Erythropoiesis and marrow stimulation

Androgen therapy has long been used clinically to stimulate erythropoiesis since the original observational study of 68 women with breast cancer which demonstrated significant, sometimes dramatic, increases in hemoglobin levels after the administration of 100 mg testosterone or dihydrotestosterone propionate injections three times weekly (Kennedy and Gilbertsen 1957). In addition, androgen therapy has smaller and less consistent effects on other bone marrow cell lineages that produce neutrophils and platelets. Androgen therapy increases hemoglobin in healthy men (Palacios etal. 1983; Wu etal. 1996) as well as augmenting the hemoglobin responses to recombinant human erythropoietin (EPO) in renal anemia (Ballal etal. 1991) and iron supplementation in iron deficiency anemia (Victor et al. 1967). Although the hemoglobin response to androgen therapy is usually modest in magnitude (typically ~10g/l), a small proportion (~1%) of normal (Palacios etal. 1983; Wu etal. 1996) or hypogonadal (Drinka et al. 1995; Krauss et al. 1991) men exhibit idiosyncratic polycythemic responses to androgen therapy. Such androgen-inducedpolycythemia may be asymptomatic or produce significant clinical effects due to hyperviscosity and/or ischemia. Androgen-induced polycythemia is usually reversible following cessation of treatment but occasionally clinical circumstances (e.g. unstable angina or transient ischemic attack) may warrant venesection. The biochemical basis of the idiosyncratic polycythemic response to testosterone is not fully understood, but it appears to be more frequent with testosterone ester injections, presumably reflecting the transient supraphysiological peak blood testosterone concentrations following each injection (see Chapter 14). More stable testosterone delivery with transdermal patches (Meikle et al. 1996) or implants (Handelsman et al. 1997) are rarely associated with polycythemia (Jockenhovel et al. 1997). Following recovery from testosterone-induced polycythemia, testosterone treatment may be resumed with careful monitoring by using a more steady-state preparation. Androgen-induced polycythemia is also occasionally related to underlying sleep apnea or respiratory failure. It is not known whether or not the androgen receptor CAG triplet repeat polymorphism in androgen sensitivity is involved (Zitzmann and Nieschlag 2003).

Sleep Apnea

Sleep Apnea

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