Objective: The purpose of this study was to determinewhether 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 fac- tor 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 μg/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 l<–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.
Our results indicate an increased prevalence of subclinical glucocorticoid deficiency in patients receiving imatinib mesylate for CML. Therefore under stressed conditions, such as intercurrent illness state, overt and untreated partial glucocorticoid deficiency in CML patients become life threatening.
In the present study, rats were administered acetylsalicylic acid (ASA), at low
and high doses, by means of a gastric tube for 30 days. Chronic administration of a high dose
of ASA (200 mg/kg body weight) resulted in a significant increase in liver plasma membrane
γ-glutamyl transpeptidase activity, cholesterol, and phospholipid levels. The enzymatic
activity and lipid levels appeared not to be affected by ASA when given at a lower dose
(50 mg/kg body weight). The changes in the enzymatic activity of plasma membrane were
positively correlated to membrane cholesterol content. These findings suggest that the hepatotoxicity
of high doses of ASA should not be overlooked during clinical use of the drug.
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