Rare Presentation of Acute Liver Injury From Herpes Simplex Virus-1 Hepatitis and Concomitant Acetaminophen Toxicity in an Immunocompetent Patient

Abstract

Introduction: Herpes simplex virus-1 (HSV-1) is an established cause of acute liver injury (ALI) in immunocompromised patients; very rarely has it been described as a factor of ALI in an immunocompetent patient. While ALI offers a broad differential including blood flow, toxins, and viral etiologies; the evaluation often is deemed complete after establishing a single unifying diagnosis. Here, we present a case of ALI from HSV 1 in the background of acetaminophen toxicity in an immunocompetent patient. Case Report: Our patient was a 37-year-old female with no significant medical history, presented with 2-day history of malaise, mild nausea, and poor oral intake. Physical exam was remarkable for scleral icterus; no signs of encephalopathy. Vital signs were stable. Admission labs showed markedly elevated AST/ALT of 7147/6729, respectively, bilirubin was 3.8, and alkaline phosphatase was minimally elevated, suggesting marked hepatocellular insult. Initial INR was 6, Tylenol level 127. On presentation, the primary concern was related to Tylenol toxicity, and NAC therapy was initiated along with one dose of oral vitamin K. 24 hours later, liver functions worsened (AST/ALT: 11597/11032, Tbili 4.3, INR 7.7), ALI work-up was further pursued, including antibody and viral testing. In the mean time, empiric acyclovir therapy was started pending HSV test results, and arrangements were being made to transfer the patient to a liver transplant center. There was a suspicion for viral etiology due to the pattern of transaminases (AST >ALT). A day later, the labs started to trend down and transaminases began to improve. Eventually, the work-up was positive for HSV-1 IgG (>10.49) and IgM (1:40). ANA, AMA, anti-smooth muscle Ab, IGG subclass, Hep A-Ab, HepBsAg, Hep Bs Ab, Hep C Ab, LKMA were negative. The patient was observed in the hospital for 3 days more as the labs normalized and then discharged home on 2 weeks of acyclovir therapy. On follow-up exam, she had returned to baseline with no evident chronic liver disease. Conclusion: HSV 1 hepatitis is an extremely rare cause of acute liver injury in an immunocompetent patient. In a patient having acute liver injury, even in those with an apparently evident acetaminophen toxicity, it is important to look for other possible causes fulminant hepatitis and empirically start acyclovir therapy, especially when AST>ALT and LFTs worsen despite appropriate therapy on NAC. Strong consideration for liver biopsy should also be undertaken. It is also important to recognize that this patient did not have any signs of encephalopathy inspite of significant liver injury. This is an unusual presentation of acute liver injury from HSV 1 hepatitis along with concomitant Tylenol toxicity.