• J. Clin. Invest. · Apr 2012

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    Hemolysis and cell-free hemoglobin drive an intrinsic mechanism for human disease.

    • Mark T Gladwin, Tamir Kanias, and Daniel B Kim-Shapiro.
    • Vascular Medicine Institute and Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA. gladwinmt@upmc.edu
    • J. Clin. Invest. 2012 Apr 1;122(4):1205-8.

    AbstractBlood transfusion represents the first and most prescribed cell-based therapy; however, clinical safety and efficacy trials are lacking. Clinical cohort studies have suggested that massive transfusion and/or transfusion of aged stored blood may contribute to multiorgan dysfunction in susceptible patients. In this issue of the JCI, Baek and colleagues report that aged stored blood hemolyzes after massive transfusion in a guinea pig model. Hemolysis led to vascular and kidney injury that was mediated by cell-free plasma hemoglobin and prevented by coinfusion of the specific hemoglobin scavenger protein, haptoglobin. These studies support an expanding body of research indicating that intravascular hemolysis is a pathological mechanism in several human diseases, including multiorgan dysfunction after either massive red blood cell transfusion or hemoglobin-based blood substitute therapy, the hemoglobinopathies, malaria, and other acquired and genetic hemolytic conditions.

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