S5706 A Rare Case of Acute Liver Injury Caused by Coinfection With Hepatitis A and Epstein-Barr Virus (EBV)

Introduction: EBV patients suffer from liver involvement ranging from mild inflammation to acute hepatitis. Hepatitis A Virus (HAV) patients can have a variable clinical presentation ranging from asymptomatic to fulminant liver failure. We report a rare case of severe acute liver injury in a patient with combined acute EBV and HAV. Case Description/Methods: A 64-year-old woman presented to urgent care with complaints of fatigue. Laboratory evaluation revealed markedly elevated liver enzymes: AST 2024 U/L (normal 0–32 U/L), alanine aminotransferase (ALT) 3,720 U/L (normal 0–33 U/L), total bilirubin 6.2 mg/dL (normal 0–1.3 mg/dL), and alkaline phosphatase 323 U/L (normal 35–104 U/L), and mildly elevated international normalized ratio of 1.4. ANA (<1:80) and anti-smooth muscle antibody (<1:20), were negative. Viral serologies were positive for Epstein-Barr virus Early Antigen IgG at 34.2 U/mL (normal 0–10.9), Viral Capsid Antigen (VCA) IgG >750 U/mL (normal 0–21.9), VCA IgM 67.2 U/mL (normal 0–43.9), and Nuclear Antigen IgG 144 U/mL (normal 0–22), suggesting recent or acute EBV infection. Hepatitis A virus (HAV) IgM was also positive, indicating acute HAV infection. Labs 5 days later showed significant improvement in AST to 411 U/L, ALT to 1425 U/L, and alkaline phosphatase 327 U/L although total bilirubin increased slightly to 7.1 mg/dL. Labs continuously improved to a total bilirubin down to 1.8 mg/dL, AST 136 U/L, ALT 318 U/L, and alkaline phosphatase 236 U/L. Her fatigue and jaundice improved. Discussion: The differential diagnosis of an increase in transaminases to ≥1000 IU/L includes ischemic hepatitis, acute viral hepatitis, and drug-induced liver injury. Hepatitis caused by EBV is common, mild, and self-limiting, although fulminant hepatic failure has been reported. Acute HAV infection is a self-limited illness; fulminant hepatic failure occurs in fewer than 1 percent of cases. Laboratory abnormalities in HAV include elevations of serum aminotransferases (often >1000 IU/dL), serum bilirubin (typically ≤10 mg/dL), and alkaline phosphatase (<400 U/L). This significant elevation in transaminases in our patient may have resulted from the combined effect of acute HAV and EBV infections, despite the patient’s relatively mild clinical symptoms. This pattern of acute liver injury, potentially driven by dual infection with HAV and EBV, should be considered in the differential diagnosis of patients presenting with marked transaminase elevations.

Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001150284.82089.df
Primary Topic
Hepatitis Viruses Studies and Epidemiology
Type
article
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article

S5706 A Rare Case of Acute Liver Injury Caused by Coinfection With Hepatitis A and Epstein-Barr Virus (EBV)

The American Journal of Gastroenterology
Hepatitis Viruses Studies and Epidemiology
article

S5706 A Rare Case of Acute Liver Injury Caused by Coinfection With Hepatitis A and Epstein-Barr Virus (EBV)

article en

Abstract

Introduction: EBV patients suffer from liver involvement ranging from mild inflammation to acute hepatitis. Hepatitis A Virus (HAV) patients can have a variable clinical presentation ranging from asymptomatic to fulminant liver failure. We report a rare case of severe acute liver injury in a patient with combined acute EBV and HAV. Case Description/Methods: A 64-year-old woman presented to urgent care with complaints of fatigue. Laboratory evaluation revealed markedly elevated liver enzymes: AST 2024 U/L (normal 0–32 U/L), alanine aminotransferase (ALT) 3,720 U/L (normal 0–33 U/L), total bilirubin 6.2 mg/dL (normal 0–1.3 mg/dL), and alkaline phosphatase 323 U/L (normal 35–104 U/L), and mildly elevated international normalized ratio of 1.4. ANA (<1:80) and anti-smooth muscle antibody (<1:20), were negative. Viral serologies were positive for Epstein-Barr virus Early Antigen IgG at 34.2 U/mL (normal 0–10.9), Viral Capsid Antigen (VCA) IgG >750 U/mL (normal 0–21.9), VCA IgM 67.2 U/mL (normal 0–43.9), and Nuclear Antigen IgG 144 U/mL (normal 0–22), suggesting recent or acute EBV infection. Hepatitis A virus (HAV) IgM was also positive, indicating acute HAV infection. Labs 5 days later showed significant improvement in AST to 411 U/L, ALT to 1425 U/L, and alkaline phosphatase 327 U/L although total bilirubin increased slightly to 7.1 mg/dL. Labs continuously improved to a total bilirubin down to 1.8 mg/dL, AST 136 U/L, ALT 318 U/L, and alkaline phosphatase 236 U/L. Her fatigue and jaundice improved. Discussion: The differential diagnosis of an increase in transaminases to ≥1000 IU/L includes ischemic hepatitis, acute viral hepatitis, and drug-induced liver injury. Hepatitis caused by EBV is common, mild, and self-limiting, although fulminant hepatic failure has been reported. Acute HAV infection is a self-limited illness; fulminant hepatic failure occurs in fewer than 1 percent of cases. Laboratory abnormalities in HAV include elevations of serum aminotransferases (often >1000 IU/dL), serum bilirubin (typically ≤10 mg/dL), and alkaline phosphatase (<400 U/L). This significant elevation in transaminases in our patient may have resulted from the combined effect of acute HAV and EBV infections, despite the patient’s relatively mild clinical symptoms. This pattern of acute liver injury, potentially driven by dual infection with HAV and EBV, should be considered in the differential diagnosis of patients presenting with marked transaminase elevations.

The American Journal of GastroenterologyVol. 120(10S2)
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Hepatitis Viruses Studies and Epidemiology
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