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Is there any relationship between imatinib mesylate medication and hypothalamic-pituitary-adrenal axis dysfunction?
O Bilgir1, L Kebapcilar, F Bilgir
1Internal Medicine Department, Bozyaka Training and Research Hospital, Izmir, Turkey.
Imatinib mesylate treatment for chronic myelogenous leukemia (CML) is linked to subclinical glucocorticoid deficiency. This HPA axis dysfunction poses life-threatening risks during illness.
Area of Science:
- Endocrinology
- Hematology
- Pharmacology
Background:
- Imatinib mesylate is a tyrosine kinase (TK) inhibitor used for chronic myelogenous leukemia (CML).
- TK plays a crucial role in the hypothalamo-pituitary-adrenal (HPA) axis regulation.
- Potential impact of TK inhibitors on HPA axis function requires investigation.
Purpose of the Study:
- To evaluate the integrity of the HPA axis in patients undergoing imatinib therapy for CML.
- To determine the prevalence of HPA axis dysfunction in this patient cohort.
Main Methods:
- Utilized Glucagon Stimulation Test (GST) to assess adrenal response.
- Employed a low-dose (1 microg) ACTH Stimulation Test (LDSST) for HPA axis evaluation.
- Assessed 25 patients diagnosed with CML and treated with imatinib.
Main Results:
- 68% of patients exhibited an impaired peak cortisol response (cut-off 500 nmol/L) during GST.
- 48% of patients failed the LDSST, indicating HPA axis deficiency.
- The majority of deficient patients presented with partial glucocorticoid deficiency.
Conclusions:
- Subclinical glucocorticoid deficiency is prevalent in CML patients treated with imatinib.
- Untreated HPA axis dysfunction can become life-threatening under stress (e.g., illness).
- Routine HPA axis monitoring may be warranted for CML patients on imatinib therapy.
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