EXTENSIVE MENINGEAL INVOLVEMENT AS THE PRIMARY MANIFESTATION OF A SYSTEMIC SMALL LYMPHOCYTIC LYMPHOMA: FAVOURABLE OUTCOME AFTER NEURAXIAL IRRADIATION WITHOUT CHEMOTHERAPY

consent, we challenged intravenous infusion trial with the plasma from those donors during his complete remission period: we filtered their plasmas by Acrodisc (0.22 pm, German Sciences Inc., Michigan, U.S.A.) to remove platelets completely, mixed 2.5 ml of them in 40 ml of saline and administered to him. This trial provoked no clinical symptoms, then we tried HLA locus A. B-matched PCs from two donors prepared for the challenging. Both of them also caused nothing, and 24 h post-transfusion platelet count increments showed much better responses ( + 13 x 1 Oy/l and + 33 x 10y/l) than that of HLA-incompatible ones (ranging from +0.4 x 10y/l to +0.9 x 10y/l). We conclude that the severe anaphylactic reaction described above, including an anaphylactic shock, was induced by undetectable anti-HLA antibodies, or alloantibodies closely linked to the HLA locus A, B of the patient (A2 and A24, B46 and B52). In our case, HLA A31, A33, B44 and/or B55 among the six donors seemed to be attributed to the reaction, though we could not further identify the antigen and the antibody involved. The failure to obtain positive skin test results may be due to inadequate exposure of antigen (platelet) to antibody in the patient’s serum, and no anaphylactic reaction to red cell preparation would also suggest a need for infusion of intact platelets ready for activation. This activation of platelets by the donor, if it occurred and contributed to the reaction, would not be a result of separating platelets by the apheresis system, because there was no reaction to platelets drawn from HLA-matched donors. Taking these facts into consideration, we also suggest that adequately activated platelets due to antibody binding British Journal of Haematology, 1993, 83