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Scholars Journal of Medical Case Reports | Volume-14 | Issue-02
Severe Reversible Conjugated Hyperbilirubinemia Induced by Ribociclib: A Transporter-Mediated Toxicity with Successful Switch to Palbociclib
Lamia Aalaoui, Sanaa Berrag, Rachid Tanz, Hassan Errihani
Published: Feb. 7, 2026 |
75
74
Pages: 198-201
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Abstract
Ribociclib, a cyclin-dependent kinase 4/6 (CDK4/6) inhibitor, is widely used as first-line therapy for hormone receptor–positive, HER2-negative metastatic breast cancer and is generally well tolerated. Hepatic adverse events are recognized, most commonly presenting as reversible elevations in serum transaminases. However, severe isolated hyperbilirubinemia, particularly with predominance of conjugated bilirubin and without associated cytolysis, remains exceptionally rare and poorly characterized. We report the case of a 56-year-old woman with a history of right-sided hormone receptor–positive, HER2-negative breast cancer who developed a histologically confirmed right adrenal metastasis and was treated with letrozole plus ribociclib. After three months of therapy, despite radiologic disease stability and biochemical response, the patient developed clinical jaundice with grade 4 hyperbilirubinemia reaching 150 µmol/L, predominantly conjugated, while liver transaminases and cholestatic enzymes remained within normal ranges. Extensive evaluation excluded infectious, autoimmune, hemolytic, and obstructive causes, and hepatobiliary imaging was unremarkable. Ribociclib was discontinued, resulting in progressive and complete normalization of bilirubin levels within two months. Following hepatic recovery, treatment was resumed with abemaciclib in combination with endocrine therapy, without recurrence of hepatotoxicity and with sustained disease control after nine months of follow-up. This case illustrates a rare and reversible pattern of ribociclib-associated hepatotoxicity, emphasizes the importance of bilirubin monitoring even in the absence of transaminase elevation, and supports the feasibility of switching to an alternative CDK4/6 inhibitor after resolution of hepatic toxicity.


