Posttransfusion purpura following bone marrow transplantation

D. A. Evenson, S. Pulkrabek, E. H. Perry, J. Radford, J. S. Miller, C. Verfaillie

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

BACKGROUND: Thrombocytopenia is a major cause of morbidity and hospital expense following bone marrow transplantation. Platelet transfusions in these patients are frequently complicated by the recipient's development of antibodies to HLA class I antigens. When these patients become refractory to the transfusion of HLA‐matched platelets, the recipient's platelet antigen phenotype must be determined, to ensure that donor platelets will be phenotypically compatible. Cases of alloimmunization to HPA‐1a and HPA‐1b resulting in refractoriness to transfused platelets and the subsequent development of a posttransfusion purpura‐like syndrome are reported. CASE REPORTS: In the first case, a 43‐year‐old woman with Stage IV infiltrating ductal breast cancer presented to the hospital for a transplant of autologous peripheral blood stem cells. After the transplant, her platelet count remained less than 10 × 109 per L, despite daily platelet transfusions, including HLA‐matched platelets. Fourteen days following the transplant, her serum was found to contain anti‐HPA‐1a. Initially, the patient was refractory to the transfusion of HPA‐1a‐negative platelets, but after treatment with intravenous immunoglobulin, she had transient increases in posttransfusion platelet counts. She was also treated with a staphylococcal protein A immunoadsorption column and has not had any such subsequent refractoriness. Her genotype has been found, by use of allele‐specific oligonucleotide hybridization with white cell DNA, to be HPA‐1b/1b. The second case involved a 32‐year‐old woman with chronic myelogenous leukemia who received an unrelated‐donor marrow transplant. Three years later, her CML recurred, and she was treated with interferon‐alpha. Four months afterward, she experienced interferon‐alpha‐induced thrombocytopenia and the interferon therapy was discontinued. She received 12 platelet transfusions in 20 days, but none was effective. Antibodies specific for HLA antigens and HPA‐1b were detected, and three HLA‐matched, HPA‐1b‐negative apheresis platelet components were given, but without effect. Two days after treatment with methylprednisolone (1 g intravenously) and prednisone (2 mg/kg/day orally), her platelet count was 26 × 109 per L, and after 8 more days, it was 102 × 109 per L, without further transfusions. She was found to be homozygous for HPA‐1a (HPA‐1a/1a). CONCLUSION: Anti‐HPA‐ 1a and anti‐HPA‐1b can cause refractoriness to platelet transfusions in bone marrow transplant patients. Testing for platelet‐specific antibodies should be considered in all patients who are refractory to HLA‐matched platelets. 1995 AABB

Original languageEnglish (US)
Pages (from-to)688-693
Number of pages6
JournalTransfusion
Volume35
Issue number8
DOIs
StatePublished - Aug 1995

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