A rationale for the use of testosterone "salvage" in treatment of men with erectile dysfunction failing phosphodiesterase inhibitors

An age-related decline of serum testosterone (T) is reported in approximately 20% to 30% of men. However, the evaluation of total T levels may be misleading because of an increase in sex hormone-binding globulin (SHBG). Free and bioavailable T levels seem to be a better biochemical marker. Observational studies show that T concentrations are consistently lower among men with cardiovascular disease but not with erectile dysfunction (ED), suggesting a possible preventive role that requires critical evaluation with prospective studies. Hormonal replacement therapy can induce both beneficial and deleterious effects on cardiovascular risk factors by decreasing serum levels of high-density lipoprotein (HDL) cholesterol, plasminogen activator inhibitor type-1, lipoprotein (a), fibrinogen, and visceral fat mass in hypogonadal men. By contrast, the possible beneficial effects of T in cardiovascular disease include antiatherogenic and coronary vasodilator effects. Shortterm interventional studies show that T produces a modest but consistent improvement in cardiac ischemia over placebo. ED is most frequently caused by pelvic arterial insufficiency resulting from atherosclerosis, and T administration in men with arteriogenic ED produces robust vasodilator effects on the cavernous arteries. The role of T supplementation on erectile function in the era of phosphodiesterase type 5-inhibitors is discussed.