The bacterial screening system has removed a significant number, but not all bacterially contaminated platelet components from the supply. The sample volume is an important factor in sensitivity due to the low number of bacteria in a platelet component pack on day 1. An effective notification and recall system is a critical part of the bacterial screening system.
Under current physical storage conditions, glucose appears necessary for the maintenance of platelets stored as concentrates in minimal volumes of plasma. The addition of acetate was associated with increased platelet activation and reduced ATP levels.
Forty-one patients with autoimmune haemolytic anaemia (AIHA), who had free antibody in their sera, were investigated for the presence of alloimmune erythrocyte antibodies using the ZZAP autoabsorption technique. Patients were subdivided into three risk categories: (I) no prior pregnancy or transfusion; (II) history of pregnancy and/or one to five transfusions; and (III) greater than 5 transfusions. A total of 13 (32%) of the 41 patients exhibited significant alloantibodies. Of 11 category-I patients 2 (18%) had significant alloantibodies. Eight (31%) of the 26 category-II patients had significant alloantibodies and 3 (75%) of the 4 category-III patients had significant alloantibodies after absorption. The majority showed Rh specificity: anti-E(8), -C(3), -Cw(1). Anti-K was found in 6 samples and 1 had anti-Fya. Alloantibodies had not been suspected prior to autoabsorption in 10 (77%) of the 13 patients with alloantibodies. These findings underline the importance of performing autoabsorption in AIHA when free autoantibody is present in the serum. Additionally, Rh phenotyping performed on ZZAP-treated cells showed complete agreement with that ascertained using pure IgM Rh typing sera and untreated cells.
Platelets suspended in a medium of 70:30 SSP+™ to plasma ratio performed at least as well as platelets in 100% autologous plasma for up to 10 days of storage. Further, results are suggestive of an apoptosis-like process being involved in the platelet storage lesion.
The enhanced HLA class I (Bg) on red blood cells (RBC) of many patients with systemic lupus
erythematosus has allowed a significant correlation to be made between their HLA-B types and haemagglutination
reactivity with lymphocytotoxic anti-HLA-B sera stimulated by pregnancy alone. Therefore the class I expression on
these RBC relates to classical, rather than non-classical, class I gene products. Studies of class I expression on RBC by
means of monoclonal antibodies (MAb) to epitopes on the heavy polypeptide chain and β2-microglobulin (β2m) have
suggested that the complete extracellular structure is present. The specific effect of chloroquine in ‘stripping HLA’ from
RBC had been assumed to support the concept that HLA class I was adsorbed from plasma. However, from our data,
we conclude that HLA class I is an intrinsic membrane component. We suggest that the action of chloroquine is to
remove β2m alone, which prevents normal class I expression and also results in conformational changes to the class I
heavy chain, but that it is not capable of removing the membrane-bound heavy chain.
The enhanced HLA class I (Bg) on red blood cells (RBC) of many patients with systemic lupus erythematosus has allowed a significant correlation to be made between their HLA-B types and haemagglutination reactivity with lymphocytotoxic anti-HLA-B sera stimulated by pregnancy alone. Therefore the class I expression on these RBC relates to classical, rather than non-classical, class I gene products. Studies of class I expression on RBC by means of monoclonal antibodies (MAb) to epitopes on the heavy polypeptide chain and beta 2-microglobulin (beta 2m) have suggested that the complete extracellular structure is present. The specific effect of chloroquine in 'stripping HLA' from RBC had been assumed to support the concept that HLA class I was adsorbed from plasma. However, from our data, we conclude that HLA class I is an intrinsic membrane component. We suggest that the action of chloroquine is to remove beta 2m alone, which prevents normal class I expression and also results in conformational changes to the class I heavy chain, but that it is not capable of removing the membrane-bound heavy chain.
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