Does Imatinib Mesylate Therapy Cause Growth Hormone Deficiency?

被引:16
|
作者
Kebapcilar, L. [1 ]
Bilgir, O. [2 ]
Alacacioglu, I. [3 ]
Payzin, B. [3 ]
Bilgir, F.
Oner, P.
Sari, I.
Calan, M.
Binicier, O. [4 ]
机构
[1] Bozyaka Training & Res Hosp, Div Endocrinol & Metab, Dept Internal Med, TR-35340 Izmir, Turkey
[2] Bozyaka Training & Res Hosp, Div Hematol, TR-35340 Izmir, Turkey
[3] Ataturk Training & Res Hosp, Div Hematol, Dept Internal Med, Izmir, Turkey
[4] Dokuz Eylul Univ, Dept Internal Med, Izmir, Turkey
关键词
Imatinib mesylate; Growth hormone deficiency; Chronic myeloid leukemia; DIAGNOSIS; LEUKEMIA;
D O I
10.1159/000226288
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective: The purpose of this study was to determine whether or not imatinib mesylate therapy induces growth hormone deficiency (GHD). Subjects and Methods: Seventeen patients with chronic myloid leukemia (CML) were enrolled in the study. The glucagon stimulation test (GST), and standard deviation scores (SDSs) of insulin-like growth factor 1 (IGF-I) and insulin-like growth factor binding protein (IGFBP-3) were used to determine GHD. The L-dopa test was performed on those with IGF-I SDSs above the -1.8 cut-off level. Results: Of the 17 patients in the study, 12 (70%) had severe GHD (serum GH level <3 mu g/l after GST). IGF-I SDSs and IGFBP-3 SDSs were below -1.8 in 12 patients (70%) and below -0.9 in 10 subjects (58%). Four of the 5 remaining subjects with IGF-I SDS >-1.8 showed insufficient GH response to L-dopa stimulation. Nine subjects (52%) had both severe GHD based on GST response and IGF-I SDS below -1.8. If an IGF-I SDS cut-off value 1<-3 were used, 5 out of 17 subjects (30%) would be classified as GH deficient. These same patients also showed severe GHD based on GST response. Conclusions: The data showed that a large number of patients on imatinib mesylate therapy had GH deficiency. A study involving a larger number of patients with a matched control group is needed to confirm the present observations. Copyright (C) 2009 S. Karger AG, Basel
引用
收藏
页码:360 / 363
页数:4
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