Can the administration of testosterone to men with late-onset hypogonadism be discontinued?

Over the last decade, in addition to the classical forms of hypogonadism attributable to defects in testicular steroidogenesis (primary hypogonadism) or defects of the hypothalamo–pituitary unit (secondary hypogonadism), a new form has been defined: late-onset hypogonadism (LOH). LOH is partially based on the ageing process of the hypothalamo–pituitary–testicular axis leading to a diminution of the efficacy of testicular steroidogenesis, but a more significant determinant of decline in testosterone levels with ageing is disease and, in particular, the so-called metabolic syndrome. The main components of the metabolic syndrome are abdominal obesity, insulin resistance, hypertension and dyslipidaemia and these components are, in principle, remediable. Administration of testosterone to elderly men with the metabolic syndrome and hypogonadal values of testosterone leads to an improvement in the components of the metabolic syndrome which, in turn, could lead to an improvement in the own testicular hormone production eventually obviating the need for testosterone administration. There is very limited experience with this approach but this strategy deserves further exploration.