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Chronic heart failure (CHF) represents a debilitating condition with morbidity and mortality comparable to other end-stage disease states.1 Non-oedematous weight loss in the context of chronic heart failure is associated with adverse prognosis, as it is a strong independent risk factor for mortality in patients with CHF and cachexia: patients with CHF with wasting have a mortality at 18 months as high as 50% compared to 17% in those without cachexia.2 A number of different mediators have been implicated in the wasting process, including activation of pro-inflammatory cytokines, secretion of neurohormones and peptides, including PYY, ghrelin, leptin, growth hormone and insulin, and a relative deficiency of micronutrients and macronutrients.3 It has been suggested that a low testosterone level may represent one of the factors contributing to the anabolic/catabolic imbalance characteristically present in many patients with advanced CHF.4
In the study by Güder et al (see page 504) total (TT) and free serum testosterone (FT), dehydroepiandrosterone sulfate (DHEAS), and sex hormone binding globulin (SHBG) were studied in a cohort of 191 patients with heart failure (mean age 64 years; NYHA class I–IV 24/35/35/6%).5 Free testosterone (0.5–3% of the total testosterone) represents the biologically active unbound testosterone fraction. The current gold-standard method of determining free testosterone is equilibrium dialysis, but this is technically demanding and laborious, and in clinical practice, a derived method for free testosterone is employed, calculated from the total testosterone, serum albumin and SHBG. There is good correlation between the two methods. The bioavailable testosterone represents the fraction of testosterone that is unbound (free) plus the albumin bound testosterone, which is readily dissociable and thus ‘bioavailable’. A reduction in free testosterone …