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D'Arena G.,Haematology and Stem Cell Transplantation Unit | Grandone E.,Haemostasis and Thrombosis Unit | Di Minno M.N.D.,University of Naples Federico II | Di Minno M.N.D.,Unit Of Cell And Molecular Biology In Cardiovascular Diseases Monzino Cardiology Center | Di Minno G.,University of Naples Federico II
Blood Transfusion

Background. Acquired haemophilia A (AHA) is a rare bleeding disorder caused by the development of specific autoantibodies against naturally occurring factor VIII (FVIII). Although about half of cases are idiopathic, AHA may be associated with several non-neoplastic conditions, autoimmune disorders, as well as haematological malignancies, such as chronic lymphocytic leukaemia and lymphoma. The long-term suppression of inhibitors is one of the mainstays of the treatment of AHA. Apart from standard immunosuppressive treatments, rituximab has been proven to be effective in AHA. Materials and methods. The aim of this review is to provide a systematic description of data available in the literature on this topic. To do so, we performed a search using the indexed online database Medline/PubMed, without temporal limits, matching the words "rituximab" and "acquired h(a)emophilia". Furthermore, additional published studies were identified in the reference list of the publications found in PubMed. Results. The review of the literature confirms that rituximab may be a safe and useful treatment for AHA. Discussion. Although rituximab is not a standard therapy for AHA, it may be useful in resistant cases. However, the definitive place of this monoclonal antibody in the therapeutic strategy for AHA (first or second-line, alone or in combination with other drugs) remains to be determined more precisely and warrants further investigation. © SIMTI Servizi Srl. Source

Ria R.,University of Bari | Musto P.,Haematology and Stem Cell Transplantation Unit | Reale A.,University of Bari | Guariglia R.,Haematology and Stem Cell Transplantation Unit | And 3 more authors.
Journal of Nuclear Medicine

Targeted radioimmunotherapy with 90Y-labeled ibritumomab tiuxetan is a novel therapeutic approach for CD20-positive relapsed or refractory non-Hodgkin lymphoma (NHL). Methods: Seven consecutive patients with CD20-positive aggressive NHL who did not fully respond to prior myeloablative chemotherapy were enrolled. A 14.8 MBq (0.4 mCi)/kg dose of 90Y- ibritumomab tiuxetan was administered to all patients, and approximately 100 d afterward 18F-FDG PET/CT was performed to assess response. Results: PET/CT showed a complete response in 5 of 7 patients. Of the 2 nonresponsive patients, 1 showed persistent disease and the other progression. Toxicity included thrombocytopenia in all 7 patients and grade IV neutropenic fever in 1 patient. Conclusion: Despite the small series studied, we suggest that radioimmunotherapy is safe for consolidation in patients treated with high-dose chemotherapy for aggressive NHL and may provide clinical benefit in extensively pretreated patients. Copyright © 2011 by the Society of Nuclear Medicine, Inc. Source

Introduction: A still not well defined proportion of patients with multiple myeloma (MM) and eligible for autologous stem cell transplantation (AuSCT) fails to mobilize CD34+ peripheral blood stem cells (PBSC) at all or to collect an adequate number for a safe procedure or sufficient for multiple transplants. These so-called "poor-mobilizers" are difficult to be predicted, due to marked difference across previous heterogeneous studies. Methods: We aimed to develop a method based on simple clinical parameters for predicting unsuccessful (<2 × 106/kg) or sub-optimal (<5 × 106/kg) collections of CD34+ PBSC in newly diagnosed MM patients eligible for AuSCT, treated with novel agents and receiving an homogeneous mobilizing therapy with cyclophosphamide and granulocyte-colony stimulating factor (G-CSF). To this purpose, 1,348 patients enrolled in five consecutive Italian clinical trials were retrospectively analysed. Age, baseline low peripheral blood cell counts, use of lenalidomide, and haematological toxicity developed during induction were taken into account as possible factors associated with poor mobilization. Results: Overall, 280 patients (20.8%) showed either sub-optimal (167 patients, 12.4%) or unsuccessful (113 patients, 8.4%) collections. All analysed parameters negatively influenced the procedure, but only age and haematological toxicity during induction maintained their significance at multivariate analysis. Based on ordinal logistic regression model, we constructed a risk heat-map where the four parameters were pooled and weighted according to their relevance as single or combined variables. This model was predictive for different probabilities of failure, suboptimal or optimal outcomes. Conclusions: We found that about one fifth of newly diagnosed MM fails to collect an adequate number of PBSC. Our model, based on a large group of patients treated frontline with novel agents and receiving the most popular mobilizing approach currently employed in Europe, is applicable in individual subjects and may contribute to the early identification of "poor mobilizer" phenotypes. © 2015 Musto et al.; licensee BioMed Central. Source

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