Eiki Miyanishi

Hemostatic Abnormalities Following Bone Marrow Transplantation

Hemostatic abnormalities in 26 patients following bone marrow transplantation (BMT) were examined. In the event-free survival group, the plasma levels of antithrombin (AT) and protein C (PC) were significantly decreased 1 and 2 weeks after BMT, and the plasma levels of thrombomodulin (TM) and tissue plasminogen activator-plasminogen activator inhibitor-1 complex (tPA-PAI-I complex) were significantly increased from 4 weeks to 13 weeks after BMT. Excepting AT, there was no significant difference in hemostatic parameters before BMT among the event-free survival, 6-month survival, and death within 6 months groups. On day 0 following BMT, only plasma AT levels were significantly lower in the 6-month survival group than in the death within 6 months group. From 1 to 3 weeks after BMT, plasma levels of AT or PC were significantly lower in the death within 6 months group than in the 6-month survival group. From 1 to 5 weeks after BMT, the plasma levels of TM and tissue type plasminogen activator-plasminogen activator inhibitor-I complex (tPA-PAI-I complex) were significantly higher in the 6-month survival group than in the death within 6 months group. From 1 to 13 weeks after BMT, the plasma levels of D-dimer or soluble fibrin monomer (SFM) were significantly higher in the death within 6 months group than in the 6-month survival group. There was no remarkable difference in plasma levels of thrombin-antithrombin comlex or plasmin-plasmin inhibitor complex following BMT between these groups of patients. These findings suggest that the decrease in the plasma AT or PC level reflects early occurrence of complications of prognostic significance and that the increase in vascular endothelial cell markers such as plasma levels of TM or tPA-PAI-I complex reflects occurrence of complications during the middle course of BMT. Plasma levels of D-dimer and SFM may be useful markers for predicting complications associated with poor prognosis after BMT.

Pathogenesis of Fever of Unknown Origin in Patients with Acute Leukemia and Granulocytopenia

Interleukin-1 (IL-1) is an endogenous pyrogen produced by blood monocytes or tissue macrophages in response to infection. Since hepatic macrophages (Kupffer cells) make up more than 90% of tissue macrophages and have a possibility of remaining intact after cytotoxic chemotherapy, they may be the major producers of IL-1 in infection during prolonged periods of severe monocytopenia in leukemic patients having modern chemotherapy treatment. Hence, the majority of febrile episodes probably due to infection in patients with acute leukemia and granulocytopenia may be caused by an inflammatory response mediated by IL-1 derived from the Kupffer cells in the liver sinuses.

HTLV‐1 unrelated adult T‐cell leukemia/lymphoma with unique phenotype and karyotype

We describe a unique case of adult T‐cell leukemia/lymphoma (ATL). The patient had typical clinicohematological features as ATL, but showed a lack of antibody to human T‐cell leukemia virus type‐1 (HTLV‐1) and was negative for HTLV‐I proviral DNA in the peripheral mononuclear cells by means of polymerase chain reaction. The phenotype of tumor cells revealed CD7+, CD5+, CD2+, CD3+, WT31−, TcR δ 1−, CD4−, CD8−, CD25−, and the karyotype showed a 5q‐, t(12;18). HTLV‐I unrelated ATL is very rare, and the karyotype as in our case has not been reported previously. Am. J. Hematol. 64:64–66, 2000.