Rituximab in the treatment of acquired factor VIII inhibitors

Wiestner, Adrian; Cho, Hearn J.; Asch, Adam S.; Michelis, Michael F.; Zeller, Jack A.; Peerschke, Ellinor I.B.; Weksler, Babette B.; Schechter, Geraldine P.

doi:10.1182/blood-2002-03-0765

Cited by 201 publications

(157 citation statements)

References 20 publications

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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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Section: Introductionmentioning

confidence: 99%

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

et al. 2005

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“…Moreover, in young female patients, such treatment can compromise fertility (Maillard et al, 2006). In contrast, rituximab was well tolerated with few side effects and no infectious complications reported in patients with acquired haemophilia (Wiestner et al, 2002;Fischer et al, 2003;Jy et al, 2003;Stasi et al, 2004;Aggarwal et al, 2005;Clatworthy & Jayne, 2006;Maillard et al, 2006;Santoro et al, 2007), and was an effective alternative for patients unable to receive cytotoxic therapy (Jy et al, 2003;Marietta et al, 2003;Stasi et al, 2004;Berezné et al, 2006;Maillard et al, 2006). Aggarwal et al (2005) have proposed an algorithm for the treatment of autoimmune haemophilia.…”

Section: Use Of Rituximab In Acquired Haemophiliamentioning

confidence: 99%

Rituximab in the treatment of autoimmune haematological disorders

2008

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SummaryCurrent treatment regimens for haematological autoimmune diseases are relatively non-selective and are often associated with considerable toxicity. Recently, it has become clear that B cells play a key role in both the development and perpetuation of autoimmunity, suggesting that B-cell depletion could be a valuable treatment approach for patients with autoimmune diseases. This article reviews data supporting the use of rituximab -an anti-CD20 monoclonal antibody that specifically depletes B cells -in four key autoimmune haematological disorders: idiopathic thrombocytopenic purpura (ITP); autoimmune haemolytic anaemia (AIHA); acquired haemophilia; and thrombotic thrombocytopenic purpura (TTP). Although treatment of ITP, AIHA, acquired haemophilia and TTP with rituximab is still relatively uncommon, results from case series and small phase II trials indicate that patients of all ages can respond to rituximab, irrespective of the number or type of prior treatments that they have received. Moreover, patients with these diseases receiving rituximab experienced predominantly mild adverse events, with only a few serious adverse events reported. These data suggest that rituximab provides an effective and well-tolerated alternative treatment option for patients with ITP, AIHA, acquired haemophilia and TTP, many of whom have limited treatment choices.

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“…56 A metodologia consiste de infusões intravenosas de rituximab (anticorpos monoclonais anti-CD20) que se liga às células B e iniciam um processo de lise celular (via sistema do complemento ou apoptose). 57,58 Esta opção de tratamento tem se mostrado bastante eficiente e uma grande quantidade de estudos relaciona a sua eficácia no tratamento de anticorpos inibidores de FVIII em indivíduos com hemofilia adquirida. [59][60][61][62] Entretanto, notificações de reações adversas relacionadas ao uso do medicamento têm sido emitidas e casos de síndrome de liberação excessiva de citocinas com resultado fatal já foram relatados.…”

Section: Tratamento Das Crises Hemorrágicas Na Presença Do Inibidorunclassified

Desenvolvimento de inibidores do fator VIII na hemofilia A

Chaves¹,

Rodrigues²

2009

Rev. Bras. Hematol. Hemoter.

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Dentre os distúrbios de coagulação hereditários nas populações humanas destaca-se, por sua gravidade, a hemofilia A (HA), uma coagulopatia recessiva ligada ao cromossomo X causada pela deficiência ou disfunção da glicoproteína plasmática denominada Fator VIII (FVIII). A incidência da HA pode chegar a 1:5.000 meninos nascidos vivos. Nos indivíduos com hemofilia A grave (aproximadamente 50% dos casos; atividade do FVIII<0,01 U/mL), a hemorragia pode ocorrer espontaneamente, enquanto Dias, pacientes com hemofilia moderada (cerca de 10% dos indiví-duos; atividade do FVIII 0.01-0.05 U/mL) apresentam um fenótipo intermediário. Pacientes portadores da forma leve da doença, observada em 30%-40% dos casos (atividade do FVIII 0,05-0,4 U/mL), sofrem de hemorragias pós-trauma ou pós-cirúrgicas. REVISTA BRASILEIRA DE HEMATOLOGIA E H E M O T E R A P I A 1As anormalidades genéticas responsáveis pela hemofilia congênita incluem deleções, inversões (mais frequentemente a inversão do intron 22), mutações sem sentido, mutações de sentido trocado e pequenas deleções no

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Rituximab in the treatment of acquired factor VIII inhibitors

Cited by 201 publications

References 20 publications

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

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

Rituximab in the treatment of autoimmune haematological disorders

Desenvolvimento de inibidores do fator VIII na hemofilia A

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