E Taaning1, F Tønnesen. 1. Department of Clinical Immunology, Glostrup Hospital, Denmark.
Abstract
BACKGROUND AND OBJECTIVES: The mechanism for the destruction of a patient's own platelets in post-transfusion purpura (PTP) is unknown. In order to test the hypothesis that the destruction of autologous platelets in PTP is related to the presence of platelet antibodies with pan-reactivity, we investigated sera from patients with PTP. MATERIALS AND METHODS: Sera from 12 patients with PTP were investigated for platelet antibodies by platelet-ELISA and monoclonal antibody-specific immobilization of platelet antigen assay. RESULTS: During the thrombocytopenic phase, antibodies of IgG and IgM classes with pan-specificity against platelet GPIIb-IIIa, GPIb-IX and GPIa-IIa were found together with HPA alloantibodies. After recovery, the pan-specific antibodies disappeared or the extent of reactivity diminished, whereas the IgG HPA alloantibodies persisted. CONCLUSION: These findings provide evidence that transient panreactive antibodies may be responsible for the autologous platelet destruction in PTP.
BACKGROUND AND OBJECTIVES: The mechanism for the destruction of a patient's own platelets in post-transfusion purpura (PTP) is unknown. In order to test the hypothesis that the destruction of autologous platelets in PTP is related to the presence of platelet antibodies with pan-reactivity, we investigated sera from patients with PTP. MATERIALS AND METHODS: Sera from 12 patients with PTP were investigated for platelet antibodies by platelet-ELISA and monoclonal antibody-specific immobilization of platelet antigen assay. RESULTS: During the thrombocytopenic phase, antibodies of IgG and IgM classes with pan-specificity against platelet GPIIb-IIIa, GPIb-IX and GPIa-IIa were found together with HPA alloantibodies. After recovery, the pan-specific antibodies disappeared or the extent of reactivity diminished, whereas the IgG HPA alloantibodies persisted. CONCLUSION: These findings provide evidence that transient panreactive antibodies may be responsible for the autologous platelet destruction in PTP.
Authors: Gavin Falk; Charles G Winans; Krista Bowens; Daniel W Bougie; Brian R Curtis; Richard H Aster Journal: Am J Hematol Date: 2016-06-03 Impact factor: 10.047