Correspondence (reply): In Reply

The use of radioactive isotopes to treat polycythemia vera as described by Schmidt in his letter was first described in 1940. Although they were easy to handle and effective, scientific discussion since has focused on the leukemogenic effect of phosphorus-32 (1). In the first two decades after phosphorus-32 had been introduced, no other therapeutic options existed: hence an increased risk of developing leukemia at a later stage was accepted in return for acute protection from potentially fatal thromboembolic complications. The thinking on this matter has changed since effective substances – such as hydroxyurea, interferon alpha, or anagrelide – have become available for cytoreduction and thus prevention of thromboembolic complications. Since in treating patients with polycythemia vera, the golden rule is "primum nil nocere," we recommend phosphorus-32 because of the increased leukemia risk only in exceptions, i.e., in patients older than 70 or in patients whose long-term medication cannot be well controlled (2).

Tsamaloukas mentioned new developments in anemia treatment that utilize novel insights into the molecular basis of the regulation of renal erythropoiesis; these are indeed fascinating. Discussing these would have exceeded the scope of our review. However, his wish for a current German language review article of primary myelofibrosis can be fulfilled (3). We thank Nieschlag for mentioning the special scenario of testosterone induced polycythemia in elderly men. The fact that androgens can increase erythropoiesis has been known for a long time (4). The conclusion from these observations is that the blood of patients receiving testosterone substitution should be monitored regularly. However, what is not known is whether androgen induced erythrocytosis is also associated with an increased risk of thromboembolic complications.