Published online Dec 28, 2021. doi: 10.13105/wjma.v9.i6.488
Peer-review started: December 29, 2020
First decision: October 11, 2021
Revised: October 14, 2021
Accepted: December 24, 2021
Article in press: December 24, 2021
Published online: December 28, 2021
Processing time: 364 Days and 3.5 Hours
Nilotinib is a specific breakpoint cluster region-Abelson leukemia virus-tyrosine kinase inhibitor that is used as an effective first- or second-line treatment in imatinib-resistant chronic myelogenous leukemia (CML) patients. Hepatotoxicity due to nilotinib is a commonly reported side effect; however, abnormal liver function test (LFT) results have been reported in asymptomatic cases. When alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels are more than five-fold the upper limit of the normal (ULN) or when the serum total bilirubin level is more than three-fold the ULN, dose modification or discontinuation of nilotinib is recommended, resulting in decreased levels of hematological indicators in certain patients with CML. Nilotinib-induced hyperbilirubinemia typically manifests as indirect bilirubinemia without elevated ALT or AST levels. Such abnormal liver functioning is thus not attributed to the presence of a true histologic lesion of the liver. The underlying mechanism may be related to the inhibition of uridine diphosphate glucuronosyltransferase activity. Therefore, nilotinib dose adjustment is not recommended for this type of hyperbilirubinemia, and in the absence of elevated liver enzyme levels or presence of abnormal LFT findings, physicians should consider maintaining nilotinib dose intensity without modifications.
Core Tip: Hepatotoxicity due to nilotinib is a commonly reported side effect; however, abnormal liver function test (LFT) results have been reported in asymptomatic cases. Nilotinib-induced hyperbilirubinemia manifests usually as indirect bilirubinemia without observation of elevated alanine aminotransferase or aspartate aminotransferase levels. The underlying mechanism may be related to the inhibition of uridine diphosphate glucuronosyltransferase activity. Therefore, in the absence of elevated levels of liver enzymes or presence of abnormal LFT findings, physicians should consider maintaining nilotinib dose intensity without modifications.