PubMed · 8578466
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S J Machin, H Kelsey, M J Seghatchian, R Warwick, I J Mackie. 1995. Platelet transfusion.. https://pubmed.ncbi.nlm.nih.gov/8578466/
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A variety of alloantigens is expressed by the platelet membrane, whereby currently seventeen platelet specific antigen systems have been recognized. However, in Caucasoids immunization occurs most frequently against only four of these alloantigen systems. Alloimmunization can cause neonatal alloimmune thrombocytopenia, post-transfusion purpura and refractoriness for platelet transfusion. The importance of all alloantigen systems is evidenced by their discovery in association with neonatal alloimmune thrombocytopenia. The genetic polymorphisms of all systems is characterized by a single base mutation which induces a single amino acid substitution. This amino acid change is associated with a change of the tertiary structure of the glycoprotein, which results in high antigeneicity. As the molecular structure of thirteen systems has been elucidated, genotypings can be performed from genomic DNA by simple polymerase chain reactions. Thus, any equipped institution can provide typed donors to meet the clinical demands, without the need for specific antisera.
Instrument platelet counts used in corrected count increment (CCI) and percent platelet recovery (PPR) formulas presume the transfused platelets are in equilibrium during the first hour after platelet transfusion. The timing of the pre-transfusion count affects CCI results, and we postulate that timing of CCI post transfusion affects CCI results. Platelet equilibrium using indium-111 platelet transfusions has not been reported. Platelet redistribution was studied in 16 healthy volunteers and 12 thrombocytopenic patients by generally infusing less than 72-hr stored single-donor platelets along with an aliquot of indium-111-labeled platelets by intravenous push. Counts were measured at 10, 15, 20, 60, and 120 min, and 24, 48, 72 hr along with continuous body scanning for 2 hr in healthy volunteers, and static organ scanning in patients and volunteers. Results indicated transfused platelets do not reach intravascular equilibrium for 60 min post-infusion and that the 10-min count cannot detect platelet refractoriness. However, total body equilibrium varies considerably between normal volunteers and thrombocytopenic patients. It is recommended to continue with the 1-hr post transfusion count.
Immune responses to platelet and neutrophil alloantigens are involved in the pathogenesis of several clinical syndromes including: neonatal alloimmune thrombocytopenia (NATP), post-transfusion purpura (PTP), refractory responses to platelet transfusion, neonatal alloimmune neutropenia (NAN), transfusion-related acute lung injury (TRALI), and chronic benign autoimmune neutropenia of infancy. Initially, platelet alloantigens were only characterized serologically. Subsequently, they were localized to specific platelet surface glycoprotein structures and ultimately defined to the level of nucleic acid polymorphisms on platelet glycoprotein genes. These advances allowed the tools of molecular biology to be applied to typing for platelet alloantigens. The advantages of such typing methods include: 1) patient platelets are no longer required for the typing assays, and therefore, platelet types can be established on extremely thrombocytopenic samples (by using peripheral blood white blood cells [WBC]); 2) The genotyping methods eliminate the requirement for rare serologic reagents. A number of different genotyping methods have been developed. These include: restriction fragment length polymorphism (RFLP), sequence specific primers (SSP), and Dot-Blot hybridization. Clinical applications of this methodology include: determining the platelet genotype of fetuses at risk for NATP, in the diagnosis of PTP, and identifying causes of refractory responses to platelet transfusions. Analogous to platelet alloantigens, a limited number of neutrophil alloantigens can now be determined by molecular biologic methods. The new methods obviate the need to isolate fresh neutrophils for serologic typing and do not require rare serologic reagents. To date, molecular polymorphisms associated with alloantigens on the neutrophil Fc gamma RIIIb surface glycoprotein have been elucidated. These include the allo-antigens NA1, NA2, and SH.