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Imatinib/nilotinib Hyperbilirubinaemia and decreased platelet count: case report

A 24-year-old man developed decreased platelet count during treatment with imatinib, and hyperbilirubinemia during treatment with nilotinib for chronic myelogenous leukaemia [routes and duration of treatment to reaction onset not stated; not all outcomes stated]. The man, who was initially hospitalised due to complaints of abdominal pain, was diagnosed with chronic myelogenous leukaemia (CML). Subsequently, his treatment was started with imatinib tablets [Glivec; imatinib mesylate] 400 mg/day. During the treatment, he complained of leg ache [aetiology not stated]. Hence, the dose of imatinib was reduced by 1 tablet/day. Additionally, laboratory tests showed a rapid decrease in his platelet count from 231×109/L to 54×109/L in 20 days, which reached a level of 34×109/L. Consequently, the man’s dose of imatinib was reduced by two tablets, and was discontinued. One month after discontinuation of the imatinib therapy, increase in the BCR-ABL/ABL ratio was noted (indicative of CML). Hence, his treatment was started with nilotinib [Tasigna] 400mg twice a day. Liver function test performed before the initiation of nilotinib therapy showed normal total bilirubin (12.6 µmol/L). After 4 weeks of nilotinib treatment, the total bilirubin (TBIL) level increased to 91 µmol/L. Therefore, his nilotinib therapy dose was decreased to 300 mg/day. After the dose reduction, TBIL count reduced to 32 µmol/L, which was maintained at approximately 30–50 µmol/L for 1 month. However, analysis of BCR-ABL/ABL ratio indicated the lack of major molecular response in CML; therefore, the dose of nilotinib was readjusted to 400 mg/day. After 1 week, the TBIL level increased to 89 µmol/L. Additionally, increased level of indirect bilirubin was noted. The levels of ALT and the other liver functional indicators were noted to be normal. Subsequent liver histological analysis revealed no signs of liver damage. The nilotinib therapy was continued at the same dose of 400 mg/day for persistent molecular response, and the levels of TBIL and IBIL remained elevated. Genetic analysis showed a uridine diphosphate glucuronosyltransferase (UGT1A1) mutation. It was concluded that, he developed hyperbilirubinaemia due to inhibition of UGT1A1 activity by nilotinib. Based on the Naranjo adverse drug reaction probability score (score of 13), a causal relation between nilotinib and hyperbilirubinaemia was assessed as ’definite’. Tan Y, et al. Nilotinib-induced liver injury: A case report. Medicine 99: e22061, No. 36, 4 Sep 2020. Available from: URL: http://doi.org/10.1097/ MD.0000000000022061

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Reactions 17 Oct 2020 No. 1826