Frontiers in pharmacology · 2026
Corticosteroid-responsive portal lymphadenopathy mimicking malignant progression induced by furmonertinib in EGFR-mutated NSCLC: a case report.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Zhu Nengyang, Long Guo, Zhu Jing, Xu Weiguo, Wu Junhua, Xie Jiajun
Аннотация
BACKGROUND: Third-generation epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are widely used in the treatment of NSCLC with EGFR mutations due to their efficacy and favourable safety profile. However, drug-induced liver injury (DILI) associated with targeted therapy may occasionally present with atypical clinical and radiological features, posing diagnostic challenges. Here, we present a rare case of severe hepatotoxicity accompanied by pseudo-progressive portal lymphadenopathy that occurred following furmonertinib treatment.
CASE PRESENTATION: A 59-year-old female patient with EGFR-mutated NSCLC initiated treatment with the third-generation EGFR-TKI furmonertinib. Two months into the therapy, the patient developed jaundice and marked elevations in total bilirubin and transaminases. Extensive laboratory investigations excluded viral hepatitis and autoimmune liver diseases. Abdominal imaging revealed newly enlarged portal lymph nodes, mimicking malignant metastasis, but without clear evidence of hepatic metastasis or biliary obstruction. Furmonertinib was discontinued and systemic corticosteroid therapy was initiated. Within 2 weeks, liver function tests had improved significantly and follow-up imaging showed that the portal lymphadenopathy had regressed. Causality assessment using the RUCAMyielded a score of 9, indicating a highly probable drug-induced liver injury.
CONCLUSION: This case highlights that severe hepatotoxicity associated with furmonertinib may present with portal lymphadenopathy that mimics disease progression. Clinicians should remain vigilant for this atypical hepatotoxicity when using EGFR-TKIs and promptly assess portal lymph node status upon the emergence of jaundice or abnormal liver function. The implementation of early intervention strategies may facilitate recovery and help avoid misinterpretation of imaging findings.
CASE PRESENTATION: A 59-year-old female patient with EGFR-mutated NSCLC initiated treatment with the third-generation EGFR-TKI furmonertinib. Two months into the therapy, the patient developed jaundice and marked elevations in total bilirubin and transaminases. Extensive laboratory investigations excluded viral hepatitis and autoimmune liver diseases. Abdominal imaging revealed newly enlarged portal lymph nodes, mimicking malignant metastasis, but without clear evidence of hepatic metastasis or biliary obstruction. Furmonertinib was discontinued and systemic corticosteroid therapy was initiated. Within 2 weeks, liver function tests had improved significantly and follow-up imaging showed that the portal lymphadenopathy had regressed. Causality assessment using the RUCAMyielded a score of 9, indicating a highly probable drug-induced liver injury.
CONCLUSION: This case highlights that severe hepatotoxicity associated with furmonertinib may present with portal lymphadenopathy that mimics disease progression. Clinicians should remain vigilant for this atypical hepatotoxicity when using EGFR-TKIs and promptly assess portal lymph node status upon the emergence of jaundice or abnormal liver function. The implementation of early intervention strategies may facilitate recovery and help avoid misinterpretation of imaging findings.