Case Presentation: A 39-year-old male with a history of seizure disorder, depression, and alcohol use disorder presented to the emergency room with new-onset jaundice and a two-week history of fatigue, decreased appetite, and dark orange urine. Social history notable for intermittent and progressive alcohol use starting at the age of 18, with most recent liquor use consisting of half of a 750mL bottle of liquor every other day. Upon arrival, he was hemodynamically stable, and lab findings showed a hemoglobin of 8.6 (normal: 13.0-17.0), total bilirubin of 20.3 (normal: 0.0-1.2), alkaline phosphatase of 140 (normal: 40-130), and AST of 85 (normal: 0-40). CT abdomen showed morphologic features consistent with cirrhosis. Patient was admitted following a new diagnosis of decompensated alcohol-related cirrhosis with hepatic encephalopathy. Infectious disease workup at admission included titers for HAV, HBV, HEV IgM, VZV, CMV, EBV, and HSV. On hospital day five, patient’s Maddrey score was determined to be 88, slightly worse than on admission, indicating a poor prognosis of his alcoholic hepatitis and prompting 40 mg prednisone daily for 7 days. On hospital day 6, hepatitis E IgM antibody returned as positive, suggestive of current or recent infection of HEV. Patient continued to improve with a course of prednisone and was discharged with out-patient follow up with hepatology.
Discussion: Typical high risk groups for HEV are pregnant women, infants, older people, immunocompromised individuals, patients with underlying chronic liver diseases, and workers that come into close contact with HEV-infected animals.(1) Though there are differences in prevalence of hepatitis E based on genotype, the most predominant genotype of hepatitis E, genotype 3, has a prevalence of 6% in the United States. (2) There is a greater seroprevalence amongst individuals born outside of the United States, suggesting that foreign acquired cases of HEV may contribute to estimated prevalence. There is also a higher prevalence among those living in the Midwest and in non-Hispanic white persons and that patients with alcohol-related liver disease have a higher likelihood of HEV infection. Certain studies have demonstrated that patients with alcoholic-related cirrhosis are fourteen times more likely than that of healthy patients, and three times higher than individuals with other causes of cirrhosis to contract HEV.(3) There is not a clear explanation as to why alcoholic cirrhosis predisposes to HEV seropositivity. Potential explanations include cirrhosis-related immune dysfunction leading to alterations in immunity and alcohol consumption inducing subclinical steatosis or fibrosis, making the liver immunologically susceptible. Other studies have analyzed how HEV infection contributes to a more rapid progression of chronic liver disease, negatively impacting overall mortality and prognosis of these patients.(4)
Conclusions: Patients with alcohol-related cirrhosis or other risk factors for HEV should be monitored more closely for seropositivity. The prevalence of HEV, particularly in patients with alcoholic cirrhosis, may be greater than previously thought in developed countries and contributing to a more rapid progression of cirrhosis-related mortality in patients with alcoholic-related cirrhosis. More studies are needed to determine the exact relationship between HEV and alcoholic cirrhosis, management of the comorbid conditions, and variations in prognosis and mortality.