Successful resumption of epoetin alfa after rituximab treatment in a patient with pure red cell aplasia

Mandreoli, Marcora; Finelli, Carlo; Lopez, Antonia; Ascani, Stefano; Vianelli, Nicola; Baccarani, Michele; Santoro, Antonio

doi:10.1053/j.ajkd.2004.06.016

Cited by 14 publications

(1 citation statement)

References 18 publications

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“…Of 15 patients with idiopathic PRCA treated with a humanized mAb to the IL-2 receptor (daclizumab), six (40%) responded to the treatment, but this therapy has not been evaluated in patients with antibody-mediated PRCA (30). Successful treatment with rituximab has also been reported in a few patients, whereas others failed to respond to this therapy (29,31). PRCA associated with parvovirus infection responds well to intravenous Ig therapy, but the results in patients with ESA-induced PRCA are poor (29).…”

Section: Treatment Of Esa-induced Prcamentioning

confidence: 99%

Pure Red Cell Aplasia Induced by Erythropoiesis-Stimulating Agents

Pollock¹,

Johnson²,

Hörl³

et al. 2008

Clinical Journal of the American Society of Nephrology

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Pure red cell aplasia in patients who are treated for anemia of chronic kidney disease with erythropoiesis-stimulating agents such as epoetin was first reported in 1998. Although the incidence of pure red cell aplasia peaked in 2002, it remains important for nephrologists to know how to investigate a suspected case of pure red cell aplasia and how to identify other causes of hyporesponsiveness to erythropoiesis-stimulating agents, which account for the vast majority of such cases. The authors reviewed the current status of information in the literature and drew on their personal experiences with patients regarding the diagnosis and management of epoetin-induced pure red cell aplasia. The mechanism for development of epoetin-induced pure red cell aplasia remains unconfirmed. It generally occurs after the production of neutralizing anti-erythropoietin antibodies. Elucidation of a suspected pure red cell aplasia case requires a systematic approach, beginning with simple measurements such as blood cell counts, because most cases of erythropoiesis-stimulating agent hyporesponsiveness are attributable to other causes. If these criteria indicate that the patient's response to erythropoiesis-stimulating agent therapy is very poor, then bone marrow examination and measurement of anti-erythropoietin antibodies is justified. If pure red cell aplasia is confirmed, then cessation of erythropoiesis-stimulating agent therapy and initiation of immunosuppressive therapy are recommended. Continued study of epoetin-induced pure red cell aplasia is needed to help nephrologists prevent or manage future cases and will have implications for the use of other protein-based therapeutic agents.

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