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Cytopenias following bone marrow transplantation may be severe and life-threatening. These have been described post-allogeneic Klumpp, 1991 : Bone Marrow Transplant 8:159-171. or post-autologous bone marrow transplants Khouri et al., 1994: J Clin Oncol 12:748-758. as well as with peripheral blood stem cell transplantation Klumpp et al., 1992: Am J Hemato/41:215-217. It can be immune mediated, associated on occasions with graft-versus-host disease (GVHD) Anasetti et al., 1989: Blood 4:1054-1058; however, in most cases, the underlying mechanism is uncertain. The treatment of post-transplant cytopenias is not well established, and they are often refractory to immunosuppressive therapy with steroids. Herein we describe two cases of neutropenia after allogeneic bone marrow transplantation that improved after therapy with high-dose intravenous im-munoglobulin. o 1996 Wiley-Liss, Inc. CASE REPORT 1 history of cryptococcal meningitis 2 years ago; the current A 47-year-old man with chronic lymphocytic leukemia was treated upon diagnosis at another institution, with chlorambucil, prednisone, and Campath-IH monoclonal antibody (mAb). Upon relapse of his disease, he was refractory to treatment with CHOP, and later to fludara-bine. He received a matched unrelated bone marrow trans-plantation for a stage Rai IV, Binet C disease. The prepara-tive regimen consisted of cyclophosphamide 60 mgkgl day bid and fractionated total body irradiation of 1,200 cGy given in four daily fractions. A combination of FK-506 and methotrexate was used for prophylaxis against GVHD, as per institutional protocols. Pretransplant, his leukocyte count was 73.2 X lo9& consisting mostly of abnormal lymphocytes; the platelet count was 27 X lo9/ L, and the hematocrit 0.253. The hospital course was complicated by fever of unknown origin that started on day 7 post-transplantation. Vancomycin and ceftazidine antibiotic therapy were started. Blood and urine cultures as well as a chest radio-graph were normal. Amphotericin B was added on day 13. Because of recurrent fever on day 17, ceftazidine was changed to imipenem and doxycycline. High-dose fluconazole was started because of prior 0 1996 Wiley-Liss, Inc. serum cryptococcal level was 1 : 16. A lumbar puncture was not possible because of persistent thrombocytopenia that was refractory to platelet transfusions. After an initial response, the patient had recurrent fever; on day 24, imi-penem and doxycycline were changed to ticarcillin-clavulanate. The patient's lymphocytosis persisted until day 13 of his transplant. His maximum neutrophil count was 0.3 X 109L This did not improve with high doses of granulo-cyte colony-stimulating factor. Vancomycin, fluconazole,
Cytopenias following bone marrow transplantation may be severe and life-threatening. These have been described post-allogeneic Klumpp, 1991 : Bone Marrow Transplant 8:159-171. or post-autologous bone marrow transplants Khouri et al., 1994: J Clin Oncol 12:748-758. as well as with peripheral blood stem cell transplantation Klumpp et al., 1992: Am J Hemato/41:215-217. It can be immune mediated, associated on occasions with graft-versus-host disease (GVHD) Anasetti et al., 1989: Blood 4:1054-1058; however, in most cases, the underlying mechanism is uncertain. The treatment of post-transplant cytopenias is not well established, and they are often refractory to immunosuppressive therapy with steroids. Herein we describe two cases of neutropenia after allogeneic bone marrow transplantation that improved after therapy with high-dose intravenous im-munoglobulin. o 1996 Wiley-Liss, Inc. CASE REPORT 1 history of cryptococcal meningitis 2 years ago; the current A 47-year-old man with chronic lymphocytic leukemia was treated upon diagnosis at another institution, with chlorambucil, prednisone, and Campath-IH monoclonal antibody (mAb). Upon relapse of his disease, he was refractory to treatment with CHOP, and later to fludara-bine. He received a matched unrelated bone marrow trans-plantation for a stage Rai IV, Binet C disease. The prepara-tive regimen consisted of cyclophosphamide 60 mgkgl day bid and fractionated total body irradiation of 1,200 cGy given in four daily fractions. A combination of FK-506 and methotrexate was used for prophylaxis against GVHD, as per institutional protocols. Pretransplant, his leukocyte count was 73.2 X lo9& consisting mostly of abnormal lymphocytes; the platelet count was 27 X lo9/ L, and the hematocrit 0.253. The hospital course was complicated by fever of unknown origin that started on day 7 post-transplantation. Vancomycin and ceftazidine antibiotic therapy were started. Blood and urine cultures as well as a chest radio-graph were normal. Amphotericin B was added on day 13. Because of recurrent fever on day 17, ceftazidine was changed to imipenem and doxycycline. High-dose fluconazole was started because of prior 0 1996 Wiley-Liss, Inc. serum cryptococcal level was 1 : 16. A lumbar puncture was not possible because of persistent thrombocytopenia that was refractory to platelet transfusions. After an initial response, the patient had recurrent fever; on day 24, imi-penem and doxycycline were changed to ticarcillin-clavulanate. The patient's lymphocytosis persisted until day 13 of his transplant. His maximum neutrophil count was 0.3 X 109L This did not improve with high doses of granulo-cyte colony-stimulating factor. Vancomycin, fluconazole,
The efficacy of IgG infusion therapy in ITP is now established even in cases resistant to other forms of therapy. However, the mechanism of action is still speculative. We assume that a correction of the elevated thrombocyte clearance is brought about at several levels. First, antibodies specific for an inciting antigen (and for which the patient is deficient) may remove free antigen and/or immune complexes which adhere to platelet surfaces, thereby rendering platelets less susceptible to clearance. Second, IgG may act nonspecifically by protecting the platelet surface from becoming covered with immune complexes. Third, monomeric IgG may display a nonspecific inhibitory effect at the level of the interaction of immunologically altered platelets with Fc receptors of mononuclear phagocytes. For the latter effect, good in vivo evidence exists. However, it must be born in mind that interaction of antibodies with Fc receptors is but one mechanisms for triggering adherence and endocytosis. A variety of other receptors and binding sites exists which may interact with immunologically altered thrombocytes. These may either trigger phagocytes on their own or facilitate the interaction of antibodies and Fc receptors. How IgG infusion influences such interactions remains to be determined.
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