Prostate cancer is the most common gender‐specific malignancy in men in the USA. Androgen‐deprivation therapy (ADT) is commonly used in the treatment of metastatic or recurrent prostate cancer. The use of ADT is increasing with the advocacy of adjuvant and neoadjuvant ADT for treating asymptomatic patients with locally advanced prostate cancer. Although the use of ADT has resulted in improved survival in men with advanced prostate cancer, ADT, with its resulting severe hypogonadism, causes profound metabolic side‐effects. We comprehensively reviewed previous reports using Medline searches of English‐language literature (1950 to the present), with the keywords ‘hypogonadism’, ‘testosterone’, ‘androgen deprivation therapy’, ‘hormonal treatment’, ‘prostate cancer’, ‘diabetes’, ‘metabolic syndrome’, and ‘cardiovascular disease’. Men with prostate cancer who undergo long‐term ADT are at greater risk of developing dyslipidaemia, insulin resistance, hyperglycaemia and metabolic syndrome. These metabolic and physiological changes are a direct result of the induced severe hypogonadism and might predispose patients to a greater risk of cardiovascular morbidity and mortality. There is a need for prospective studies aimed and designed to investigate the metabolic and cardiovascular adverse effects of ADT, and assess the benefit/risk ratio, especially in special populations such as diabetics.

A definitive role of testosterone in erectile function has been controversial; however, recent evidence is becoming available which substantiates a key function for this hormone. Testosterone deficiency is associated with a decline in erectile function and testosterone levels are inversely correlated with increasing severity of erectile dysfunction. Erectile dysfunction can be caused by multifactorial pathologies. In particular, erectile dysfunction may be the first symptom of cardiovascular disease. Animal studies have demonstrated that castration causes vascular smooth muscle cell atrophy, venous leakage, adipocytes in the subtunical space, loss of elastic fibers and increase in collagen deposition. Testosterone increases the expression of nitric oxide synthase and phosphodiesterase type 5, both principal enzymes involved in the erectile process. Testosterone replacement alone in hypogonadal men can restore erectile function. A significant proportion of men who fail to respond to a PDE5 inhibitor are testosterone deficient. Testosterone replacement therapy can convert over half of these men into phosphodiesterase type 5 responders. It is now recommended that testosterone levels should be assessed in all patients with erectile dysfunction.

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INTRODUCTION AND OBJECTIVE:Previous studies have suggested that diabetes mellitus (DM) may increase the risk of kidney and bladder cancer; however, little is known about the glycemic status and duration of DM. We analyzed the risk of kidney and bladder cancer according to the baseline glycemic status and duration of DM in a longitudinal nationwide cohort.METHODS: This study was conducted in a cohort of 9,773,462 participants !20 years old who underwent a Korean National Health Examination in 2009 and were followed up until December 2017. Coxproportional hazard models were used to evaluate the risk of kidney and bladder cancer in relation to the glycemic status and duration of DM.RESULTS: During follow-up (mean 7.3 years), kidney and bladder cancer occurred in 11,219 and 13,769 participants, respectively, at least 1 year after enrollment. DM was associated with an increased risk of kidney and bladder cancer (hazard ratio, 95% confidence interval; 1.14, 1.09e1.20 and 1.23, 1.17e1.28). Compared to fasting glucose <100 mg/dL, abnormal glycemic status and longer DM duration were associated with increased risk of kidney and bladder cancer: impaired fasting glucose (IFG) (1.