Tumor lysis syndrome soon after treatment with hydroxyurea followed by nilotinib in two patients with chronic-phase chronic myelogenous leukemia

Jiang, Hua; Iwaki, Yasunobu; Inoue, Morihiro; Hagihara, Masao

doi:10.1007/s12185-013-1356-2

Cited by 11 publications

(10 citation statements)

References 16 publications

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“…Renal dysfunction has been reported with other TKIs, including imatinib, [6][7][8][9][10]14,[34][35][36] nilotinib, [37][38][39] and dasatinib, 6,9,[11][12][13][14][40][41][42][43] suggesting a possible drug class effect. This is supported by the similar frequency and characteristics of renal decline observed with imatinib and bosutinib treatment in our analyses.…”

Section: Discussionmentioning

confidence: 97%

Effects of Bosutinib Treatment on Renal Function in Patients With Philadelphia Chromosome-Positive Leukemias

Cortes

Gambacorti‐Passerini

Kim

et al. 2017

Clinical Lymphoma Myeloma and Leukemia

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Section: Discussionmentioning

confidence: 97%

Effects of Bosutinib Treatment on Renal Function in Patients With Philadelphia Chromosome-Positive Leukemias

Cortes

Gambacorti‐Passerini

Kim

et al. 2017

Clinical Lymphoma Myeloma and Leukemia

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“…The elderly patient in our center did not experience AKI during the rst year of Imatinib treatment but developed AKI with estimated glomerular ltration rate of 16.14ml/min two years after Nilotinib administration. In 2013, Jin (15) reported Nilotinib-related AKI, which was caused by tumor lysis syndrome (TLS). TLS is characterized by abnormal metabolism and usually occurred at the initial anti-tumor treatment.…”

Section: Discussionmentioning

confidence: 99%

Late Occurrence of Hyperbilirubinemia and Renal Dysfunction During Nilotinib Treatment for an Elderly Chronic Myeloid Leukemia: A Case Report

Huang¹,

Lian²,

Zhu³

et al. 2021

Preprint

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Background: Compared with the first-generation tyrosine kinase inhibitor (TKI), Nilotinib exhibited potent inhibition for BCR-ABL kinase activity, approved of the first-line and second-line TKI treatment of CML patients. Nilotinib was generally well tolerated with mild hematologic and non-hematologic adverse events. Hyperbilirubinemia, the most common non-hematologic adverse events, was confirmed presented mostly with grade I-II, rarely with grade III-IV in several large-scale clinical trails and real-world treatment. Case presentation: we report a rare case of elderly CML with severe bilirubin and creatinine elevation after receiving Nilotinib as second-line treatment for 2 years. After TKI suspension, hepatic and renal function improved quickly, but degree IV bone marrow suppression persisted for rather a long time. Monosomy 7 clone was detected at the point when renal dysfunction occurred, which indicated disease progression to accelerated phase. When Imatinib and Dasatinib were administrated alternately, a large area of acute cerebral infarction occurred unexpectedly after blood cell count recovered. So far, Imatinib treatment was continued, the patient is still stable state at the 6 months follow up.Conclusions: The report alerted clinicians to obsereve the incidence of adverse events during long-term TKIs therapy. Also, clinicans might consider the occurrence of monosomy clone when faced with poor efficacy or intolerance.

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“…In this case, the elevated TBIL level obviously improved through dose adjustment at the beginning of the TBIL level elevation, which also affected the response of the Bcr-Abl/Abl IS ratio. Hua et al [ 17 ] reported that a 44-year-old man with CML developed metabolic acidosis within 10 hours of nilotinib administration, which rapidly progressed to multiorgan and hepatic failure (bilirubin, 4.4 mg/dL; ALT, 1031 U/L). Furthermore, the autopsy showed massive liver necrosis.…”

Section: Discussionmentioning

confidence: 99%

Nilotinib-induced liver injury

Ya¹,

Ye²,

Zhou³

2020

Medicine

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Introduction: Nilotinib is a selective inhibitor of the BCR-ABL tyrosine kinase receptor and is used in the management of chronic myelogenous leukemia (CML). Nilotinib therapy at high doses is associated with elevated serum bilirubin levels. If the serum bilirubin level exceeds 3 times the upper limit of normal, the recommendation is to either adjust nilotinib dosage or temporarily discontinue the treatment. However, it is unclear whether hyperbilirubinemia indicates obvious liver histology damage. Patient concerns: A 24-year-old man with confirmed CML was treated with nilotinib therapy and developed hyperbilirubinemia after the treatment. Although the first remission of the hyperbilirubinemia was achieved after dose adjustment, the hematological parameters deteriorated. Thus, we initiated an antineoplastic therapy (at the standard dose) until complete remission of the CML was achieved. The pathogenic mechanism of hyperbilirubinemia may be related to the inhibition of uridine diphosphate-glucuronosyltransferase (UGT1A1) activity. Liver histological analysis revealed no significant liver damage. In addition, the patient had no family history of hyperbilirubinemia and liver disease. Diagnosis: The patient was admitted to our hospital under the diagnosis of hyperbilirubinemia, and histopathology by liver biopsy showed no obvious damage. We also detected a UGT1A1 mutation [ex1 c.686C > A (p.Pro229Gln)] in the patient and his mother. Interventions: When the nilotinib dose was decreased to 300 mg daily, the total bilirubin (TBIL) level decreased to 30 to 50 μmol/L for 1 month. However, because the Bcr-Abl/Abl IS ratio did not correspond to the major molecular response (MMR; <0.1%), the nilotinib dose was readjusted to 400 mg daily. One week later, the TBIL and indirect bilirubin levels increased to 89 and 79 μmol/L, respectively. The levels of alanine transaminase and other liver functional indicators were normal. Outcomes: A Naranjo Adverse Drug Reaction (ADR) Probability Scale score of 13 indicates that hyperbilirubinemia is attributed to ADR caused by nilotinib rather than by drug-induced liver injury. Conclusion: Although reducing the nilotinib dose can alleviate the occurrence of hyperbilirubinemia, the effect of MMR is also reduced. Treatment of CML without dose adjustment or discontinuation of nilotinib therapy may be more advantageous.

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Tumor lysis syndrome soon after treatment with hydroxyurea followed by nilotinib in two patients with chronic-phase chronic myelogenous leukemia

Cited by 11 publications

References 16 publications

Effects of Bosutinib Treatment on Renal Function in Patients With Philadelphia Chromosome-Positive Leukemias

Effects of Bosutinib Treatment on Renal Function in Patients With Philadelphia Chromosome-Positive Leukemias

Late Occurrence of Hyperbilirubinemia and Renal Dysfunction During Nilotinib Treatment for an Elderly Chronic Myeloid Leukemia: A Case Report

Nilotinib-induced liver injury

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