Myelodysplastic syndrome (MDS) with erythroid hypoplasia, a rare form of MDS, has not yet been clearly defined. We report four patients with MDS with erythroid hypoplasia who received immunosuppressive therapy. All were elderly, had severe transfusion‐dependent anaemia, morphological evidence of myelodysplasia and a low percentage (3·2–13·6%) of erythroid precursors. Administration of cyclosporin A (CsA) improved their anaemia; all transfusion‐dependent patients achieved transfusion‐independence. An inverted CD4/8 ratio was seen in three patients who also demonstrated T‐cell receptor (TCR)‐β and ‐γ gene rearrangements by Southern blotting and clonality by polymerase chain reaction. Treatment with CsA can be an attractive alternative treatment for patients with MDS with erythroid hypoplasia, which may be associated with a clonal abnormality in T cells.

Myelofibrosis is usually observed in myeloproliferative disorders, such as chronic myeloid leukemia. However, there are only a few reports showing an association between T-cell lymphoma and myelofibrosis. We report a case of peripheral T-cell lymphoma, unspecified (diffuse large cell) type, involving the bone marrow that was associated with severe myelofibrosis. In the present case, the plasma concentration of transforming growth factor-beta1 (TGF-beta1) was increased to 8.95 ng/ml (normal range: 1.56-3.24 ng/ml). No lymphadenopathy or skin lesions were observed during the entire clinical course. Although the mechanism of secondary myelofibrosis is still unclear, elevated plasma TGF-beta1 might be involved in the pathogenesis of bone marrow fibrosis in the present case.

Vitamin K 2 (VK2) effectively induces apoptosis in leukemia cell lines, including HL-60 and U937. However, combined treatment of cells with VK2 plus la, 25-dihydroxyvitamin D 3 (VD3) resulted in suppression of VK2-inducing apoptosis and pronounced induction of monocytic differentiation as compared with that by VD3 alone. After achieving monocytic differentiation by pre-exposure to VK2 and VD3, the cells became resistant to various apoptotic stimuli including VK2-and H 2 0 2-treatment and serum deprivation. Accumulation of cytoplasm p21 CIP1 along with disappearance of nuclear p21 CIP1 was detected in cells in response to 96-h treatment with VK2 plus VD3. A stable transfectant, U937-ANLS-p21 clpl , which lacked the nuclear localization signal of p21 CIP1 and showed overexpression of cytoplasm p21 CIP1 without monocytic differentiation, was resistant to apoptosis. These data suggest that a change of intracellular distribution of p21 CIP1 from nucleus to cytoplasm along with differentiation appears to be anti-apoptotic. Clinical benefits of using VK2 for treatment of patients with leukemia and myelodysplastic syndrome (MDS) have been reported. Our data suggest that VK2 plus VD3 may be an effective combination for differentiation-based therapy for leukemia and also MDS whose cytopenias are mediated though apoptosis.

Leukemia cutis is a localized or disseminated skin infiltration by leukemic cells. A 64-year-old man was diagnosed with acute myeloid leukemia (AML) complicated by disseminated intravascular coagulation. During the course of treatment with gabexate mesilate, the substance accidentally leaked from the infusion site in his elbow. One month later, a dark red erythema and induration accompanied by severe pain appeared in the area proximal to the gabexate mesilate injection site. The biopsy specimen demonstrated not only inflammation but infiltration of leukemic cells as well. Immunohistochemical staining for intercellular adhesion molecule-1 and platelet/endothelial cell adhesion molecule-1 showed strong expression of endothelial cells and leukemic cells. We speculate that the gabexate mesilate might have played a role in the induction of leukemia cutis via adhesion molecules in our case.

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