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Innovation in transfusion medicine and blood banking: documenting the record in 50 years of TRANSFUSION

I n many industries, as much as 30% to 40% of revenue may come from products introduced in the previous 5 years—even from well-established companies. It is important for innovation to be part of blood banking and/or transfusion medicine not necessarily to increase revenue but to provide the best possible transfusion therapy for patients. Ten scientific discoveries and technologic advances have transformed transfusion medicine and blood banking (Table 1). When defined broadly and viewed over a substantial period of time, these have had a huge impact on patient care. Many of these discoveries have been documented during the 50 years of publication of TRANSFUSION. With the development of apheresis, for the first time the yield from a blood donation was not limited to the amount of whole blood loss that the donor could sustain. The use of marrow as a blood component and recruitment of community volunteers as marrow donors represented the beginning of clinical use of cells other than peripheral blood and opened the way to many novel cellular therapies. Blood banks took the lead in marrow donor recruitment. Now the United States’ National Marrow Donor Program has more than 7 million people who have volunteered to be donors and they have provided marrow or stem cells for more than 29,000 transplants. The molecular structure of most red blood cell (RBC) antigens is known and the genes that control their expression have been cloned. Understanding the role of the white blood cell (WBC) has had a tremendous impact on transfusion medicine. This spectrum has ranged from the role of WBC antibodies and cytokines in transfusion reactions and platelet (PLT) refractoriness and its prevention by leukoreduction leading to HLA matching donors for PLTs and the role of the lymphocyte in transfusion-associated graftversus-host disease (GVHD) leading to the introduction of irradiation of blood products and understanding the passenger lymphocyte syndrome in which transient lymphocyte proliferation can produce RBC antibodies reactive with the recipient’s RBCs leading to hemolysis. Antigens and antibodies unique to PLTs and neutrophils are involved in diseases such as autoimmune thrombocytopenia or neutropenia and homologs of hemolytic disease in the newborn, neonatal alloimmune thrombocytopenia, and neutropenia. These antigens and antibodies affect the recovery and survival of transfused cells. Paid donors pose a higher risk of transfusiontransmitted infections than volunteer donors. The conversion to an all-volunteer blood supply was accomplished with a great deal of anxiety and considerable tension but had a huge impact on blood safety. For decades our testing for blood safety was limited to syphilis and hepatitis B. Although the conversion to an allvolunteer donor system increased blood safety, the human immunodeficiency virus epidemic initiated major changes in the approach to blood safety. Many new tests of donated blood were added. Equally importantly, many questions were added to the medical history, and these were very effective in improving blood safety. The major factors that control hematopoiesis have been identified and these can be used to drive hematopoiesis in certain directions. This manipulation can be done in patients, donors, or in the laboratory. Erythropoietin replaced the need for approximately 500,000 units of RBCs per year in patients with renal disease and cancer. Granulocyte–colony-stimulating (G-CSF) factor is used to speed hematopoietic engraftment and to treat neutropenia. G-CSF has become a standard part of stem cell donation and a major clinical trial has begun to evaluate higher yields of granulocyte concentrates obtained from G-CSF–stimulated donors. Plasma fractionation has been refined to produce a variety of products that have enabled new immunology From the Department of Laboratory Medicine & Pathology, University of Minnesota, Minneapolis, Minnesota. Address reprint requests to: Jeffrey McCullough, MD, Department of Laboratory Medicine & Pathology–MMC 609, University of Minnesota, 420 Delaware Street SE, Minneapolis, MN 55455; e-mail: mccul001@umn.edu. Received for publication May 13, 2010; accepted May 26, 2010. doi: 10.1111/j.1537-2995.2010.02787.x TRANSFUSION 2010;50:2542-2546.