Payam Hakimian

Nitrofurantoin: the return of an old friend in the wake of growing resistance.

To re‐evaluate the first‐ and second‐line therapies for treating uncomplicated urinary tract infection (UTI), as although fluoroquinolones are commonly used for this purpose, its level of use is thought to be inappropriately excessive and will eventually have a detrimental impact; thus we hypothesise that nitrofurantoin might be the best choice for this indication, due to its low frequency of use and its high susceptibility rate in common UTI pathogens.

Metabolic and cardiovascular effects of androgen deprivation therapy

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.

Erectile Dysfunction and Testosterone Deficiency

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.