Two childhood acute myelogenous leukemia (AML) patients receiving intrathecal (IT) and intravenous (IV) cytosine arabinoside (Ara-C) developed progressive ascending paralysis, resulting in death in one patient. Necropsy findings on this patient included spinal cord demyelination characteristic of Ara-C neurotoxicity. An unusual aspect of these two cases was the delay between cessation of IT therapy and the onset of neurologic symptoms. These patients received relatively low total doses of IT Ara-C and standard doses of IV Ara-C. Previous studies have shown that Ara-C equilibrates readily between serum and cerebrospinal fluid; this implies that total IV and IT doses of Ara-C may be additive in relation to development of neurotoxicity. For these reasons, use of IV and IT Ara-C in childhood AML must be approached with greater caution, especially if neurologic abnormalities develop during or after therapy. Cancer 57:1083-1088, 1986. RANSIENT and permanent paraplegia after adminis
A 16-year-old female developed a hemolytic uremic syndrome 9 months after undergoing bone marrow transplantation for acute lymphoblastic leukemia during second relapse. There appears to be no etiologic relationship between the post-transplant immune status and the hemolytic uremic syndrome. The patient succumbed later to recurrent leukemia.
A 25-year-old female developed idiopathic thrombocytopenic purpura 1 year after undergoing bone marrow transplantation for acute myelogenous leukemia. She had a complete response after splenectomy. The patient’s posttransplant immune status and the possible relationship between idiopathic thrombocytopenic purpura and her posttransplant state are discussed.
A 28-yr-old woman with acute malignant myelosclerosis received, as primary treatment, ablative chemotherapy and total body radiation therapy followed by bone marrow transplantation from her histocompatible brother. The patient is now well more than 15 mo after bone marrow transplantation, with normal peripheral blood counts, a normal bone marrow, no evidence of graft-versus-host disease, and is on no therapy. In light of the poor results obtained with conventional chemotherapy in this disease, bone marrow transplantation may represent the treatment of choice for patients who have an appropriate donor.
Six cases of immune hemolytic anemia attributed to donor-derived red cell antibodies after allogeneic bone marrow transplantation (BMT) are reported. In 2/6 cases, severe intravascular hemolysis was seen, 6/6 required increased red cell transfusion, and 1/6 was treated by plasma exchange. All recipients were receiving cyclosporine to prevent graft-v- host disease. Investigations showed that in each case, the donor lacked ABO or Rho(D) red cell antigens present in the recipient. The direct antiglobulin test was positive in 6/6. Relevant serum antibody (anti-A, four cases; anti-B, one case; anti-D, one case) was first detected one to three weeks after BMT. Eluates made from recipient red cells showed the same specificity as serum antibody. Maximum hemolysis occurred nine to 16 days after BMT, suggesting that active production of antibody by “passenger” donor lymphocytes was the likely mechanism of hemolysis, rather than passive transfer of antibody in the marrow infusion. Retrospective analysis of 21 consecutive cyclosporine-treated BMT patients receiving marrow lacking ABO or D antigens present in the recipient showed that (1) 15/18 patients tested had red cell antibody production against recipient red cell antigens; (2) despite the frequent presence of antibody specific for recipient red cell antigens, only 3/21 patients developed clinically significant hemolysis; (3) clinical hemolysis could not be predicted by donor or recipient red cell antibody titers. We conclude that although red cell antibody against recipient antigens is frequently produced after minor ABO and D mismatched BMT in cyclosporine-treated recipients, only 10% to 15% of cases develop clinically significant immune hemolysis. The data presented show that the most likely source of antibody is “passenger” donor lymphoid cells.
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