William J Savage

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. ncbi Allergic agonists in apheresis platelet products are associated with allergic transfusion reactions
    William J Savage
    Department of Pathology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    Transfusion 52:575-81. 2012
  2. ncbi New insights into paroxysmal nocturnal hemoglobinuria
    William J Savage
    The Division of Pediatric Hematology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Hematology 12:371-6. 2007
  3. ncbi Atopic predisposition of recipients in allergic transfusion reactions to apheresis platelets
    William J Savage
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Transfusion 51:2337-42. 2011
  4. ncbi Plasma glial fibrillary acidic protein levels in children with sickle cell disease
    William J Savage
    Divisions of Transfusion Medicine and Pediatric Hematology, Johns Hopkins University School of Medicine, 600 N Wolfe St, Baltimore, MD 21287, USA
    Am J Hematol 86:427-9. 2011
  5. ncbi Allergic transfusion reactions to platelets are associated more with recipient and donor factors than with product attributes
    William J Savage
    Department of Pathology, Division of Transfusion Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Transfusion 51:1716-22. 2011
  6. ncbi Biomarkers in pediatrics: children as biomarker orphans
    William J Savage
    Division of Transfusion Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Proteomics Clin Appl 4:915-21. 2010
  7. ncbi Plasma glial fibrillary acidic protein levels in a child with sickle cell disease and stroke
    William J Savage
    Division of Transfusion Medicine, Department of Pathology, Johns Hopkins University, Baltimore, MD, USA
    Acta Haematol 125:103-6. 2011
  8. ncbi ABO antibody titers are not predictive of hemolytic reactions due to plasma-incompatible platelet transfusions
    Matthew S Karafin
    Department of Pathology, Johns Hopkins University, Baltimore, Maryland, USA
    Transfusion 52:2087-93. 2012
  9. ncbi Prevention of allergic transfusion reactions to platelets and red blood cells through plasma reduction
    Aaron A R Tobian
    Department of Pathology, Johns Hopkins University, Baltimore, MD 21287, USA
    Transfusion 51:1676-83. 2011
  10. ncbi The impact of apheresis platelet manipulation on corrected count increment
    Matthew Karafin
    Department of Pathology, Johns Hopkins University, Baltimore, Maryland 21287, USA
    Transfusion 52:1221-7. 2012

Detail Information

Publications17

  1. ncbi Allergic agonists in apheresis platelet products are associated with allergic transfusion reactions
    William J Savage
    Department of Pathology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    Transfusion 52:575-81. 2012
    ..To assess product factors associated with ATRs, we investigated candidate mediators in apheresis platelet (PLT) products associated with ATRs and controls...
  2. ncbi New insights into paroxysmal nocturnal hemoglobinuria
    William J Savage
    The Division of Pediatric Hematology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Hematology 12:371-6. 2007
    ..The recently FDA approved complement inhibitor eculizumab has been shown to decrease hemolysis, decrease erythrocyte transfusion requirements, and improve quality of life for PNH patients...
  3. ncbi Atopic predisposition of recipients in allergic transfusion reactions to apheresis platelets
    William J Savage
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Transfusion 51:2337-42. 2011
    ..The biologic mechanisms of allergic transfusion reactions (ATRs) are largely unknown. We sought to compare the atopic predisposition of platelet (PLT) recipients who experienced an ATR to nonreactive control recipients...
  4. ncbi Plasma glial fibrillary acidic protein levels in children with sickle cell disease
    William J Savage
    Divisions of Transfusion Medicine and Pediatric Hematology, Johns Hopkins University School of Medicine, 600 N Wolfe St, Baltimore, MD 21287, USA
    Am J Hematol 86:427-9. 2011
    ..Plasma GFAP is elevated among children with SCD and may be associated with subclinical brain injury...
  5. ncbi Allergic transfusion reactions to platelets are associated more with recipient and donor factors than with product attributes
    William J Savage
    Department of Pathology, Division of Transfusion Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Transfusion 51:1716-22. 2011
    ..Mechanisms of allergic transfusion reactions (ATRs) are not well understood. The aim of this study was to distinguish recipient-, donor-, and product-specific factors associated with ATRs...
  6. ncbi Biomarkers in pediatrics: children as biomarker orphans
    William J Savage
    Division of Transfusion Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Proteomics Clin Appl 4:915-21. 2010
    ..This review focuses on the fundamentals of biomarkers, the additional considerations needed for applying biomarker research to children, and recommendations for advancing pediatric biomarker research...
  7. ncbi Plasma glial fibrillary acidic protein levels in a child with sickle cell disease and stroke
    William J Savage
    Division of Transfusion Medicine, Department of Pathology, Johns Hopkins University, Baltimore, MD, USA
    Acta Haematol 125:103-6. 2011
    ..Stroke in SCD can occur in the setting of acute illness, and a biomarker that could predict the onset and triage ill children to therapeutic intervention more quickly would be useful...
  8. ncbi ABO antibody titers are not predictive of hemolytic reactions due to plasma-incompatible platelet transfusions
    Matthew S Karafin
    Department of Pathology, Johns Hopkins University, Baltimore, Maryland, USA
    Transfusion 52:2087-93. 2012
    ....
  9. ncbi Prevention of allergic transfusion reactions to platelets and red blood cells through plasma reduction
    Aaron A R Tobian
    Department of Pathology, Johns Hopkins University, Baltimore, MD 21287, USA
    Transfusion 51:1676-83. 2011
    ..This study evaluated whether removing plasma from apheresis platelets (APs) or red blood cells (RBCs) by concentrating or washing transfusion products can decrease the incidence of ATRs...
  10. ncbi The impact of apheresis platelet manipulation on corrected count increment
    Matthew Karafin
    Department of Pathology, Johns Hopkins University, Baltimore, Maryland 21287, USA
    Transfusion 52:1221-7. 2012
    ..However, these processes may damage platelets (PLTs). This study evaluated whether concentrating or washing APs decrease the corrected count increment (CCI)...
  11. ncbi Bacterial culture reduces but does not eliminate the risk of septic transfusion reactions to single-donor platelets
    Alice K Fuller
    Department of Pathology, Hemapheresis and Transfusion Services Division, The Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
    Transfusion 49:2588-93. 2009
    ..6 per 100,000; 95% confidence interval [CI], 0.17-36.9 per 100,000) transfusions. The goal of this study was to determine if bacterial testing of SDPs reduced the rate of SPTRs in our hospital...
  12. ncbi Glial fibrillary acidic protein as a biomarker for neonatal hypoxic-ischemic encephalopathy treated with whole-body cooling
    Christopher S Ennen
    Department of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Am J Obstet Gynecol 205:251.e1-7. 2011
    ..Glial fibrillary acidic protein (GFAP) is specific to astrocytes in the central nervous system. We hypothesized that serum GFAP would be increased in neonates with hypoxic-ischemic encephalopathy (HIE) treated with whole-body cooling...
  13. ncbi Congenital T cell deficiency in a patient with CHARGE syndrome
    Julie Hoover-Fong
    McKusick Nathans Institute of Genetic Medicine, Department of Pediatrics, Johns Hopkins University, Baltimore, MD, USA
    J Pediatr 154:140-2. 2009
    ..We report a patient with molecularly confirmed CHARGE syndrome, which included a congenital T cell deficiency, who was treated with peripheral blood mononuclear cell transplantation...
  14. ncbi Hemoglobin drift after cardiac surgery
    Timothy J George
    Division of Cardiac Surgery, Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21287, USA
    Ann Thorac Surg 94:703-9. 2012
    ..The purpose of this study was to define the natural progression of hemoglobin levels in postoperative cardiac surgery patients...
  15. ncbi Multiplex assays for biomarker research and clinical application: translational science coming of age
    Qin Fu
    The Johns Hopkins Bayview Proteomics Center, Johns Hopkins University, Baltimore, MD 21224, USA
    Proteomics Clin Appl 4:271-84. 2010
    ..We also discuss choosing an appropriate platform, judging the performance of assays, obtaining reliable, quantitative results for translational research and clinical applications in the biomarker field...
  16. ncbi Glycosylphosphatidylinositol-anchored protein deficiency confers resistance to apoptosis in PNH
    William J Savage
    Division of Hematology, Johns Hopkins University School of Medicine, Baltimore, MD 21205 2196, USA
    Exp Hematol 37:42-51. 2009
    ..Investigate the contribution of PIG-A mutations to clonal expansion in paroxysmal nocturnal hemoglobinuria (PNH)...
  17. ncbi Natural history of paroxysmal nocturnal hemoglobinuria clones in patients presenting as aplastic anemia
    Jeffrey J Pu
    Division of Hematology, Department of Medicine, School of Medicine, Johns Hopkins University, Baltimore, MD, USA
    Eur J Haematol 87:37-45. 2011
    ..To investigate the natural history of paroxysmal nocturnal hemoglobinuria (PNH) clones in patients with acquired aplastic anemia (AA)...