Efficacy of imatinib mesylate in the treatment of idiopathic hypereosinophilic syndrome

被引:129
作者
Cortes, J
Ault, P
Koller, C
Thomas, D
Ferrajoli, A
Wierda, W
Rios, MB
Letvak, L
Kaled, ES
Kantarjian, H
机构
[1] Univ Texas, MD Anderson Canc Ctr, Dept Leukemia, Houston, TX 77030 USA
[2] Novartis Pharmaceut, E Hanover, NJ USA
关键词
D O I
10.1182/blood-2003-01-0081
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Idiopathic hypereosinophilic syndrome (HES) is a myeloproliferative disorder characterized by persistent eosinophilia and organ involvement. Different treatments have been investigated in HES with modest success. It has been suggested that imatinib is active in HES. We treated 9 patients with HES with 100 mg imatinib daily. Doses for patients without response after 4 weeks were increased to 400 mg daily. Prior therapy had failed for 7 patients. Five patients responded: 4 achieved sustained complete remission lasting a median of 12+ weeks (range, 9+ to 36+ weeks), and 1 had a transient response. One patient died in complete remission. Responses occurred within 4 weeks of therapy; only 1 responder required an increase in dose to 400 mg daily. Three of 4 nonresponders failed to respond to an increase in dose. Toxicity was minimal. We conclude that imatinib therapy is effective for HES. (C) 2003 by The American Society of Hematology.
引用
收藏
页码:4714 / 4716
页数:3
相关论文
共 22 条
[1]   The mechanism of IL-5 signal transduction [J].
Adachi, T ;
Alam, R .
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 1998, 275 (03) :C623-C633
[2]  
Assa'ad AH, 2000, CHEM IMMUNOL, V76, P208
[3]   Response of idiopathic hypereosinophilic syndrome to treatment with imatinib mesylate [J].
Ault, P ;
Cortes, J ;
Koller, C ;
Kaled, ES ;
Kantarjian, H .
LEUKEMIA RESEARCH, 2002, 26 (09) :881-884
[4]   ACTIVATION OF HUMAN EOSINOPHILS BY PLATELET-DERIVED GROWTH-FACTOR [J].
BACH, MK ;
BRASHLER, JR ;
STOUT, BK ;
JOHNSON, HG ;
SANDERS, ME ;
LIN, AH ;
GORMAN, RR ;
BIENKOWSKI, MJ ;
ISHIZAKA, T .
INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY, 1992, 97 (02) :121-129
[5]  
Buchdunger E, 1996, CANCER RES, V56, P100
[6]  
Buchdunger E, 2000, J PHARMACOL EXP THER, V295, P139
[7]   HYPEREOSINOPHILIC SYNDROME - ANALYSIS OF 14 CASES WITH REVIEW OF LITERATURE [J].
CHUSID, MJ ;
DALE, DC ;
WEST, BC ;
WOLFF, SM .
MEDICINE, 1975, 54 (01) :1-27
[8]   Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells [J].
Druker, BJ ;
Tamura, S ;
Buchdunger, E ;
Ohno, S ;
Segal, GM ;
Fanning, S ;
Zimmermann, J ;
Lydon, NB .
NATURE MEDICINE, 1996, 2 (05) :561-566
[9]   Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. [J].
Druker, BJ ;
Talpaz, M ;
Resta, DJ ;
Peng, B ;
Buchdunger, E ;
Ford, JM ;
Lydon, NB ;
Kantarjian, H ;
Capdeville, R ;
Ohno-Jones, S ;
Sawyers, CL .
NEW ENGLAND JOURNAL OF MEDICINE, 2001, 344 (14) :1031-1037
[10]   THE IDIOPATHIC HYPEREOSINOPHILIC SYNDROME - CLINICAL, PATHOPHYSIOLOGIC, AND THERAPEUTIC CONSIDERATIONS [J].
FAUCI, AS ;
HARLEY, JB ;
ROBERTS, WC ;
FERRANS, VJ ;
GRALNICK, HR ;
BJORNSON, BH .
ANNALS OF INTERNAL MEDICINE, 1982, 97 (01) :78-92