title: Granulocyte colony-stimulating factor (G-CSF) dependent hematopoiesis with monosomy 7 in a patient with severe aplastic anemia after ATG/CsA/G-CSF combined therapy.
abstract: We report a case of secondary myelodysplastic syndrome (MDS) with monosomy 7, which evolved from severe aplastic anemia (SAA) after long-term use of granulocyte colony-stimulating factor (G-CSF). A 36 year old female was admitted for detailed examination and treatment of pancytopenia. SAA was diagnosed based on hypoplastic bone marrow and a normal chromosome study. She was treated with anti-thymocyte globulin (ATG), ciclosporin A (CsA) and G-CSF, which resulted in gradual improvement of not only the myeloid but also the erythroid-megakaryocyte series. However, bone marrow dysplasia with monosomy 7 was observed after 7 months of a combination therapy of immunosuppressant and G-CSF, which prompted the discontinuation of G-CSF administration. Thereafter, bone marrow hypoplasia gradually progressed, resulting in a second aplastic crisis. During this process, the proportion of marrow cells showing monosomy 7 decreased, and the proportion with normal karyotype increased. Re-administration of G-CSF induced a trilineage, though dysplastic, hematological response; but the monosomy 7 positive population increased again. These observations indicated the presence of G-CSF dependent hematopoiesis associated with monosomy 7 in this patient. Although many G-CSF related MDS/AML cases with this leukemia-specific abnormal karyotype have been reported with emphasis on the harmful effects of G-CSF, G-CSF was useful even after the appearance of monosomy 7 as a means of avoiding life-threatening infection in this patient.
authors.affiliation: Third Department of Internal Medicine, Yamaguchi University School of Medicine, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Nishimura
authors.forename: T
authors.initials: T
authors.lastname: Yamada
authors.forename: T
authors.initials: T
authors.lastname: Andoh
authors.forename: T
authors.initials: T
authors.lastname: Tao
authors.forename: M
authors.initials: M
authors.lastname: Emoto
authors.forename: T
authors.initials: T
authors.lastname: Ohji
authors.forename: K
authors.initials: K
authors.lastname: Matsuda
authors.forename: N
authors.initials: N
authors.lastname: Kameda
authors.forename: Y
authors.initials: Y
authors.lastname: Satoh
authors.forename: A
authors.initials: A
authors.lastname: Matsutani
authors.forename: Y
authors.initials: Y
authors.lastname: Azuno
authors.forename: Y
authors.initials: Y
authors.lastname: Oka
mesh_terms: D000328:Adult; D000741:Anemia, Aplastic / Q000188:drug therapy* / Q000235:genetics*; D000961:Antilymphocyte Serum / Q000009:adverse effects / Q000627:therapeutic use*; D002897:Chromosomes, Human, Pair 7 / Q000235:genetics*; D016572:Cyclosporine / Q000009:adverse effects / Q000627:therapeutic use*; D004305:Dose-Response Relationship, Drug; D004359:Drug Therapy, Combination; D005260:Female; D016179:Granulocyte Colony-Stimulating Factor / Q000009:adverse effects / Q000627:therapeutic use*; D006410:Hematopoiesis / Q000502:physiology*; D006801:Humans; D007166:Immunosuppressive Agents / Q000009:adverse effects / Q000627:therapeutic use*; D009006:Monosomy / Q000503:physiopathology
chemical_list: D000961:Antilymphocyte Serum; D007166:Immunosuppressive Agents; D016179:Granulocyte Colony-Stimulating Factor; D016572:Cyclosporine