Search

Summary. By applying the platelet suspension immunofluorescence test (PSIFT), platelet-specific alloantibodies responsible for post-transfusion purpura were detected in eight patients within a period of 2 years. All patients were female and had previously received blood or had been pregnant. The platelet-specific alloantibodies had the specificity anti-Zwa in all the patients, who were all Zw(a -). In two patients the platelets were tested in the acute phase of the disease and found to be coated with IgG. In one patient an ether eluate was prepared from the platelets that reacted strongly with Zw(a +) platelets, but weakly with platelets from Zwb-homozygous individuals. The sera of these two patients, and of two others whose platelets were not directly tested, taken in the acute phase of the purpura, reacted strongly with Zwa-positive platelets. The four sera also reacted, however weakly, with Zwa-negative platelets, with autologous platelets taken during remission and with platelets from patients with Glanzmann's disease. It is postulated that Zwa-anti-Zwa complexes, present in the eluate and the sera, caused the reaction with Zwa-negative platelets and the patients’own platelets. Immunochemical characterization of the post-transfusion purpura antibodies showed that in all patients these were IgG, in two combined with IgM antibodies. Antibodies of the sub-class IgG1 were found in all patients, sometimes together with IgG3. In the indirect immunofluorescence test with anti-complement serum, the PTP antibodies in only four sera were able to fix complement. In only two of these sera were these complement-binding antibodies detectable in the 51Cr-lysis technique and then in a much lower titre than in the immunofluorescence technique.

Both 51Cr-survival studies with donor platelets and allogenic skin transplantations were performed in a patient with immune unresponsiveness to platelet antigens, i.e., HLA-and platelet-specific antigens. The patients, who suffered from hypoplastic anaemia, was successfully transfused with random donor platelets during 13 months. The serum of this patient contained only granulocyte-and mononuclear-cell-reactive antibodies, but no platelet-reactive antibodies. A nearly normal survival time of the donor platelets as well as a prolonged rejection time of a skin allograft of the same donor support the serological findings. The 51Cr-platelet survival time was not influenced by a leucocyte concentrate from the same donor, which was administered at the same time. Thus, in our patient, no increased platelet destruction could be induced via the so-called innocent bystander mechanism.

Summary. A serological follow-up study was undertaken in 47 patients with bone-marrow failure, who were repeatedly transfused with random donor granulocytes and/or platelets. Sera, obtained at regular intervals, were investigated in the leucoagglutination test, the lymphocytotoxic test and the immunofluorescence test on paraformaldehyde-fixed platelets, granulocytes and lymphocytes. The frequency of alloimmunization was high (73%). Not only HLA antibodies, but also blood-cell-specific alloantibodies were detected in the sera of the alloimmunized patients, e.g. lymphocyte-specific, platelet-specific and granulocyte-specific antibodies. The immunofluorescence test on platelets was also used as a crossmatch, and when this test was positive it was always found that after platelet transfusion the increment value was nil.