Adverse drug reactions of imatinib in patients with chronic myeloid leukemia: A single-center surveillance study

Francis, Jose; Palaniappan, Muthiah; Dubashi, Biswajit; Pradhan, S.C.; Chandrasekaran, Adithan

doi:10.4103/0976-500x.149141

Cited by 10 publications

(8 citation statements)

References 14 publications

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“…Imatinib is a tyrosine kinase inhibitor clinically applied against leukemia and metastatic gastrointestinal stromal tumors (Cismowski, 2007a). Nausea, vomiting, abdominal pain, and elevated serum transaminase level are associated with imatinib therapy (Cismowski, 2007a; Francis et al., 2015; Cross et al., 2006; Tonyali et al., 2010). On the other hand, nephrotoxicity and acute renal failure might accompany imatinib administration (Cismowski, 2007a).…”

Section: Introductionmentioning

confidence: 99%

The potential role of mitochondrial impairment in the pathogenesis of imatinib-induced renal injury

Emadi

Abdoli

Ghanbarinejad

et al. 2019

Heliyon

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Imatinib is a tyrosine kinase inhibitor widely administered against chronic myeloid leukemia. On the other hand, drug-induced kidney proximal tubular injury, electrolytes disturbances, and renal failure is a clinical complication associated with imatinib therapy. There is no precise cellular mechanism(s) for imatinib-induced renal injury. The current investigation aimed to evaluate the role of mitochondrial dysfunction and oxidative stress in the pathogenesis of imatinib nephrotoxicity. Rats received imatinib (50 and 100 mg/kg, oral, 14 consecutive days). Serum and urine biomarkers of renal injury and markers of oxidative stress in the kidney tissue were assessed. Moreover, kidney mitochondria were isolated, and mitochondrial indices, including mitochondrial depolarization, dehydrogenases activity, mitochondrial permeabilization, lipid peroxidation (LPO), mitochondrial glutathione levels, and ATP content were determined. A significant increase in serum (Creatinine; Cr and blood urea nitrogen; BUN) and urine (Glucose, protein, gamma-glutamyl transferase; γ-GT, and alkaline phosphatase; ALP) biomarkers of renal injury, as well as serum electrolytes disturbances (hypokalemia and hypophosphatemia), were evident in imatinib-treated animals. On the other hand, imatinib (100 mg/kg) caused an increase in kidney ROS and LPO. Renal tubular interstitial nephritis, tissue necrosis, and atrophy were evident as tissue histopathological changes in imatinib-treated rats. Mitochondrial parameters were also adversely affected by imatinib administration. These data represent mitochondrial impairment, renal tissue energy crisis, and oxidative stress as possible mechanisms involved in the pathogenesis of imatinib-induced renal injury and serum electrolytes disturbances.

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Section: Introductionmentioning

confidence: 99%

The potential role of mitochondrial impairment in the pathogenesis of imatinib-induced renal injury

Emadi

Abdoli

Ghanbarinejad

et al. 2019

Heliyon

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“…Imatinib is associated with mild to moderate toxicity, mostly reversible by dose reduction or discontinuation of the drug. In a study by Francis J et al ,[ 18 ] it was observed that thrombocytopenia was the most common adverse effect with a percentage occurrence of 57.9%, which is midway between the frequency reports in earlier Indian studies (17.5%–98.0%). Whereas, it was observed that maximum number of patients (46%) was having no side effects of Imatinib therapy; 23% patients suffered from edema, 12% from rashes, 9% with asthenia, 6% hyper pigmentation, 3% hypo pigmentation and 1% with pleural effusion.…”

Section: Discussionmentioning

confidence: 69%

Clinical spectrum and treatment response in patient of chronic myeloid leukemia in correlation with ABO blood group

Bharti

Meher

Gupta

et al. 2022

Journal of Family Medicine and Primary Care

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Background: Several studies have been conducted to evaluate and investigate the molecular mechanisms underlying alterations in ABO blood group antigens in oncogenesis. We observed that no study has been reported yet that correlate cytological, molecular and haematological responses of Imatinib therapy in chronic myeloid leukemia (CML) patients with different types of blood groups. Objective: To determine the distribution of CML in the ABO blood group, clinical spectrum of CML in different blood groups, and treatment response of CML patients in correlation with ABO and Rh blood groups. Material and Methods: All the patients included in the study were diagnosed on the basis of clinical features, peripheral smears and bone marrow aspiration findings. Real-time reverse transcriptase polymerase chain reaction (PCR) and cytogenetic analysis were done in all patients at the time of initiation of therapy. Blood grouping and Rh typing of each patient were done at the initiation of therapy. Results: Out of 100 included patients, 58 were male and 42 were female patients. It was observed that 45 (45%) patients were having a B+ blood group; 33% patients were having O+ blood group, followed by A+ (10%), AB+ (8%), A− (2%), B− (1%) and AB− (1%). Around 43.64% study subjects with O + blood groups showed complete cytogenetic response, followed by B+ (41.82%), A+ (10.91), A− (1.82) and AB+ (1.82). An equal number of patients (40% each) with O+ and B+ blood groups, followed by A+ (20%) showed undetectable Abelson-breakpoint cluster region (BCR-ABL)/ratio (%). About 75% of patients showed complete haematological response (CHR) and 25% showed PHR. Patients with B+ and O+ blood groups (41.33%) showed a CHR. It was observed that a maximum number of patients were suffering from symptoms of an abdominal mass (37%), 43.24% of patients with B+ blood group showed an abdominal mass, followed by O+ (35.13%), A+ and AB+ (8.11% each), B − and AB− (2.70% each). Conclusion: This study revealed that study subjects with B+ and O+ blood groups showed better cytogenetic, molecular and haematological responses as compared with patients with other blood groups at 6 and 12 months of treatment with Imatinib.

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“…Imatinib can cause side effects including weight gain, fatigue (Jabbour & Kantarjian, 2020), bone and muscle pain, as well as increased creatinine. A study conducted by Francis et al reported that 68% of CML patients treated with Imatinib experienced various side effects, especially hematological toxicity-thrombocytopenia as much as 21% (Francis et al, 2015).…”

Section: Resultsmentioning

confidence: 99%

Differences In Hematology And Bcr-Abl Molecular Profiles In Patients With Chronic Myeloid Leukemia Undergoing Tyrosine Kinase Inhibitor Therapy

Santosa

Shidqi

Muslim³

et al. 2022

Med.Lab.Tech.J.

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Chronic myeloid leukemia (CML) is a myeloproliferative malignancy due to the formation of the BCR-ABL fusion gene in chronic myeloid leukemia. This condition causes excessive cell proliferation, resulting in an increase in the number of leukocytes. Tyrosine Kinase Inhibitor (TKI) is a first-line therapy that helps reduce the percentage of the BCR-ABL fusion gene in patients with chronic myeloid leukemia. This study was conducted to determine differences in the hematological profiles (hemoglobin levels, leukocyte counts, platelet counts) and molecular BCR-ABL in patients with chronic myeloid leukemia before and after 12 months of tyrosine kinase inhibitors therapy. This analytic observational study was administered using a cross-sectional design to in analyzing the medical records of CML patients who underwent TKI therapy at the Sub Specialist Polyclinic of Internal Medicine Hematology Oncology Ulin Banjarmasin Regional Hospital from March 2021-April 2022. Dependent T-test and McNemar's test were performed in data analysis which results showed that 12 month tyrosine kinase inhibitor therapy could increase the hemoglobin levels, decrease leukocyte counts, platelet counts as well as decreasing the percentage of BCR-ABL gene fusion in patients with chronic myeloid leukemia. In conclusion, significant differences were found in the hematological profiles (p<0.001) and the molecular BCR-ABL (p<0.001) before and after 12 months of tyrosine kinase inhibitor therapy

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Adverse drug reactions of imatinib in patients with chronic myeloid leukemia: A single-center surveillance study

Cited by 10 publications

References 14 publications

The potential role of mitochondrial impairment in the pathogenesis of imatinib-induced renal injury

The potential role of mitochondrial impairment in the pathogenesis of imatinib-induced renal injury

Clinical spectrum and treatment response in patient of chronic myeloid leukemia in correlation with ABO blood group

Differences In Hematology And Bcr-Abl Molecular Profiles In Patients With Chronic Myeloid Leukemia Undergoing Tyrosine Kinase Inhibitor Therapy

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