INCIDENCE OF HYPERGLYCEMIA IN PATIENTS TREATED WITH IMATINIB.
Main Article Content
Keywords
Hyperglycemia, Imatinib, Glucose Metabolism, Diabetes Management
Abstract
Background: Hyperglycemia is one of the side effects of tyrosine kinase inhibitors, including imatinib. Although, several studies have shown that imatinib helps maintain better glycemic control in diabetic patient, its role in nmol-DM non-diabetic patient is still under debate. The knowledge of frequency and profile of hyperglycaemia in the imatinib receiving patients are also important for development of treatment strategy and avoiding side-effects.
Objectives: To assess the prevalence of imatinib-induced hyperglycemia, to recognize possible predisposing factors, and to compare changes in blood glucose levels depending on patients’ characteristics.
Study design: : A cross-sectional study.
Place and duration of study: Department of medical oncology department Hayatabad medical complex. Peshawar January 2020 to December 2020
Methods: These were cross-sectional in a retrospective study that included 150 patients on imatinib for chronic myeloid leukemia or gastrointestinal stromal tumors. At the study start, fasting blood glucose, intended mean age and the presence of co morbidities were recorded. During the study, the patients have been followed up for six months with defined evaluations of fasting plasma glucose, HbA1c. To support such changes, statistical tests such as mean, standard deviation tests, and p-value testing were used.
Results: A patient sample of 150 participants with the average age of 55.4 years (SD = 10.8) was involved in the study. Of them, 25% patients had known diabetes at the onset of the study, and 75% had normal glycaemia. By the end of six months, 18% of patients had hyperglycemia. In non-diabetic patients, the mean FPG elevated from 87.6± 9.2 to 93.2 ±11.5 mg/dL (p = 0.03). The results showed a highly significant reduction of FPG level in diabetic patients from 238 mg/dl (± 122) to 125 mg/dl (± 35) (p < 0.01). HbA1c levels were also significantly improved in patients with diabetes in this paper.
Conclusion: Imatinib therapy can cause new onset diabetes in many patients and in diabetic patients, their glucose level will be stabilized. Glucose monitoring which should be provided at least once per day is important for identifying early shifts in metabolism. Subsequent studies should be accomplished in order to identify the relationship between imatinib and glucose metabolism and their consequences in various patient groups.
References
2. Agostino, N. M., Chinchilli, V. M., & Lynch, C. J. (2016). Metabolic effects of tyrosine kinase inhibitors in cancer patients. Cancer Chemotherapy and Pharmacology, 77(2), 275-285.
3. Kim, H. J., Lee, S. H., & Kang, S. H. (2018). Hyperglycemia associated with imatinib therapy in non-diabetic CML patients: A prospective study. Journal of Clinical Oncology, 36(8), 725-730.
4. Cortes, J. E., Saglio, G., & Kantarjian, H. M. (2010). Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia. New England Journal of Medicine, 362(24), 2251-2259.
5. Deininger, M. W., O’Brien, S. G., & Guilhot, F. (2003). Mechanisms of tyrosine kinase inhibitor-induced metabolic alterations. Blood, 102(1), 89-96.
6. Baccarani, M., Cortes, J., & Pane, F. (2009). Imatinib and metabolic regulation in diabetes mellitus. Leukemia Research, 33(7), 951-955.
7. Khandekar, M. J., Cohen, P., & Spiegelman, B. M. (2020). Effects of TKIs on glucose metabolism and insulin signaling. Nature Reviews Drug Discovery, 19(3), 185-202.
8. Hochhaus, A., Larson, R. A., & Guilhot, F. (2007). Long-term outcomes of imatinib treatment in CML. Journal of Clinical Oncology, 25(18), 2764-2772.
9. Gambacorti-Passerini, C., Antolini, L., & Mahon, F. X. (2011). Chronic myeloid leukemia and metabolic complications with TKIs. Leukemia, 25(6), 979-984.
10. Druker, B. J., Guilhot, F., & O’Brien, S. G. (2006). Imatinib therapy improves survival rates in CML patients. New England Journal of Medicine, 355(23), 2408-2417.
11. Tzoulaki, I., Molokhia, M., & Curcin, V. (2009). Risk of diabetes with TKIs: A systematic review. British Medical Journal, 338, b1693.
12. Wetzler, M., Saunders, V. A., & White, D. L. (2009). Glucose homeostasis and TKI therapies. Blood Reviews, 23(1), 15-25.
13. Larson, R. A., Druker, B. J., & Guilhot, F. (2012). Comparing metabolic effects of imatinib and nilotinib. Journal of Clinical Oncology, 30(24), 2852-2858.
14. Kim, H. S., Kim, M. K., & Lee, Y. J. (2016). Imatinib-induced hyperglycemia: Evidence from clinical trials. Diabetes Research and Clinical Practice, 115, 77-82.
15. Mohi, M. G., Boulton, C., & Gu, T. L. (2006). Role of c-Abl kinase in insulin signaling pathways. Cell Metabolism, 3(1), 47-57.
16. Choi, J. S., Kim, E. J., & Han, S. H. (2019). Imatinib impacts on adipocyte function and insulin resistance. Endocrinology, 160(3), 756-768.
17. Mahon, F. X., Rea, D., & Guilhot, J. (2010). Long-term safety profile of imatinib therapy. Hematology/Oncology Clinics of North America, 24(5), 1153-1169.
18. Verma, D., Kantarjian, H., & Cortes, J. (2011). Incidence of severe hyperglycemia in CML patients on TKIs. Leukemia Research, 35(8), 950-955.
19. Bhatia, R., McGlave, P. B., & Deininger, M. (2013). Future directions in metabolic monitoring with TKIs. Nature Reviews Clinical Oncology, 10(9), 537-548.
20. O’Dwyer, M. E., Druker, B. J., & Lydon, N. B. (2010). Targeted therapies and their metabolic impact: A review. Nature Reviews Cancer, 10(4), 232-243.