P6126 - Influenza A-Induced Acute Liver Injury: A Rare Adverse Effect

Sara Sadeghi, MD, Prasad Rajalingamgari, MD, Fahmida Hossain, BSc, Justin Wagner, DO, John Trillo, MD
NYC Health + Hospitals/South Brooklyn Health, Brooklyn, NY

Introduction: Influenza A virus (IAV) has extrapulmonary manifestations, such as acute liver injury (ALI) which is rare and under-documented. This under-recognition can delay diagnosis and management, increasing the risk of severe outcomes.
This case report highlights an unassuming presentation of IVA-induced ALI, emphasizing the importance of recognizing extrapulmonary manifestations of viral infections. Maintaining a high index of suspicion is crucial for timely diagnosis and intervention.

Case Description/

Methods: This is a case of a 65-year-old African-American female with significant comorbidities, presented with altered mental status and difficulty walking.
Labs were remarkable for elevated liver enzymes with predominantly hepatocellular pattern of liver injury, AKI on CKD, and positive PCR for IVA. CT head was negative for any acute pathology. The patient’s home medications include atorvastatin, carbamazepine, cyclobenzaprine, famotidine, fluoxetine, gabapentin, hydroxyzine, metformin, multivitamin, propranolol, senna, Seroquel, vitamin B1, Vivitrol. There had been no recent changes to the medications’ list or doses. A recent lab from one month ago showed no acute changes from the baseline.
The patient underwent an MRCP, which was noral. Serum toxicology, acetaminophen and salicylate levels, viral/autoimmune hepatitis studies were also unremarkable. Serum carbamazepine level was < 3.0. The patient’s LFTs were trending downward and reached near-baseline levels after one week. With acute liver injury secondary to medications and other ethologies ruled out, a diagnosis of IVA-induced hepatitis was made.

Discussion: Experimental studies showed that influenza caused ALI with hepatocellular pattern in mice. Systemic inflammation and epithelial barrier dysfunction, facilitates the spread of IAV to the liver, resulting in inflammation and damage. Additionally, oxidative stress causes mitochondrial dysfunction, which may subsequently impair liver fat metabolism.
Several clinical clues point towards IVA causality of ALI in our patient. Carbamazepine can cause elevated liver enzymes usually after 6 to 12 weeks of therapy, whereas our patient has been on carbamazepine for years with no recent changes in dose or frequency. Additionally, labs from a month ago showed liver enzymes to be at baseline. These findings along with the IVA infection point towards IAV-induced ALF.
Given the potential for ALI, especially in severely ill patients, routine liver enzyme testing is recommended in the management of IAV infection.

Disclosures:
Sara Sadeghi indicated no relevant financial relationships.
Prasad Rajalingamgari indicated no relevant financial relationships.
Fahmida Hossain indicated no relevant financial relationships.
Justin Wagner indicated no relevant financial relationships.
John Trillo indicated no relevant financial relationships.

Sara Sadeghi, MD, Prasad Rajalingamgari, MD, Fahmida Hossain, BSc, Justin Wagner, DO, John Trillo, MD. P6126 - Influenza A-Induced Acute Liver Injury: A Rare Adverse Effect, ACG 2025 Annual Scientific Meeting Abstracts. Phoenix, AZ: American College of Gastroenterology.