S5936 Influenza A-Induced Acute Liver Injury: A Rare Adverse Effect

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 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 woman 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, acute kidney infection on chronic kidney disease, and positive PCR for IAV. Computed tomography 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 normal. Serum toxicology, acetaminophen and salicylate levels, viral/autoimmune hepatitis studies were also unremarkable. Serum carbamazepine level was <3.0. The patient’s liver function tests were trending downward and reached near-baseline levels after 1 week. With acute liver injury secondary to medications and other etiologies 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 acute liver failure. Given the potential for ALI, especially in severely ill patients, routine liver enzyme testing is recommended in the management of IAV infection.