The collection of PBSC for transplantation requires repetitive leukapheresis, typically via central venous catheters (CVC). To assess the complications of this procedure, we reviewed 75 consecutive PBSC transplant candidates requiring 554 leukapheresis on a Haemonetics V50 Plus apheresis system. CVC occlusion necessitating thrombolytic therapy or cancellation of the procedure was the most commonly observed complication, occurring among 37 patients on 86 occasions (15.9% of CVC-aided collections). Thrombolytic therapy was successful in 85%. Of the patients, 16% experienced an infectious complication during the PBSC harvesting; chemotherapy mobilization significantly increased this risk, whereas growth factor mobilization was protective (p < 0.02). Hematologic complications including anemia (median postapheresis nadir hemoglobin 8.8 g/dl) and transient thrombocytopenia (median postapheresis nadir 64,000/microliters) required transfusional support among 30.7% and 14.7% of patients, respectively. The use of chemotherapy mobilization was correlated with increased need for support of both red cells and platelets (p < 0.001). Additional complications included catheter placement problems, symptomatic citrate-related hypocalcemia, transient hypotension, and machine-related malfunctions. Although the complications of the PBSC harvests were manageable, given their frequency the decision to pursue this form of hematopoietic rescue in preference to traditional operative bone marrow harvesting must address these risks.

The differential diagnosis of unexpected neutropenia following bone marrow transplantation includes several potentially life-threatening complications including graft rejection, overwhelming infection, relapse of the underlying neoplasm, and intrinsic graft failure. However, a number of recent reports document that the differential diagnosis also includes autoimmune neutropenia, which, although potentially life-threatening, often responds well to corticosteroids or splenectomy. Autoimmune neutropenia has been reported following both autologous and allogeneic bone marrow transplantation. Herein we report a 31-year-old woman who developed a rapidly falling neutrophil count 11 days following peripheral blood stem cell transplantation for non-Hodgkin's lymphoma. A laboratory evaluation supported a diagnosis of autoimmune neutropenia, and the neutropenia resolved following treatment with steroids and granulocyte-colony stimulating factor.

No abstract

In vitro coculture studies were performed in five patients with severe aplastic anemia (SAA) and their normal HLA-matched donors before and after allogeneic bone marrow transplantation (BMT) to determine whether the erythropoietic function of T cells is abnormal in this disorder. These coculture studies used fresh or cryopreserved marrow T lymphocytes with fresh or cryopreserved marrow T cell-depleted target cells. Four of five aplastic patients had little or no transfusion exposure before studies. The composite results showed that, in comparison to the erythropoietic effects of normal HLA-identical marrow T lymphocytes or engrafted T lymphocytes, T lymphocytes collected from the aplastic patients before BMT consistently suppressed or failed to support CFUE and BFUE growth optimally from autologous marrow, HLA- identical marrow, or engrafted aplastic T cell-depleted marrows. This T cell abnormality was not observed in four multiply transfused leukemics and three patients with myelodysplastic syndrome. Marker analyses of SAA marrow T lymphocytes performed before and after BMT suggested that the erythropoietic functional abnormality was due to abnormal marrow T cell composition reflecting an excess of activated Tac+, T3+, T11+ lymphocytes. Collectively, these in vitro studies provide firmer in vitro evidence implicating T cells in the pathogenesis of SAA. The erythropoietic T cells abnormalities in SAA are fully corrected by allogeneic BMT.