Post-transfusion purpura due to anti HPA–1a antibodies – a retrospective case report

Post-transfusion purpura is a life-threatening adverse reaction associated with a reduction in platelet counts below 10 x 109/L and bleeding. It usually occurs in women who, due to their pregnancies, have developed antibodies directed against human platelet antigen (HPA), most often anti-HPA 1a. The case described by us concerned an 83-year-old woman who received two units of red blood cells (RBC) due to severe secondary anemia. Seven days after the transfusion, she developed skin symptoms of thrombocytopenic diathesis, gastrointestinal bleeding, and a reduced number of platelets (3 x 109/L), and the patient’s serum (genotype HPA-1b/1b) was positive for anti-platelet antibodies with HPA-1a specificity and directed against human leukocyte antigen (HLA) class I and class II antibodies, unresponsive to the lymphocytotoxic test. Prompt diagnosis by our transfusion medicine consultant and the initiation of treatment with intravenous immunoglobulins certainly shortened the duration of thrombocytopenia and bleeding, and possibly also saved the patient’s life.

Genotyping of Eight Human Platelet Antigen Systems in Serbian Blood Donors: Foundation for Platelet Apheresis Registry

Introduction: The aim of this study was to investigate the allele and genotype frequencies of 8 human platelet antigen (HPA) systems among blood donors from the Blood Transfusion Institute of Serbia and to compare them with published studies. These data would be useful to establish the basis for a platelet apheresis donor registry. Material and Methods: Seventy-two unrelated male platelet apheresis/blood donors from Serbia were typed for 8 HPA systems (HPA-1 to HPA-6, HPA-9, and HPA-15) via the FluoGene method, based on polymerase chain reaction-sequence-specific amplification (PCR-SSP; PCR using sequence-specific primers) with fluorometric signal detection. Allele and genotype frequencies were estimated by direct counting and compared to the expected genotype frequencies according to the Hardy-Weinberg principle. The transfusion mismatch probability was calculated for every HPA specificity. Results: The allele frequencies were: HPA-1a, 0.868; HPA-1b, 0.132; HPA-2a, 0.917; HPA-2b, 0.083; HPA-3a, 0.611; HPA-3b, 0.389; HPA-5a, 0.903; HPA-5b, 0.097; HPA-9a, 0.993; HPA-9b, 0.007; HPA-15a, 0.472; and HPA-15b, 0.528. For HPA-4 and HPA-6 only allele a was detected. Discussion: The HPA allele frequencies of European populations showed no significant differences in comparison with our results. Statistically significant differences were revealed in comparison with some populations of non-European origin. In the tested donors no HPA-2 bb genotype was detected, but we found 1 donor with the rare HPA-9b allele. The biggest transfusion mismatch probability in the Serbian population is for systems HPA-15 (37.4%) and HPA-3 (36.2%), which means that more than a third of random transfusions could cause mismatch in these systems. This study was enabled by the introduction of molecular HPA typing, and it provides initial results of the HPA allele and genotype frequencies in the population of blood donors in Serbia. They will be used to provide a compatible blood supply on demand for treating patients with alloimmune thrombocytopenic disorders. The successful implementation of PCR-SSP with fluorometric signal detection could be further complemented in the future by the introduction of high-throughput methods, which will largely depend on the available financial resources.