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Platelet functions were studied in 16 patients with multiple myeloma (MM) and 4 with primary macroglobulinemia (PM). The fall in immunoglobulins on therapy was correlated with the status of platelet function. Effect of incubation of normal platelets with immunoglobulins derived from these patients on kaolin-induced platelet factor 3 (PF3) release was studied to elucidate the mechanism of platelet function defect. Results show increased bleeding time, absence or poor platelet adhesion and aggregation, poor PF3 availability and reduced total PF3 in platelets more consistently in PM but to a lesser extent in MM. Normalisation or partial reduction in globulins on therapy was associated with improvement in platelet functions. Incubation of normal platelets with immunoglobulins enhanced the kaolin-induced PF3 availability. It is suggested that in vivo platelet activation may bring about the PF3 release which subsequently manifests as poor PF3 availability and reduction in its total contents.

TABLE I. Cytogenetlc and Molecular Follow-Up Study of the Patient Date of sample Karyotype (no. of mitoses) Molecular analysis Diagnosis 3/84 46 XY t(9:22)(q34;ql1)(19) ND BMT 4/86 4/87 46,XY (63) ND 3/88 46.XY (16) ND 4/89 46,XY (46)46.XY 1(9;22)(q34;qI l)t(8:14)(p22;qlI)(l) ND 10189 46,XY (10) M-bcr rearrangement 5/90 46.XY (65) M-bcr rcarrangement 1/91 46,XY 1(9:22)(q34;qI 1).1(8;14)(p22;qI 1)(20) Failure excluded with the same degree of certitude, for lack of sufficient serum and erythrocyte samples. More traditional clues to this hypothesis were, however, lacking. Three years after BMT. bone marrow karyotype revealed one cell 46,XY t(9;22)t(8; 14). Cytogenetical and molecular follow-up is summarized in Table I. Following karyotype controls were normal, but molecular analysis revealed M-bcr rearrangement by PCR method. In January, 1991, the patient showed evidence of hematological relapse and bone marrow karyotype revealed 20 cells 46.XY t(9;22). t(8;14)(p22;qlI). He received rIFNa,, treatment, with achievement of an hematological response at time of this report. We concluded that paternity is possible few years after BMT in patients who received TBI. Therefore, assumption of probable sterility in male allogeneic bone mamw recipients should be made cautiously. Although this is only an anecdotal report, we confirmed, as have others 121, that the late reappearance of even a unique leukemic cell and/or M-bcr rearrangement may preclude CML relapse. The relationship between paternity and relapse is very speculative. Nevertheless, these two events may represent different aspects of an insufficient conditioning regimen. T. FACON REFERENCESI . Sanders JE. Buckner D, Leonard JM. Sullivan KM. Witherspoon RP. Deeg J. Storb R. Thomas ED: Late effects on gonaldal function of cyclophosphamide. total body irradiation, and marrow transplantation. Transplantation 36252, 1983. 2. Hughes TP. Morgan GJ, Martial P. Goldman JM: Detection of residual leukemia after bone marrow transplant for chronic myeloid leukemia: Role of polymerase chain reaction in predicting relapse. Blood 77:874. 1991.

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