Clinical Significance of Transient Asymptomatic Elevations in Aminotransferase (TAEAT) in Oncology
- PMID: 35848749
- PMCID: PMC9311471
- DOI: 10.1097/COC.0000000000000932
Clinical Significance of Transient Asymptomatic Elevations in Aminotransferase (TAEAT) in Oncology
Abstract
Monitoring for liver injury remains an important aspect of drug safety assessment, including for oncotherapeutics. When present, drug-induced liver injury may limit the use or result in the discontinuation of these agents. Drug-induced liver injury can exhibit with a wide spectrum of clinical and biochemical manifestations, ranging from transient asymptomatic elevations in aminotransferases (TAEAT) to acute liver failure. Numerous oncotherapeutics have been associated with TAEAT, with published reports indicating a phenomenon in which patients may be asymptomatic without overt liver injury despite the presence of grade ≥3 aminotransferase elevations. In this review, we discuss the occurrence of TAEAT in the context of oncology clinical trials and clinical practice, as well as the clinical relevance of this phenomenon as an adverse event in response to oncotherapeutics and the related cellular and molecular mechanisms that may underlie its occurrence. We also identify several gaps in knowledge relevant to the diagnosis and the management of TAEAT in patients receiving oncotherapeutics, and identify areas warranting further study to enable the future development of consensus guidelines to support clinical decision-making.
Copyright © 2022 The Author(s). Published by Wolters Kluwer Health, Inc.
Conflict of interest statement
J.H.L. has no known competing financial interests or personal relationships, that could have appeared to influence the work reported in this paper. S.K.K. and C.D.B. are employed by and own stock in Amgen Inc. A.H.W. has served on advisory boards for Novartis, Janssen, Amgen, Roche, Pfizer, AbbVie, Servier, Celgene-BMS, Macrogenics, Agios, and Gilead; received research funding to his institution from Novartis, AbbVie, Servier, Celgene-BMS, Astra Zeneca, and Amgen; served on the speakers’ bureau for AbbVie, Novartis, and Celgene. M.S. served in a consulting or advisory role for Amgen, Celgene, Gilead Sciences, Janssen, Novartis, Pfizer, and Seattle Genetics; served on the speakers’ bureau for Amgen, Celgene, Gilead Sciences, Janssen, Novartis, and Pfizer; received travel, accommodations, and expenses from Amgen, Celgene, and Gilead Sciences; received research funding from Amgen, Celgene, Gilead Sciences, Miltenyi Biotec, MorphoSys, Novartis, and Seattle Genetics. The other authors declare no conflicts of interest.
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