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Background/Case Studies: Group O red blood cells (RBCs) are the universal donor red cells; they can be given to a recipient with any other blood group. Although it is usually the standard practice to select ABO group specific blood as the first choice for patients requiring transfusion, there are many situations where group O blood is given to non-O recipients. Transfu-sion of group O blood to non-O recipients, or the transfusion of Rh negative (D-) blood to Rh positive (D1) recipients, can result in shortages of O or D-blood, respectively. Current patterns of group O and D- blood utilization are not well understood. Study Design/Methods: Hospital transfusion services collected ABO and Rh groups of transfused RBC units and of recipients during the 2013 calendar year. Units administered to recipients of unknown ABO or Rh group were excluded. Two analyses were performed: How often group O RBCs were transfused to non-O recipients, and how often D- units (of any ABO group) were transfused to D1 recipients. The hospitals were divided into 3 categories: Small (<250 beds), medium (250-1000 beds), and large (>1000 beds). Results/Findings: Data was received from 30 centers in 9 countries. There were 7 small, 17 medium and 6 large hospital respondents. In total, these 30 centers transfused a total of 415,696 RBC units, of which 2257 (0.5%) were units excluded from the D mismatch analysis because the D type of the recipient was unknown. The ABO groups of all recipients were known. Overall 11.1% of the O units were transfused to non-O recipients. The percentage of O RBCs transfused to non-O recipients was similar among the small, medium and large sized hospital respondents (12.4, 12.8 and 8.5%, respectively). The rate of group O RBC transfusion to non-O recipients at the small hospitals ranged from 0-33.0%, at the medium hospitals from 0-22.0%, and at the large hospitals from 5.0-10.0%. In terms of D- RBC transfusion to D1 recipients, overall 29.8% of the D- units were transfus

BACKGROUND: Transfusion of group O blood to non-O recipients, or transfusion of D- blood to D+ recipients, can result in shortages of group O or D- blood, respectively. This study investigated RBC utilization patterns at hospitals around the world and explored the context and policies that guide ABO blood group and D type selection practices. STUDY DESIGN AND METHODS: This was a retrospective study on transfusion data from the 2013 calendar year. This study included a survey component that asked about hospital RBC selection and transfusion practices and a data collection component where participants submitted information on RBC unit disposition including blood group and D type of unit and recipient. Units administered to recipients of unknown ABO or D group were excluded. RESULT(S): Thirty-eight hospitals in 11 countries responded to the survey, 30 of which provided specific RBC unit disposition data. Overall, 11.1% (21,235/191,397) of group O units were transfused to non-O recipients; 22.6% (8777/38,911) of group O D- RBC units were transfused to O D+ recipients, and 43.2% (16,800/38,911) of group O D- RBC units were transfused to recipients that were not group O D-. Disposition of units and hospital transfusion policy varied within and across hospitals of different sizes, with transfusion of group O D- units to non-group O D- patients ranging from 0% to 33%. CONCLUSION(S): A significant proportion of group O and D- RBC units were transfused to compatible, nonidentical recipients, although the frequency of this practice varied across sites.Copyright © 2017 AABB

Background/Case Studies: Group O red blood cells (RBCs) are the universal donor red cells; they can be given to a recipient with any other blood group. Although it is usually the standard practice to select ABO group specific blood as the first choice for patients requiring transfusion, there are many situations where group O blood is given to non-O recipients. Transfu-sion of group O blood to non-O recipients, or the transfusion of Rh negative (D-) blood to Rh positive (D1) recipients, can result in shortages of O or D-blood, respectively. Current patterns of group O and D- blood utilization are not well understood. Study Design/Methods: Hospital transfusion services collected ABO and Rh groups of transfused RBC units and of recipients during the 2013 calendar year. Units administered to recipients of unknown ABO or Rh group were excluded. Two analyses were performed: How often group O RBCs were transfused to non-O recipients, and how often D- units (of any ABO group) were transfused to D1 recipients. The hospitals were divided into 3 categories: Small (<250 beds), medium (250-1000 beds), and large (>1000 beds). Results/Findings: Data was received from 30 centers in 9 countries. There were 7 small, 17 medium and 6 large hospital respondents. In total, these 30 centers transfused a total of 415,696 RBC units, of which 2257 (0.5%) were units excluded from the D mismatch analysis because the D type of the recipient was unknown. The ABO groups of all recipients were known. Overall 11.1% of the O units were transfused to non-O recipients. The percentage of O RBCs transfused to non-O recipients was similar among the small, medium and large sized hospital respondents (12.4, 12.8 and 8.5%, respectively). The rate of group O RBC transfusion to non-O recipients at the small hospitals ranged from 0-33.0%, at the medium hospitals from 0-22.0%, and at the large hospitals from 5.0-10.0%. In terms of D- RBC transfusion to D1 recipients, overall 29.8% of the D- units were transfus

BACKGROUND: Transfusion of group O blood to non-O recipients, or transfusion of D- blood to D+ recipients, can result in shortages of group O or D- blood, respectively. This study investigated RBC utilization patterns at hospitals around the world and explored the context and policies that guide ABO blood group and D type selection practices. STUDY DESIGN AND METHODS: This was a retrospective study on transfusion data from the 2013 calendar year. This study included a survey component that asked about hospital RBC selection and transfusion practices and a data collection component where participants submitted information on RBC unit disposition including blood group and D type of unit and recipient. Units administered to recipients of unknown ABO or D group were excluded. RESULT(S): Thirty-eight hospitals in 11 countries responded to the survey, 30 of which provided specific RBC unit disposition data. Overall, 11.1% (21,235/191,397) of group O units were transfused to non-O recipients; 22.6% (8777/38,911) of group O D- RBC units were transfused to O D+ recipients, and 43.2% (16,800/38,911) of group O D- RBC units were transfused to recipients that were not group O D-. Disposition of units and hospital transfusion policy varied within and across hospitals of different sizes, with transfusion of group O D- units to non-group O D- patients ranging from 0% to 33%. CONCLUSION(S): A significant proportion of group O and D- RBC units were transfused to compatible, nonidentical recipients, although the frequency of this practice varied across sites.Copyright © 2017 AABB

INTRODUCTION: Platelet-activating antiplatelet factor 4/heparin (anti-PF4/heparin) antibodies are the major cause of heparin-induced thrombocytopenia (HIT). However, the relative utility of functional (platelet activation) vs. antigen [enzyme-immunoassay (EIA)] assays, and the significance of assay discrepancies remain unresolved. METHODS: Consecutive patient sera (n = 1650) referred for diagnostic HIT testing were screened prospectively by both the heparin-induced platelet activation (HIPA) test and anti-PF4/heparin EIA - including individual classes (IgG, IgA, IgM) - with clinical correlations studied. Platelet microparticle and annexin-V-binding properties of the sera were also investigated. RESULTS: Only 205 (12.4%) sera tested positive in either the HIPA and/or EIA: 95 (46.3%) were positive in both, 109 (53.1%) were only EIA-positive, and, notably, only one serum was HIPA-positive/EIA-negative. Of 185 EIA-positive sera, only 17.6% had detectable IgM and/or IgA without detectable IgG. Among sera positive for EIA IgG, optical density values were higher when the sera were HIPA-positive (1.117 vs. 0.768; P < 0.0001), with widely overlapping values. Two HIPA-positive but EIA-IgG-negative sera became HIPA-negative following IgG depletion, suggesting platelet-activating antibodies against non-PF4-dependent antigens. Clinical correlations showed that HIPA-negative/EIA-positive patients did not develop thrombosis and had reasons other than HIT to explain thrombocytopenia. IgM/A antibodies did not increase microparticle penetration, but increased annexin-V binding. CONCLUSIONS: The anti-PF4/heparin EIA has high ( approximately 99%) sensitivity for HIT. However, only about half of EIA-positive patients are likely to have HIT. Anti-PF4/heparin antibodies of IgM/A class and non-PF4-dependent antigens have only a minor role in HIT.

OBJECTIVE: To assess the crossreactivity of glucosamine sulfate, used for treatment of degenerative joint disease with antibodies induced in heparin-induced thrombocytopenia (HIT). BACKGROUND: HIT is a severe adverse effect of heparin therapy induced by an immunological mechanism. The antibodies in HIT are induced by a complex of heparin and, in most cases, platelet factor 4. Hereby generation of the antigen is not strictly dependent on heparin. Heparin can be substituted by a variety of polysulfated carbohydrates. In vitro and in vivo crossreactivity of HIT antibodies has been demonstrated for a chemically polysulfated chondroitin-like substance (Arteparon, Luitpoldwerke, Munich, Germany), formerly used for chondroprotection. Another drug widely used in the treatment of degenerative joint disease is glucosamine sulfate. Glucosamine is a building block of glycosaminoglycans, of which heparin is the clinically most important. Many patients with degenerative joint disease use glucosamine sulfate. This group is also at the highest risk to develop HIT following joint replacement surgery. METHODS: We examined the interactions of glucosamine sulfate (DONA 200-S, Opfermann, Wiehl, Germany) with platelets and antibodies of patients with HIT in and without the presence of heparin. Sera of 5 HIT patients and platelets of 4 healthy donors were used. The binding of HIT antibodies to PF4/glucosamine sulfate complexes was assessed by an ELISA. RESULTS: HIT antibodies did not activate platelets in the presence of glucosamine sulfate in a serotonin-release assay. Preincubation with glucosamine sulfate did not inhibit platelet activation by HIT antibodies in the presence of heparin (0.2 IU/ml). Antibodies bonded to PF4/heparin but not to PF4/glucosamine sulfate complexes. CONCLUSIONS: In contrast to sulfated glycosaminoglycans, there is no evidence for an immunological crossreactivity of HIT antibodies between heparin and glucosamine sulfate.