and/or azoospermia (absent sperm in semen). Adult-onset testosterone deficiency has varied manifestations depending on the degree and duration of the deficiency. As adults, affected patients have poor muscle development, a high-pitched voice, a small scrotum, decreased phallic and testicular growth, sparse pubic and axillary hair, and an absence of body hair. Childhood-onset testosterone deficiency (see Male Hypogonadism in Children) is unrecognized until puberty is delayed. Second- or third-trimester onset of testosterone deficiency results in microphallus and undescended testes. Congenital hypogonadism of first-trimester onset results in inadequate male sexual differentiation (see also Sexual Differentiation, Adrenarche, and Puberty).
If levels of FSH and LH increase in response to IV GnRH, puberty is simply delayed. Semen analysis should be performed in all men who are seeking fertility treatment. Serum FSH and LH levels can be drawn as a single blood sample are usually ≤ 5 mIU/mL (5 IU/L) before puberty and between 5 and 15 mIU/mL (5 and 15 IU/L) in adulthood.
A fuller explanation may be that prostate cancer is very sensitive to changes in serum testosterone when at low concentrations, but is insensitive at higher concentrations because of saturation of the androgen receptors (93). In fact, prostate cancer is correlated with age in men, and older men tend to have less, not more, testosterone. The authors demonstrated that, as a result of this, approximately 35% of hypogonadal patients did not receive treatment (20). However, the increase in size of the prostate needs to carefully monitored, and the patient needs to be made aware that there might be increased voiding symptoms during treatment (2,4,9,79,89). BMD measurement in a male with osteopenia/osteoporosis or low trauma fracture can be repeated in 1–2 years after testosterone replacement therapy is initiated (2,79).
Likewise, in the Baltimore study the percentage of men with low testosterone increased from 12% in men in their 50s, to 49% in men over 80 years of age (23). The Hypogonadism in Males (HIM) study estimated the overall prevalence of hypogonadism at approximately 39% in men aged 45 years or older (18). In the Baltimore Longitudinal Study on Ageing, it was found that 19% of men over 60 years had low testosterone. Certain medications and illnesses can also affect the hypothalamic–pituitary system resulting in hypogonadism (17). Secondary hypogonadism can be caused by a number of conditions (Table 3) including hypothalamic and pituitary disorders or lesions, hyperprolactinemia and Kallmann syndrome (which causes a GnRH deficiency) (16). Apart from the vital role that it plays during puberty in stimulating the development of male secondary sexual characteristics and their maintenance thereafter, it has multiple other physiological effects.

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