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It has been suggested that use of recombinant soluble thrombomodulin (rTM) is superior to conventional drugs in treatment of disseminated intravascular coagulation (DIC) complicating acute leukemia. However, its safety and efficacy have not been fully examined in prospective studies. Here, we performed a multicenter prospective study to examine outcomes of rTM treatment for DIC in patients with acute leukemia. Of 33 patients registered in this study, 13 had acute myeloid leukemia (AML), three had acute lymphoblastic leukemia (ALL), and 17 had acute promyelocytic leukemia (APL). The cumulative rates of DIC resolution at day 7 and day 35 were 56 and 81% in AML/ALL and 53 and 77% in APL, respectively. The median time from the initiation of rTM to DIC resolution was 4 days in AML/ALL and 6 days in APL patients. Adverse events related to hemorrhage occurred in two AML/ALL patients (13%) and three APL patients (18%). Of these, one AML/ALL patient died with intracranial hemorrhage, and two APL patients died with intracranial hemorrhage and pulmonary hemorrhage. These results suggest that rTM may improve the survival of acute leukemia patients with DIC by inhibiting early death related to hemorrhagic events, as reported previously.

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BACKGROUND Isohemagglutinins against ABO antigens absent on both recipient and donor red blood cells (RBCs) increase or decrease after ABO‐incompatible hematopoietic stem cell transplantation (HSCT). However, few reports have described the changes in the isohemagglutinin titers and the characteristics in patients with recurrent hematologic conditions after ABO‐incompatible HSCT. CASE REPORT A 59‐year‐old female with acute erythroid leukemia received a peripheral blood stem cell transplant from her HLA‐haploidentical daughter. The patient was typed as group O with anti‐ A (4+) and B (4+) isohemagglutinins, while the donor was typed as group B. The bone marrow cells achieved complete donor cell chimerism on Day 13 after HSCT. On Day 120, the patient showed 97% B RBC type with persistent anti‐A (3+) and without anti‐B antibodies. On Day 375, her leukemia relapsed, and recipient type O RBCs and anti‐B antibodies sequentially reemerged. However, clinicolaboratory hemolysis and erythroid aplasia were not detected in the patient. RESULTS The post‐HSCT sera agglutinated the allo B RBCs, but not the donor B RBCs, while the pre‐HSCT sera agglutinated both RBCs. The burst‐forming/colony‐forming units of erythroid formation from the donor peripheral blood stem cells were impaired by only the pre‐HSCT sera and not by the post‐HSCT sera. CONCLUSION To our knowledge, this is the first report investigating the characteristic changes of isohemagglutinins between the pre‐ and post‐HSCT sera in a patient with recurrent acute myeloid leukemia. The present study suggests that the plasma cells producing anti‐donor B RBCs in the patient have been selectively eliminated or induced into an anergic state by the post‐HSCT immunologic reconstruction.