Long-term administration of G-CSF for aplastic anaemia is closely related to the early evolution of monosomy 7 MDS in adults

被引:57
作者
Kaito, K
Kobayashi, M
Katayama, T
Masuoka, H
Shimada, T
Nishiwaki, K
Sekita, T
Otsubo, H
Ogasawara, Y
Hosoya, T
机构
[1] Jikei Univ, Sch Med, Dept Internal Med 2, Minato Ku, Tokyo 1058461, Japan
[2] Jikei Univ, Sch Med, Kashiwa Hosp, Dept Gen Internal Med, Tokyo 1058461, Japan
关键词
aplastic anaemia; monosomy; 7; MDS; G-CSF; cyclosporine;
D O I
10.1046/j.1365-2141.1998.01014.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 pears, 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 mu g/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.
引用
收藏
页码:297 / 303
页数:7
相关论文
共 35 条
[1]  
APPELBAUM FR, 1987, EXP HEMATOL, V15, P1134
[2]   ANTILYMPHOCYTE GLOBULIN, CYCLOSPORINE, AND GRANULOCYTE-COLONY-STIMULATING FACTOR IN PATIENTS WITH ACQUIRED SEVERE APLASTIC-ANEMIA (SAA) - A PILOT-STUDY OF THE EBMT SAA WORKING PARTY [J].
BACIGALUPO, A ;
BROCCIA, G ;
CORDA, G ;
ARCESE, W ;
CAROTENUTO, M ;
GALLAMINI, A ;
LOCATELLI, F ;
MORI, PG ;
SARACCO, P ;
TODESCHINI, G ;
COSER, P ;
IACOPINO, P ;
VANLINT, MT ;
GLUCKMAN, E .
BLOOD, 1995, 85 (05) :1348-1353
[3]   TRANSIENT EXPRESSION OF TRISOMY-21 AND MONOSOMY-7 FOLLOWING CYCLOSPORINE-A IN A PATIENT WITH APLASTIC-ANEMIA [J].
BARRIOS, NJ ;
KIRKPATRICK, DV ;
LEVIN, ML ;
VARELA, M .
LEUKEMIA RESEARCH, 1991, 15 (06) :531-533
[4]   APLASTIC-ANEMIA .1. PATHOGENESIS, DIAGNOSIS, TREATMENT, AND PROGNOSIS [J].
CAMITTA, BM ;
STORB, R ;
THOMAS, ED .
NEW ENGLAND JOURNAL OF MEDICINE, 1982, 306 (11) :645-652
[5]  
DALE DC, 1993, BLOOD, V81, P2496
[6]  
DEPLANQUE MM, 1988, BRIT J HAEMATOL, V70, P55
[7]  
DEPLANQUE MM, 1989, BRIT J HAEMATOL, V73, P121
[8]  
DONEY K, 1992, BLOOD, V79, P2566
[9]   TREATMENT OF APLASTIC-ANEMIA WITH ANTILYMPHOCYTE GLOBULIN AND METHYLPREDNISOLONE WITH OR WITHOUT CYCLOSPORINE [J].
FRICKHOFEN, N ;
KALTWASSER, JP ;
SCHREZENMEIER, H ;
RAGHAVACHAR, A ;
VOGT, HG ;
HERRMANN, F ;
FREUND, M ;
MEUSERS, P ;
SALAMA, A ;
HEIMPEL, H .
NEW ENGLAND JOURNAL OF MEDICINE, 1991, 324 (19) :1297-1304
[10]  
GABRILOVE J, 1992, BLOOD, V80, P1382