Masaaki Fukutoku

Sweet's syndrome during therapy with granulocyte colony-stimulating factor in a patient with aplastic anaemia

Summary. A patient with aplastic anaemia developed Sweets syndrome (a febrile neutrophilic dermatosis) during granulocyte colony‐stimulating factor (G‐CSF) therapy. Three repeated episodes of appearance and disappearance of erythematous nodules after administration and withdrawal of G‐CSF confirmed that G‐CSF induced Sweets syndrome in the patient. Sweets syndrome has been reported in patients with myelodysplastic syndrome and acute leukaemia, but not in patients with aplastic anaemia. This is the first report of a patient with aplastic anaemia who developed G‐CSF‐induced Sweets syndrome.

Interleukin-7 (IL-7)-induced proliferation of CD8+ T-chronic lymphocytic leukemia cells

Interleukin-7 (IL-7) is a growth factor for pro-B cells, pre-B cells, and thymocytes and is known to induce the proliferation of normal human peripheral T cells. Moreover, human B and T acute leukemia cells with immature surface markers proliferate in response to IL-7. Here we describe a case of T-chronic lymphocytic leukemia, in which the leukemic cells showed a proliferative response to human recombinant IL-7in vitro. The patient was a 74-year-old woman with anemia and thrombocytopenia, whose bone marrow was fibrosed and infiltrated with pathologic cells. Surface markers of the leukemic cells were CD2(+), CD3(+), CD5(+), CD7(+), CD8(+), and CD4(−). Both T-cell receptor β-chain and γ-chain genes were found to be rearranged by immunogenotypic analysis. The leukemic cells proliferated in response to IL-7 dose dependently. The DNA synthesis of CLL cells was stimulated by not only IL-7 but also IL-2 and IL-4. The IL-7-induced proliferation was not inhibited by antibodies to IL-2 receptors or the anti-IL-4 antibody. These findings indicate that IL-7 may induce the proliferation of peripheral CD8+ T cells, even on its pathological counterpart.