This report presents a case of a 52-year-old male patient diagnosed with light-chain(AL)cardiac amyloidosis complicated by acute heart failure(NYHA IV,HFrEF,LVEF 30%).Upon hospitalization,the patient was treated with tolvaptan(15 mg·d-1),spironolactone,empagliflozin,metoprolol succinate and other medications.Within 24 hours of tolvaptan initiation,the patient's alanine aminotransferase(ALT)rising sharply to 1,573 U·L-1 and aspartate aminotransferase(AST)peaking at 3,223 U·L-1.Additional abnormalities included elevated alkaline phosphatase(ALP),total bilirubin(TBil),direct bilirubin(DBil),and prolonged prothrombin time(PT),suggesting acute severe liver injury.Tolvaptan-induced drug-induced liver injury(DILI)was highly suspected.The physician promptly discontinued tolvaptan on day 3 of hepatic deterioration and initiated aggressive hepatoprotective therapy,including intravenous polyenylphosphatidylcholine and reduced glutathione.After about 2 weeks,the transaminases were essentially normalized.The RUCAM system categorized the causal relationship between tolvaptan and the observed DILI as"probable".This case underscores the potential for tolvaptan to provoke acute severe hepatotoxicity,emphasizing the need for heightened clinical vigilance particularly in high-risk populations with multisystem involvement,such as AL amyloidosis.Strict monitoring of liver function tests,especially during the early treatment phase,is strongly advised to mitigate this serious adverse effect.

This report presents a case of a 52-year-old male patient diagnosed with light-chain(AL)cardiac amyloidosis complicated by acute heart failure(NYHA IV,HFrEF,LVEF 30%).Upon hospitalization,the patient was treated with tolvaptan(15 mg·d-1),spironolactone,empagliflozin,metoprolol succinate and other medications.Within 24 hours of tolvaptan initiation,the patient's alanine aminotransferase(ALT)rising sharply to 1,573 U·L-1 and aspartate aminotransferase(AST)peaking at 3,223 U·L-1.Additional abnormalities included elevated alkaline phosphatase(ALP),total bilirubin(TBil),direct bilirubin(DBil),and prolonged prothrombin time(PT),suggesting acute severe liver injury.Tolvaptan-induced drug-induced liver injury(DILI)was highly suspected.The physician promptly discontinued tolvaptan on day 3 of hepatic deterioration and initiated aggressive hepatoprotective therapy,including intravenous polyenylphosphatidylcholine and reduced glutathione.After about 2 weeks,the transaminases were essentially normalized.The RUCAM system categorized the causal relationship between tolvaptan and the observed DILI as"probable".This case underscores the potential for tolvaptan to provoke acute severe hepatotoxicity,emphasizing the need for heightened clinical vigilance particularly in high-risk populations with multisystem involvement,such as AL amyloidosis.Strict monitoring of liver function tests,especially during the early treatment phase,is strongly advised to mitigate this serious adverse effect.