title: Long-term administration of G-CSF for aplastic anaemia is closely related to the early evolution of monosomy 7 MDS in adults.
abstract: There is an increasing incidence of the evolution of myelodysplastic syndrome (MDS) from aplastic anaemia (AA) with immunosuppressive treatment. In paediatric patients G-CSF is also reported to increase MDS evolution, but this process is not precisely understood in children or in adults. Therefore risk factors of MDS evolution in adults are evaluated here. Of 72 patients, five developed MDS. In 47 patients without cyclosporine (CyA) or antithymocyte globulin (ATG) therapy, only one developed MDS with trisomy 8, 242 months after diagnosis. But of 25 patients treated with either CyA or ATG, four developed monosomy 7 MDS within 3 years. Of these 25 patients, 18 were treated with G-CSF and the four patients (22.2%) who developed MDS were found in this group. The cumulative dose and the duration of G-CSF administration were significantly elevated in patients who developed MDS when compared with those who did not, 822.3 +/- 185.0 v 205.4 +/- 25.5 microg/kg (P<0.05) and 187.5 +/- 52.5 v 72.0 +/- 24.6 d (P<0.002), respectively. However these two values for CyA did not differ significantly. Statistically, treatment with CyA, G-CSF and combined G-CSF and CyA were significantly related to MDS evolution. The administration of G-CSF for more than a year was the most important factor (P=0.00). These results suggested that a close relationship exists between G-CSF and subsequent monosomy 7 MDS from AA in adults who receive immunosuppressive therapy. Long-term administration of G-CSF should be prohibited in order to prevent MDS evolution.
authors.affiliation: Department of Internal Medicine II, Kashiwa Hospital, Jikei University School of Medicine, Tokyo, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Kaito
authors.forename: M
authors.initials: M
authors.lastname: Kobayashi
authors.forename: T
authors.initials: T
authors.lastname: Katayama
authors.forename: H
authors.initials: H
authors.lastname: Masuoka
authors.forename: T
authors.initials: T
authors.lastname: Shimada
authors.forename: K
authors.initials: K
authors.lastname: Nishiwaki
authors.forename: T
authors.initials: T
authors.lastname: Sekita
authors.forename: H
authors.initials: H
authors.lastname: Otsubo
authors.forename: Y
authors.initials: Y
authors.lastname: Ogasawara
authors.forename: T
authors.initials: T
authors.lastname: Hosoya
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000741:Anemia, Aplastic / Q000628:therapy*; D002897:Chromosomes, Human, Pair 7; D016572:Cyclosporine / Q000009:adverse effects; D004334:Drug Administration Schedule; D005260:Female; D005500:Follow-Up Studies; D016179:Granulocyte Colony-Stimulating Factor / Q000009:adverse effects* / Q000627:therapeutic use; D006801:Humans; D007166:Immunosuppressive Agents / Q000009:adverse effects; D008297:Male; D008875:Middle Aged; D009006:Monosomy; D009190:Myelodysplastic Syndromes / Q000209:etiology*; D012189:Retrospective Studies; D012307:Risk Factors; D015996:Survival Rate
chemical_list: D007166:Immunosuppressive Agents; D016179:Granulocyte Colony-Stimulating Factor; D016572:Cyclosporine