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Updated: Aug 10, 2025

Human Liver Microphysiological System for Assessing Drug-Induced Liver Toxicity In Vitro
Published on: January 31, 2022
Ribociclib-induced hepatotoxicity.
Muhammed Muhiddin Er1, Murat Araz1, Engin Hendem1
1Department of Medical Oncology, Necmettin Erbakan University School of Medicine, Konya, Turkey.
Switching from ribociclib to palbociclib successfully resolved persistent hepatotoxicity in a metastatic breast cancer patient. Palbociclib was well-tolerated at a full dose, demonstrating its potential as an alternative CDK4/6 inhibitor.
Area of Science:
- Oncology
- Pharmacology
- Clinical Medicine
Background:
- Cyclin-dependent kinase (CDK) 4/6 inhibitors are crucial in treating hormone receptor-positive, HER2-negative metastatic breast cancer.
- Ribociclib, a CDK4/6 inhibitor, has demonstrated efficacy but can be associated with adverse events, including hepatotoxicity.
- Management of treatment-related toxicities is essential for maintaining therapeutic continuity and patient outcomes.
Observation:
- A 71-year-old postmenopausal female with luminal metastatic breast cancer experienced persistent Grade 3 hepatotoxicity while on ribociclib therapy.
- The patient's ribociclib treatment was discontinued due to the severe liver toxicity.
- Palbociclib was initiated as a subsequent therapy to manage the metastatic breast cancer.
Findings:
- Upon switching to palbociclib, the patient's transaminase levels normalized, indicating resolution of hepatotoxicity.
- Palbociclib was administered at a full dose of 125 mg without inducing further toxicity.
- This suggests a potential for successful treatment escalation or substitution with palbociclib in cases of ribociclib-induced hepatotoxicity.
Implications:
- Palbocicpciclib can serve as a viable alternative for patients experiencing significant hepatotoxicity with ribociclib.
- Careful laboratory monitoring for neutropenia and transaminase elevation remains important even with palbociclib.
- This case highlights the importance of individualized treatment adjustments in CDK4/6 inhibitor therapy for metastatic breast cancer.
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