title: Treatment of erythropoietin-induced pure red cell aplasia: a retrospective study.
abstract: BACKGROUND
  Recombinant human erythropoietin is the standard treatment for anaemia related to chronic kidney disease, and its widespread use has been favoured by a very high therapeutic index. However, since 1998, more than 200 patients worldwide with chronic kidney disease treated in this way have developed neutralising antibodies to erythropoietin, causing pure red cell aplasia. We aimed to collate clinical and pathological features in patients unequivocally shown to have erythropoietin-induced pure red cell aplasia.
  
  
  METHODS
  We retrospectively obtained data from the files of 47 patients with pure red cell aplasia. We assessed treatment and outcome of patients and defined recovery from pure red cell aplasia as an increase in reticulocyte counts to more than 20 000 per microL in patients who were no longer transfusion-dependent.
  
  
  RESULTS
  When patients developed pure red cell aplasia, all were receiving erythropoietin subcutaneously, and the product most typically prescribed was epoetin alfa (Eprex, Ortho Biotech). The median delay between start of erythropoietin treatment and occurrence of pure red cell aplasia was 11 months (IQR 7.5-14). Nine patients received no immunosuppressive treatment, and none of these recovered. Of 37 patients who received immunosuppressive therapy, 29 (78%) recovered. All six patients who received a kidney transplant recovered within 1 month, and recovery rates were between 56% and 88% in patients treated with corticosteroids, corticosteroids plus cyclophosphamide, or ciclosporin. No relapse of pure red cell aplasia happened after stopping immunosuppressive treatment, but no patient was rechallenged with erythropoietin.
  
  
  CONCLUSIONS
  Immunosuppressive treatment accelerates recovery from erythropoietin-induced pure red cell aplasia.
authors.affiliation: Department of Nephrology, Tenon Hospital, Assistance Publique-Hôpitaux de Paris, and Pierre and Marie Curie University, Paris, France.
authors.forename: David
authors.initials: D
authors.lastname: Verhelst
authors.forename: Jérôme
authors.initials: J
authors.lastname: Rossert
authors.forename: Nicole
authors.initials: N
authors.lastname: Casadevall
authors.forename: Anne
authors.initials: A
authors.lastname: Krüger
authors.forename: Kai-Uwe
authors.initials: KU
authors.lastname: Eckardt
authors.forename: Iain C
authors.initials: IC
authors.lastname: Macdougall
mesh_terms: D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D000368:Aged; D000740:Anemia / Q000188:drug therapy / Q000209:etiology; D004921:Erythropoietin / Q000009:adverse effects*; D005260:Female; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000627:therapeutic use; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007676:Kidney Failure, Chronic / Q000150:complications; D008297:Male; D008875:Middle Aged; D011994:Recombinant Proteins; D012010:Red-Cell Aplasia, Pure / Q000139:chemically induced* / Q000628:therapy*; D012189:Retrospective Studies
chemical_list: D000305:Adrenal Cortex Hormones; D016756:Immunoglobulins, Intravenous; D007166:Immunosuppressive Agents; D011994:Recombinant Proteins; D004921:Erythropoietin