Anti-CD20 monoclonal antibody for the treatment of severe, immune-mediated, pure red cell aplasia and hemolytic anemia

Zecca, Marco; Stefano, Piero De; Nobili, Brúno; Locatelli, Franco

doi:10.1182/blood.v97.12.3995

Cited by 141 publications

(114 citation statements)

References 12 publications

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“…Rituximab has been used with varying success in the treatment of antibody-mediated cytopenias including autoimmune hemolytic anemia [2,5,6,[10][11][12]15,16]. In our patient who had warm IgM autoantibodymediated autoimmune hemolytic anemia, a disease with a known poor clinical outcome, it seems to have been a safe and effective therapy.…”

Section: Discussionmentioning

confidence: 99%

“…Because rituximab also removes normal antibody-producing B lymphocytes, it has been used to treat patients with antibody-mediated cytopenias *Correspondence to: Mary Wakim, MD, Division of Clinical Immunology and Allergy, CHLA, 4650 Sunset Blvd., Mailstop #75, Los Angeles, CA 90027. E-mail: Mwakim@chla.usc.edu with some success [5][6][7][8][9][10][11][12][13][14][15][16]. We report a case of a 6-yearold child with common variable immunodeficiency and autoimmune hemolytic anemia due to warm reactive IgM autoantibody that responded to therapy with rituximab.…”

Section: Introductionmentioning

confidence: 99%

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Successful anti‐CD20 monoclonal antibody treatment of severe autoimmune hemolytic anemia due to warm reactive IgM autoantibody in a child with common variable immunodeficiency

et al. 2004

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Autoimmune hemolytic anemia due to warm reactive IgM autoantibodies is unusual, severe, and often fails to respond to standard immunosuppressive therapies in both adults and children. A 6-year-old girl with common variable immunodeficiency had longstanding steroid dependent, splenectomy-unresponsive, warm IgM autoantibody-mediated autoimmune hemolytic anemia. Rituximab, a monoclonal antibody directed against CD20 antigen, was used to deplete B lymphocytes and reduce autoantibody production. She received a total of six doses of rituximab (375 mg/m 2 ). Therapy was well tolerated, and B-lymphocytes were effectively depleted from the peripheral blood. The patient was completely tapered off glucocorticoids. The patient has remained off immunosuppressive agents for 16 months despite the return of B lymphocytes to the peripheral circulation. She continues to require IVIG. Early treatment with rituximab might be an option for patients with warm reactive IgM autoantibody-mediated autoimmune hemolytic anemia not responding to other treatments or experiencing untoward side effects from those treatments. Am.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Successful anti‐CD20 monoclonal antibody treatment of severe autoimmune hemolytic anemia due to warm reactive IgM autoantibody in a child with common variable immunodeficiency

et al. 2004

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“…Rituximab, a chimeric anti-CD20 monoclonal antibody, causes a rapid depletion of B cells [9]. Although rituximab was originally introduced for the treatment of malignant lymphomas [10,11], several recent studies have shown that rituximab may also be effective in the treatment of ITP and other autoimmune diseases [12,19,[37][38][39][40][41][42][43][44][45][46][47][48][49][50][51][52]. The current results of all published case reports and clinical trials using rituximab in the treatment of immune thrombocytopenias have most recently been reported showing an overall response rate of about 50% [34].…”

Section: Introductionmentioning

confidence: 99%

Rituximab chimeric anti‐CD20 monoclonal antibody treatment for adult refractory idiopathic thrombocytopenic purpura

et al. 2005

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Idiopathic thrombocytopenic purpura is an autoimmune disease which involves opsonization of platelets by autoantibodies directed against different surface glycoproteins, leading to their premature destruction by the reticuloendothelial system. Management of patients with refractory ITP is difficult. Recent studies have shown that rituximab, a chimeric anti‐CD20 monoclonal antibody, is useful in the treatment of these patients, with overall response rates of about 50%. Most published reports have included a small number patients including case reports. The present study reports the results of a retrospective Danish multicenter study of rituximab in the treatment of adult patients with refractory ITP. Thirty‐five patients (median age 52 years, range 17–82 years, 17 males) were included. One patient had immune thrombocytopenia and neutropenia. All patients had received prednisolone (Pred). Next to Pred, 25 patients had been treated with high‐dose IgG, and in 16 patients a splenectomy had been performed. Sixteen patients had been treated with azathioprine. Other treatments included, e.g., cyclosporine, danazol, cyclophosphamide, vincristine, interferon, and dexamethasone. The patients were treated with a dose regimen of 375 mg/m2 i.v. approximately once weekly for 4 consecutive weeks. Six patients received a fixed dose of 500 mg disregarding their weight supplemented by 100 mg of methylprednisone i.v. or 50–100 mg of Pred given as premedication together with an antihistamine just before infusion of rituximab. The large majority of patients also received Pred and, in some cases, other concomitant immunosuppressive treatment during part of their rituximab treatment. A complete response (CR) was defined as a rise in the platelet count > 100 × 109/L, a partial response (PR) as a rise in the platelet count > 50 × 109/L, and a minor response (MR) as a rise in the platelet count < 50 × 109/L. No response (NR) was defined as no increase in the platelet count. Because 4 patients were treated twice, a total of 39 outcomes of rituximab treatment were evaluated. Rituximab proved to be effective in 17 of 39 treatments [overall response 44% with 7 CR (18%) (1 patient showed a CR twice), 6 PR (15%), and 4 MR (10%)]. In 9/13 cases of CR or PR, the response (platelet level > 50 × 109/L) was prompt, 1–2 weeks after the first infusion. The remaining patients responded 3–8 weeks later. Patients with CR and PR have been in remission for a median of 47 weeks. In general the side effects were few. In 2 cases, the treatment was stopped because of side effects either during or after the first infusion. Two fatal outcomes were recorded. A 71‐year‐old female with severe lung disease died 6 days after the first infusion of respiratory failure. The other patient, a 73‐year‐old man also with severe chronic obstructive lung disease, died of pneumonia approximately 13 weeks following the last rituximab treatment. It is concluded that rituximab may be a useful alternative therapy in patients with severe and symptomatic ITP refractory to conventional treatment. Am. J. Hematol. 78:275–280, 2005. © 2005 Wiley‐Liss, Inc.

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“…In the event of development of isohemagglutinin-mediated PRCA, the goal of therapy is to exhaust the residual pool of cells producing isohemagglutinins. Recently, rituximab has been shown to be effective in a number of patients with autoimmune antibody-mediated syndromes, such as ITP, 13 and hemolytic anemia with PRCA. 14 Hence, we hypothesized that it could be a good candidate in isohemagglutinin-mediated PRCA after BMT.…”

Section: Discussionmentioning

confidence: 99%

Successful treatment of pure red cell aplasia with a single dose of rituximab in a child after major ABO incompatible peripheral blood allogeneic stem cell transplantation for acquired aplastic anemia

Maschan

Скоробогатова

Balashov

et al. 2002

Bone Marrow Transplant

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Summary:Pure red cell aplasia (PRCA) is a well-known although infrequent hematologic complication after allogeneic bone marrow transplantation. PRCA occurs in cases of major ABO-mismatch between donor and recipient and is believed to be due to inhibition of donor erythroid progenitors by residual host isohemagglutinins. We report a 10-year-old boy with post-hepatitis aplastic anemia (AA) who developed PRCA after HLA-matched familial peripheral blood stem cell transplantation (SCT) following conditioning with Cph 200 mg/kg + ATG 90 mg/kg. Granulocyte engraftment occurred on day +18, platelet engrafted on day +40, while reticulocytopenia at 0% persisted until day +118, and erythroid precursors were totally absent from bone marrow. After a single dose of rituximab 200 mg/m 2 administered on day +118 PRCA resolved and on day +132 the reticulocytes rose to 5.7%. On day +139 the Hb reached 137 g/l and the erythroid lineage in BM increased to 21%. We conclude that due to the rapid recovery from PRCA and lack of side effects, rituximab should be tried as firstline treatment of PRCA after allo-SCT. Bone Marrow Transplantation (2002) 30, 405-407. doi:10.1038/sj.bmt.1703668 Keywords: pure red cell aplasia; allogeneic stem cell transplantation; rituximab Pure red cell aplasia (PRCA) is an infrequent but wellrecognized complication of allogeneic bone marrow transplantation. Most cases of PRCA occur after transplantations with major donor-recipient ABO mismatch and are due to the long persistence of residual titers of natural recipient anti-A, 1 or very rarely, anti-B antibodies, 2 causing inhibition of donor erythroid progenitors. Additional risk factors include use of reduced intensity conditioning and immunosuppression with CsA in the post-transplant

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Anti-CD20 monoclonal antibody for the treatment of severe, immune-mediated, pure red cell aplasia and hemolytic anemia

Cited by 141 publications

References 12 publications

Successful anti‐CD20 monoclonal antibody treatment of severe autoimmune hemolytic anemia due to warm reactive IgM autoantibody in a child with common variable immunodeficiency

Successful anti‐CD20 monoclonal antibody treatment of severe autoimmune hemolytic anemia due to warm reactive IgM autoantibody in a child with common variable immunodeficiency

Rituximab chimeric anti‐CD20 monoclonal antibody treatment for adult refractory idiopathic thrombocytopenic purpura

Successful treatment of pure red cell aplasia with a single dose of rituximab in a child after major ABO incompatible peripheral blood allogeneic stem cell transplantation for acquired aplastic anemia

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