When Treatment Turns Toxic: Acute Liver Failure Following Remdesivir Therapy
et al., American Journal of Respiratory and Critical Care Medicine, doi:10.1093/ajrccm/aamag162.5165, May 2026
Case report of a 90-year-old hospitalized patient showing acute liver failure following remdesivir treatment. The patient developed acute liver failure within 24 hours of receiving one dose of remdesivir, with AST >7000 U/L, ALT 4446 U/L, INR 13.9, lactate 4.7 mol/L, and hepatic encephalopathy. After discontinuation and initiation of N-acetylcysteine and prothrombin complex concentrate, liver function improved over 72 hours. Viral, autoimmune, and ischemic etiologies were excluded, and the temporal relationship supported drug-induced liver injury.
Gérard, Zhou, Wu, Kamo, Choi, Kim show increased risk of acute kidney injury, Leo, Briciu, Muntean, Petrov, Arch show increased risk of liver injury, Negru, Cheng, Mohammed, Kwok, Zhu show increased risk of cardiac disorders, and Kwok, Merches, Akinci, Tang, Bagheri show increased risk of mitochondrial toxicity with remdesivir.
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Tawfik et al., 1 May 2026, peer-reviewed, 3 authors.
Abstract: ## Abstract citation ID: aamag162.5165 C53-17 When Treatment Turns Toxic: Acute Liver Failure Following Remdesivir Therapy
J. A. Tawfik, F. De Leon, C. Hayward
Harbor-UCLA Medical Center, Torrance, CA, United States
Introduction: Acute liver failure (ALF) is the development of severe liver injury with hepatic encephalopathy and impaired synthetic function (INR ≥ 1.5) in a patient without prior liver disease. Drug-Induced liver Injury (DILI) is a leading cause of ALF. The diagnosis requires high index of suspicion. Remdesivir, a nucleotide analog widely used for COVID-19, is generally well tolerated but has been associated with hepatotoxicity, most often with mild transaminase elevations. We present a rare case of ALF attributed to remdesivir-induced DILI.
Case Presentation: A 90-year-old male with atrial fi brillation, heart failure with reduced ejection fraction, and chronic kidney disease presented with progressive shortness of breath and productive cough. Vitals were notable for mild tachycardia, with hypoxia necessitating 2L nasal cannula. Exam was remarkable for mild volume overload. Initial labs demonstrated normocytic anemia, thrombocytopenia, acute kidney injury, and normal liver function panel. COVID-19 was positive, and blood cultures later grew methicillin-resistant Staphylococcus Aureus (MRSA), presumably from a respiratory source, as imaging demonstrated a right lower lobe in fi ltrate. He was started on ceftriaxone, azithromycin, vancomycin, and remdesivir, receiving one dose. Of note, patient remained on his home apixaban. Within 24 hours, he developed acute liver failure with AST > 7000U/L, ALT 4446 U/L, INR 13.9, and lactate 4.7 mol/L. Patient also had waxing and waning mental status, concerning for hepatic encephalopathy. Imaging showed chronic hepatic steatosis without evidence of thrombus or obstructive pathology. A transthoracic echocardiogram was obtained and revealed worsening LVEF (now 10-20%), without valvular vegetations. Workup for viral, autoimmune, and ischemic etiologies was negative. Remdesivir was discontinued, and N-acetylcysteine (NAC) protocol was initiated. He received vitamin K and prothrombin complex concentrate (PCC) for coagulopathy. Apixaban was discontinued. Over the next 72 hours, his transaminases and INR improved (ALT down to 1793, INR to 3.1), and lactate normalized. He remained hemodynamically stable, afebrile, and on room air throughout. Blood cultures cleared within 48 hours, and vancomycin was continued for 14 days for MRSA bacteremia.
Discussion: This case highlights a rare but severe presentation of remdesivir-induced DILI in an elderly patient with multiple comorbidities. The temporal relationship between remdesivir administration and abrupt transaminitis, coagulopathy, and encephalopathy, with exclusion of other etiologies, supports the diagnosis. Prompt recognition, discontinuation of the offending agent, and supportive care with NAC and PCC led to clinical and biochemical improvement. Clinicians should remain vigilant for DILI in patients receiving remdesivir, especially those with underlying cardiac dysfunction and congestive hepatopathy.
This abstract is funded by: None
DOI record:
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"abstract": "<jats:title>Abstract</jats:title>\n <jats:sec>\n <jats:title>Introduction</jats:title>\n <jats:p>Acute liver failure (ALF) is the development of severe liver injury with hepatic encephalopathy and impaired synthetic function (INR ≥1.5) in a patient without prior liver disease. Drug-Induced liver Injury (DILI) is a leading cause of ALF. The diagnosis requires high index of suspicion. Remdesivir, a nucleotide analog widely used for COVID-19, is generally well tolerated but has been associated with hepatotoxicity, most often with mild transaminase elevations. We present a rare case of ALF attributed to remdesivir-induced DILI.</jats:p>\n </jats:sec>\n <jats:sec>\n <jats:title>Case Presentation</jats:title>\n <jats:p>A 90-year-old male with atrial fibrillation, heart failure with reduced ejection fraction, and chronic kidney disease presented with progressive shortness of breath and productive cough. Vitals were notable for mild tachycardia, with hypoxia necessitating 2L nasal cannula. Exam was remarkable for mild volume overload. Initial labs demonstrated normocytic anemia, thrombocytopenia, acute kidney injury, and normal liver function panel. COVID-19 was positive, and blood cultures later grew methicillin-resistant Staphylococcus Aureus (MRSA), presumably from a respiratory source, as imaging demonstrated a right lower lobe infiltrate. He was started on ceftriaxone, azithromycin, vancomycin, and remdesivir, receiving one dose. Of note, patient remained on his home apixaban. Within 24 hours, he developed acute liver failure with AST &gt;7000 U/L, ALT 4446 U/L, INR 13.9, and lactate 4.7 mol/L. Patient also had waxing and waning mental status, concerning for hepatic encephalopathy. Imaging showed chronic hepatic steatosis without evidence of thrombus or obstructive pathology. A transthoracic echocardiogram was obtained and revealed worsening LVEF (now 10-20%), without valvular vegetations. Workup for viral, autoimmune, and ischemic etiologies was negative. Remdesivir was discontinued, and N-acetylcysteine (NAC) protocol was initiated. He received vitamin K and prothrombin complex concentrate (PCC) for coagulopathy. Apixaban was discontinued. Over the next 72 hours, his transaminases and INR improved (ALT down to 1793, INR to 3.1), and lactate normalized. He remained hemodynamically stable, afebrile, and on room air throughout. Blood cultures cleared within 48 hours, and vancomycin was continued for 14 days for MRSA bacteremia.</jats:p>\n </jats:sec>\n <jats:sec>\n <jats:title>Discussion</jats:title>\n <jats:p>This case highlights a rare but severe presentation of remdesivir-induced DILI in an elderly patient with multiple comorbidities. The temporal relationship between remdesivir administration and abrupt transaminitis, coagulopathy, and encephalopathy, with exclusion of other etiologies, supports the diagnosis. Prompt recognition, discontinuation of the offending agent, and supportive care with NAC and PCC led to clinical and biochemical improvement. Clinicians should remain vigilant for DILI in patients receiving remdesivir, especially those with underlying cardiac dysfunction and congestive hepatopathy.</jats:p>\n <jats:p>This abstract is funded by: None</jats:p>\n </jats:sec>",
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Late treatment
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