Hepatotoxicity of epidermal growth factor receptor - tyrosine kinase inhibitors (EGFR-TKIs)

Area of Science:

• Oncology
• Hepatology
• Pharmacology

Background:

• Drug-induced liver injury (DILI) is a common adverse reaction.
• Cancer patients face increased liver dysfunction risk, complicating anticancer drug use.
• Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are crucial in treating solid tumors but can cause significant hepatotoxicity.

Purpose of the Study:

• To review the clinical features and incidence of hepatotoxicity associated with EGFR-TKIs.
• To explore recent advances in understanding the mechanisms of EGFR-TKI-induced liver injury.
• To discuss rechallenging and therapeutic strategies for managing EGFR-TKI hepatotoxicity.

Main Methods:

• Literature review of clinical studies and research on EGFR-TKI hepatotoxicity.
• Analysis of reported clinical features and incidence rates.
• Synthesis of current knowledge on mechanisms, clinical management, and treatment strategies.

Main Results:

• EGFR-TKIs are associated with increasing hepatotoxicity, limiting their clinical application.
• Mechanisms of liver injury are complex, with direct hepatocyte damage from DNA synthesis inhibition being one known factor.
• Specific mechanisms beyond direct toxicity remain largely unclear, and effective solutions are limited.

Conclusions:

• Hepatotoxicity is a critical challenge in EGFR-TKI therapy for cancer patients.
• Further research into the mechanisms of EGFR-TKI-induced liver injury is essential.
• Developing effective management and therapeutic strategies is crucial for safe clinical application.