Approximately 20–50% of HIV-infected men receiving highly active antiretroviral therapy are hypogonadal. In a case–control study of 40 cancer survivors it was found that 90% of those on opioid treatment were hypogonadal compared with only 40% of the control group (69). Various epidemiological studies in men have examined associations between testosterone and estradiol levels and BMD. There is an inverse linear relationship between total testosterone and BMI, and free testosterone concentrations also decrease with increasing BMI. Utilising data from the NHANES III survey, it was found that men in the lowest free testosterone tertile were four times as likely to have diabetes as those in the highest free testosterone tertile (47). Interestingly, low testosterone concentrations predict the development of type 2 diabetes. The concentrations of C-reactive protein in these patients are twice as high as those in eugonadal type 2 diabetics, whose C-reactive protein levels are already elevated compared with non-diabetics.
The Endocrine Society recommends that the diagnosis of testosterone be made in men who have both consistent signs and symptoms and low total testosterone levels. A recent study showed that supervised diet and exercise increased testosterone levels in hypogonadal men with metabolic syndrome and newly diagnosed type 2 diabetes. The withdrawal of testosterone therapy in hypogonadal patients that had been stabilised on this therapy leads to an increase in insulin resistance within 2 weeks and prior to significant weight gain (59). C-reactive protein, a marker for systemic inflammation, has been found to be markedly elevated in patients with secondary hypogonadism and type 2 diabetes. The Massachusetts Male Ageing Study (MMAS) measured a combination of testosterone levels and hypogonadal symptoms and found between 6% and 12% of men had symptomatic androgen deficiency (21).
Long-acting opioids such as methadone, morphine sulphate, fentanyl and oxycodone for the treatment of chronic pain often result in opioid-induced androgen deficiency (OPIAD). Systemic glucocorticoids can reduce testosterone biosynthesis in the testis; in addition, glucocorticoids impact the HPG axis by inhibiting the release of LH (17,68). Other common secondary causes are smoking, low calcium intake and vitamin D deficiency or insufficiency (61).
The Sertoli cells of the testes, in addition to stimulating spermatogenesis, also secrete the glycoprotein hormone inhibin, which provides negative feedback to the pituitary, inhibiting the secretion of FSH (11). For this reason, free and albumin-bound testosterones together are termed bioavailable testosterone (BAT). Testosterone binds strongly to SHBG, and it is therefore largely the free and albumin-bound testosterone that is available for biological action (10). FSH, follicle-stimulating hormone; GnRH, gonadotropin-releasing hormone; LH, luteinizing hormone LH acts on the interstitial Leydig cells of the testes, stimulating them to produce testosterone, whereas FSH stimulates spermatogenesis and Sertoli cell function (6,7).
The correlation of voiding symptoms and prostate size is poor, so there may not be any changes in urine flow rates and prostate voiding symptoms. The development of BPH requires androgens, but many studies have failed to show an association with testosterone treatment. Patients with benign prostatic hyperplasia (BPH) treated with androgens are at an increased risk for worsening of signs and symptoms of BPH.

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