Abstract
Objective: There is a high incidence of anemia in patients with advanced prostate cancer (PC) under androgen deprivation. Pathophysiology of this anemia remains unclear. Erythropoietin (EPO) is the main growth factor inducing erythropoesis in response to hypoxia. In this study, function of the EPO-system following androgen deprivation was tested in standardized animal model. Methods: Animals were ...
Abstract
Objective: There is a high incidence of anemia in patients with advanced prostate cancer (PC) under androgen deprivation. Pathophysiology of this anemia remains unclear. Erythropoietin (EPO) is the main growth factor inducing erythropoesis in response to hypoxia. In this study, function of the EPO-system following androgen deprivation was tested in standardized animal model. Methods: Animals were pretreated by either orchiectomy, injection of cyproteroneacetate or flutamide. After hypoxic stimulation, EPO mRNA expression and EPO serum levels were studied. Results: In all animals, EPO mRNA expression and EPO serum levels were increased following hypoxic stimulation. Compared to the control group, this increase was even more pronounced after androgen deprivation. None of the different forms of androgen deprivation had a negative stimulating effect on EPO expression. Conclusion: Unexpectedly, androgen deprivation did not suppress EPO mRNA expression and EPO serum concentrations. Instead, stimulation of the EPO system was even more pronounced after androgen deprivation. A deficient EPO system does not appear to contribute to the clinically observed anemia in patients treated by androgen deprivation.
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