Antibody-mediated pure red cell aplasia (PRCA) treatment and re-treatment: multiple options

Rossert, Jérôme; Macdougall, Iain C.; Casadevall, Nicole

doi:10.1093/ndt/gfh1090

Cited by 24 publications

(23 citation statements)

References 18 publications

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“…Therefore, one study recommended that a successful therapeutic strategy for patients with anti-EPO PRCA should consist of stopping administration of all ESAs and initiating cyclosporine therapy. However, if cyclosporine does not increase reticulocyte (Ret) counts, treatment with other immunosuppressive drugs, such as corticosteroids plus cyclophosphamide, or kidney transplantation should be considered [7]. Tacrolimus and cyclosporine are calcineurin inhibitors, with similar pharmacological functions but different receptors [8].…”

Section: Introductionmentioning

confidence: 99%

Pure red cell aplasia induced by anti-erythropoietin antibodies, well-controlled with tacrolimus

Hashimoto

Harada

Kamijo³

2016

Int J Hematol

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Anti-erythropoietin (anti-EPO) antibody-related pure red cell aplasia (PRCA) is a rare but serious complication that can occur during the administration of erythropoiesis-stimulating agents. Treatment with the calcineurin inhibitor cyclosporine has shown benefits in patients with anti-EPO PRCA. The efficacy of tacrolimus, another calcineurin inhibitor, in patients with anti-EPO PRCA has not been determined. The present report is the first our knowledge to describe the successful treatment of a patient with anti-EPO PRCA using tacrolimus. A 73-year-old man was markedly anemic 8 months after starting epoetin beta treatment. He was diagnosed with anti-EPO PRCA. Cyclosporine was started, but he experienced side effects. He was switched from cyclosporine to tacrolimus. No side effects were observed, and his anti-EPO PRCA was improved 6 months later, despite the persistence of anti-EPO antibodies. Tacrolimus was continued until the disappearance of the antibodies. Following the cessation of tacrolimus, PRCA did not relapse. Antibody remained detectable at the time of clinical remission, indicating that immunosuppressive therapy should be continued while monitoring the antibody titer. When the antibody titer decreases to the negative range, cessation of the immunosuppressive therapy does not result in disease relapse.

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Section: Introductionmentioning

confidence: 99%

Pure red cell aplasia induced by anti-erythropoietin antibodies, well-controlled with tacrolimus

Hashimoto

Harada

Kamijo³

2016

Int J Hematol

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“…Early recognition of PRCA and withholding of ESA therapy are essential, but cessation of ESA treatment alone generally will not cure ESA-induced PRCA (25). In cases of PRCA induced by other drugs (unrelated to anti-erythropoietin antibody production), the PRCA generally remits within 1 to 2 wk after elimination of exposure to the causative agent.…”

Section: Treatment Of Esa-induced Prcamentioning

confidence: 99%

“…Verhelst et al (29) reported higher recovery rates when corticosteroids were given together with cyclophosphamide (87%) than when corticosteroids were given alone. In patients with CKD and ESA-induced PRCA, oral cyclosporine therapy resulted in hematologic recovery in more than two thirds of the investigated PRCA cases (25). 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).…”

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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“…While there are only a handful of cases reported in the literature in which this has been attempted [27][28][29], it does appear that successful rechallenge is possible, particularly if immunosuppression is continued to inhibit antibody production. There is at least one case, however, of relapse of antibody-mediated PRCA after rechallenge [30], and the possibility that this may occur should be recognized.…”

Section: Management Of Epoetin-induced Pure Red Cell Aplasiamentioning

confidence: 99%

Epoetin-induced pure red cell aplasia: diagnosis and treatment

Macdougall

2007

Current Opinion in Nephrology and Hypertension

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Management of pure red cell aplasia as a complication of erythropoiesis-stimulating agent therapy consists of stopping the drug and implementing an immunosuppressive regimen to reduce or abolish erythropoietin antibody production. A recent animal study suggested that a possible alternative strategy may be to administer a novel peptide-based erythropoietin receptor agonist called Hematide that does not cross react with antierythropoietin antibodies, and will allow ongoing stimulation of erythropoiesis; this is the subject of a current clinical trial.

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Antibody-mediated pure red cell aplasia (PRCA) treatment and re-treatment: multiple options

Cited by 24 publications

References 18 publications

Pure red cell aplasia induced by anti-erythropoietin antibodies, well-controlled with tacrolimus

Pure red cell aplasia induced by anti-erythropoietin antibodies, well-controlled with tacrolimus

Pure Red Cell Aplasia Induced by Erythropoiesis-Stimulating Agents

Epoetin-induced pure red cell aplasia: diagnosis and treatment

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