Background and objectives To detect HPA‐15 alloantibodies, we previously developed a human platelet antigen 15 (HPA‐15)‐expressing cell line‐based modified rapid monoclonal antibody immobilization of platelet antigen (CL‐MR‐MAIPA) assay. In this study, the protocol was modified for easier performance by introducing the mixed‐passive haemagglutination (MPHA) principle. Material and methods In total, 20 samples that tested negative for HPA alloantibodies and eight that tested positive for HPA‐15 alloantibodies (two and six positive for HPA‐15a and HPA‐15b antibodies, respectively) by CL‐MR‐MAIPA assay were used in this study. HPA‐15 cell lines were incubated with serum/plasma and then solubilized. The lysate was transferred to a round‐bottom well, which was coated with anti‐human CD109 monoclonal antibodies. After incubation and repeated washings, sheep red blood cells, coated with anti‐human IgG, were added to the wells. Haemagglutination was assessed the next day. Results The proposed cell line‐based immune complex capture‐dependent mixed‐passive haemagglutination (CL‐IC‐MPHA) assay consisted of four steps, but required only 2 h to perform, except for overnight incubation for haemagglutination. Two HPA‐15a alloantibody samples were reactive only for HPA‐15a cells, and six HPA‐15b alloantibody samples were reactive only for HPA‐15b cells with the CL‐IC‐MPHA assay. The 20 samples that tested negative for HPA alloantibodies did not react with HPA‐15a or HPA‐15b cells. These data indicated that the CL‐IC‐MPHA assay was highly specific and sensitive. Unfortunately, the CL‐IC‐MPHA assay's analytic sensitivity was twofold to eightfold lower than that of the CL‐MR‐MAIPA assay. Conclusion A novel, easy‐to‐perform protocol was successfully developed to detect HPA‐15 alloantibodies with high specificity and sensitivity.

The cytotoxicity of self-curing PMMA dental resin to oral epithelial cells was eliminated by mixing the resin with NAC.

Background Alloantibodies against human platelet antigen (HPA)‐15 are sometimes detected in patients with platelet transfusion refractoriness (PTR); however, little is known about their impact on PTR. Study Design and Methods Two patients who possessed HPA‐15 alloantibodies (Patient 1, anti‐HPA‐15b; Patient 2, anti‐HPA‐15a) and human leukocyte antigen (HLA) antibodies were enrolled. The efficacy of HPA‐15–compatible vs –incompatible platelet transfusion was compared by focusing on ABO‐ and HLA‐matched transfusions on the basis of the 24‐hour corrected count increment (CCI‐24 hours) for platelets. The titers of HPA‐15 antibodies in the patients' sera were also monitored. Results The patients received 71 and 12 ABO‐compatible, HLA‐matched platelet transfusions, respectively, during the monitoring periods. Among these transfusions, CCI‐24 hours could be calculated in 27 and 10 transfusions, respectively, and the HPA‐15 genotype of the donors was determined. There were no significant differences in the CCI‐24 hours between the HPA‐15 compatible and incompatible transfusions in both patients (P = .30 and .56, respectively, Mann‐Whitney U test). There was no significant change in the HPA‐15b antibody titer in Patient 1 during the monitoring period, while the HPA‐15a antibody level in Patient 2 was undetectable at the end of the monitoring period, although the titer was low at the beginning. Conclusion The efficacy of HPA‐15–incompatible platelet transfusions was not necessarily inferior to that of HPA‐15 compatible ones. Although the case number was limited, our results suggest that HPA‐15 antibodies do not have a significant impact on the effects of platelet transfusion.

No abstract