Leukapheresis and low-dose chemotherapy do not reduce early mortality in acute myeloid leukemia hyperleukocytosis: A systematic review and meta-analysis

Division of Haematology/Oncology, The Hospital for Sick Children, Toronto, Canada., Pediatric Hematology and Oncology, Johann Wolfgang Goethe University, Frankfurt, Germany., Leeds General Infirmary, Leeds Teaching Hospitals, NHS Trust, Leeds, UK; Centre for Reviews and Dissemination, University of York, York, UK., Division of Haematology/Oncology, The Hospital for Sick Children, Toronto, Canada., Program in Child Health Evaluative Sciences, The Hospital for Sick Children, Toronto, Canada., Program in Child Health Evaluative Sciences, The Hospital for Sick Children, Toronto, Canada; Department of Clinical Epidemiology & Biostatistics, McMaster University, Hamilton, Canada., Division of Haematology/Oncology, The Hospital for Sick Children, Toronto, Canada; Program in Child Health Evaluative Sciences, The Hospital for Sick Children, Toronto, Canada. Electronic address: lillian.sung@sickkids.ca.

Leukemia Research. 2014;38((4):):460-8.
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Abstract
The role of leukapheresis and low-dose chemotherapy is unclear in decreasing early mortality in acute myeloid leukemia (AML) patients with hyperleukocytosis. This systematic review was conducted to describe early mortality (deaths during first induction) in patients with AML with an initial white blood count>100x10(9)L(-1) stratified by the approach to leukapheresis and hydroxyurea/low-dose chemotherapy. Twenty-one studies were included. Weighted mean early deaths rate (20 studies, 1354 patients) was 20.1% (95% confidence interval 15.0-25.1). Neither leukapheresis strategy (p=0.67) nor hydroxyurea/low-dose chemotherapy (p=0.23) influenced the early death rate. Early mortality related to hyperleukocytosis in AML is not influenced by universal or selected use of leukapheresis or hydroxyurea/low-dose chemotherapy. Copyright 2014 Elsevier Ltd. All rights reserved.
Study details
Study Design : Systematic Review
Language : English
Credits : Bibliographic data from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine