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Updated: Aug 13, 2026

Continuous Manual Exchange Transfusion for Patients with Sickle Cell Disease: An Efficient Method to Avoid Iron Overload
Published on: March 14, 2017
Management of patients with hematologic malignancies and aplastic anemia who are refractory to platelet transfusions
1Department of Medicine, Georgetown University Medical Center, NW, Washington, DC 20007, USA.
Patients with hematologic malignancies or aplastic anemia may have reduced responses to platelet transfusions after multiple transfusions of standard red blood cells or platelet components. This situation, conventionally described as 'refractoriness' to platelet transfusions, may result from immune or non-immune causes. Non-immune causes include fever, infections, hypersplenism, disseminated intravascular coagulation, antibiotics, or veno-occlusive disease. Immune causes include platelet-reactive alloantibodies, which are typically antibodies to human leukocyte antigens (HLA) or, less commonly, antibodies to human platelet antigens (HPA). Transfused HLA-matched platelets often have satisfactory posttransfusion survivals, but few transfusion services have the donor and logistical resources to sustain a prolonged course of platelet transfusions requiring four-antigen matches. The availability of commercially marketed kits for crossmatching samples of potential donors' platelets with a recipient's serum has facilitated donor-recipient matching. Also, platelet crossmatching may be used to select a suitable unit of from several candidates platelets that have been identified to be partial HLA matches. The high likelihood of decreased efficacy of platelet transfusions in HLA-alloimmunized recipients makes avoidance of exposure to HLA-bearing leukocytes a priority. This goal is facilitated by lowering transfusion 'triggers' for cellular blood components, particularly for prophylactic platelet transfusions, by reducing the leukocyte content of components by leukocyte-reduction filters and, possibly by ultraviolet-B irradiation of leukocyte-containing products.
Patients with hematologic malignancies or aplastic anemia may have reduced responses to platelet transfusions after multiple transfusions of standard red blood cells or platelet components. This situation, conventionally described as 'refractoriness' to platelet transfusions, may result from immune or non-immune causes. Non-immune causes include fever, infections, hypersplenism, disseminated intravascular coagulation, antibiotics, or veno-occlusive disease. Immune causes include platelet-reactive alloantibodies, which are typically antibodies to human leukocyte antigens (HLA) or, less commonly, antibodies to human platelet antigens (HPA). Transfused HLA-matched platelets often have satisfactory posttransfusion survivals, but few transfusion services have the donor and logistical resources to sustain a prolonged course of platelet transfusions requiring four-antigen matches. The availability of commercially marketed kits for crossmatching samples of potential donors' platelets with a recipient's serum has facilitated donor-recipient matching. Also, platelet crossmatching may be used to select a suitable unit of from several candidates platelets that have been identified to be partial HLA matches. The high likelihood of decreased efficacy of platelet transfusions in HLA-alloimmunized recipients makes avoidance of exposure to HLA-bearing leukocytes a priority. This goal is facilitated by lowering transfusion 'triggers' for cellular blood components, particularly for prophylactic platelet transfusions, by reducing the leukocyte content of components by leukocyte-reduction filters and, possibly by ultraviolet-B irradiation of leukocyte-containing products.
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