title: Acute myeloid leukemia possibly producing thrombopoietic factor(s).
abstract: A 75-year-old man developed a cluster of differentiation (CD)4-positive but human T-cell lymphotropic virus type I (HTLV-I)-negative T lymphoid neoplasm with overwhelming cutaneous involvement and mild thrombocytosis. Twelve courses tetrahydropyranyl adriamycin, cyclophosphamide, vincristine and prednisone (THP-COP) combination chemotherapy led him to complete remission. After four months of complete remission, however, atypical immature cells (blasts) appeared in peripheral blood and bone marrow. Surface marker analysis revealed the blasts to be CD2-, CD3-, CD4-, CD5-, CD7+, CD8-, CD10, CD13 +/-, CD19-, CD20-, CD25-, CD33+ and human leukocyte antigen-DR (HLA-DR+). Staining for myeloperoxidase, esterases, PAS and platelet peroxidase were all negative. The patient was diagnosed as having both CD7 and CD33 positive acute myeloid leukemia (AML). The relation between the T cell lymphoid neoplasm and AML was not clear. Thrombocytosis became more marked after acute leukemia occurred and the platelet count varied in parallel with the blast cell count in peripheral blood. When the leukemic cell count was high, thrombopoietic activity could be detected in the serum. In addition, conditioned medium obtained from primarily-cultured blasts had detectable thrombopoietic activity, which implied the blasts directly to produce a thrombopoietic factor(s). Analysis of the serum concentration for cytokines with associated thrombopoietic activity indicated that the blasts possibly produced a thrombopoietic factor(s) distinct from interleukin (IL)6, IL3, leukemia inhibitory factor (LIF), erythropoietin and granulocyte macrophage-colony stimulating factor. To our knowledge, this is the first reported case of an acute myeloid leukemia with marked thrombopoiesis (more than 2000 x 10(3)/microliter of maximum platelet count in peripheral blood.
authors.affiliation: Fourth Department of Internal Medicine, Faculty of Medicine, University of Tokyo.
authors.forename: A
authors.initials: A
authors.lastname: Fujita
authors.forename: M
authors.initials: M
authors.lastname: Matsuoka
authors.forename: Y
authors.initials: Y
authors.lastname: Shimonaka
authors.forename: N
authors.initials: N
authors.lastname: Imai
authors.forename: S
authors.initials: S
authors.lastname: Asano
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism; D000208:Acute Disease; D000368:Aged; D015703:Antigens, CD / Q000032:analysis; D019011:Antigens, CD7; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D000945:Antigens, Differentiation, T-Lymphocyte / Q000032:analysis; D001853:Bone Marrow / Q000473:pathology / Q000503:physiopathology; D015704:CD4 Antigens / Q000032:analysis; D015815:Cell Adhesion Molecules / Q000032:analysis; D006410:Hematopoiesis / Q000502:physiology; D006801:Humans; D007377:Interleukin-3 / Q000494:pharmacology; D015850:Interleukin-6 / Q000494:pharmacology; D007951:Leukemia, Myeloid / Q000097:blood* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008533:Megakaryocytes / Q000473:pathology / Q000502:physiology; D008562:Membrane Glycoproteins / Q000032:analysis; D063268:Sialic Acid Binding Ig-like Lectin 3; D012878:Skin Neoplasms / Q000097:blood* / Q000473:pathology / Q000503:physiopathology; D013922:Thrombocytosis / Q000473:pathology* / Q000503:physiopathology
chemical_list: D015703:Antigens, CD; D019011:Antigens, CD7; D015214:Antigens, Differentiation, Myelomonocytic; D000945:Antigens, Differentiation, T-Lymphocyte; C571163:CD33 protein, human; D015704:CD4 Antigens; D015815:Cell Adhesion Molecules; D007377:Interleukin-3; D015850:Interleukin-6; D008562:Membrane Glycoproteins; D063268:Sialic Acid Binding Ig-like Lectin 3; D000110:Acetylcholinesterase