Editor,—We read with great interest the paper of McCrudden et al concerning acute hepatitis E (HEV) in the UK ((2000) Gut 46:732–3; OpenUrlPubMedWeb of Science). We agree wholeheartedly with the authors that this form of hepatitis is on the increase in industrialised countries. In Italy, the reported prevalence of anti-HEV IgG positivity ranges from 0.74% to 1.94%,1 although a recent study found a prevalence of 2.6% in one small town in central Italy.2 A value of 1.5% has been reported for the general adult population of the Republic of San Marino.3

We have recently observed two cases of acute hepatitis E with no evidence of any known risk factors.

Case 1. In September 1997, a 45 year old Italian woman (not pregnant) was admitted with a one week history of fever (38°C), dark urine, and upper abdominal pain. The past medical history was unremarkable, and the patient denied recent travel abroad. There was no history of the use of drugs, alcohol, or herbal products that would justify a suspicion of toxic hepatitis.

Transaminase levels were elevated on admission and reached maximum levels approximately one week later (aspartate aminotransferase (AST) 1990 IU/l; alanine aminotransferase (ALT) 1626 IU/l). Eight days after admission total bilirubin was 280.44 μmol/l, direct bilirubin 210.33 μmol/l, alkaline phosphatase 469 IU/l, and lactate dehydrogenase 1011 IU/l. The patient was hepatitis A (HAV) IgG positive and negative for anti-HAV IgM, hepatitis C (HCV), hepatitis B (HBV), hepatitis G (HGV), cytomegalovirus (CMV), and Epstein-Barr virus (EBV) markers. Serum antinuclear, antismooth muscle, and antimitochondrial antibodies were absent. The patient was positive for anti-HEV IgG and negative for anti-HEV IgM.

On abdominal sonography the liver appeared mildly enlarged with no intra- or extrahepatic bile duct dilatation. One month later there was a significant increase in anti-HEV IgG, and serum transaminase levels began to drop. The patient was discharged, and six weeks later jaundice had disappeared and transaminases were within normal limits.

The patient has been followed for approximately three years, during which time she has remained asymptomatic with normal transaminases, bilirubin, alkaline phosphatase, and γ-glutamyl transpeptidase levels. Anti-HEV IgG titres have decreased but are still positive.

Case 2. A 60 year old housewife presented in our outpatient clinic with a one week history of jaundice, pale stools, and dark urine preceded by malaise, anorexia, and fever. On liver ultrasonography no bile stones or obstruction were found. She had no identifiable risk factors for liver disease, and no history of foreign travel, contact with infected individuals, or toxic exposure. She refused hospitalisation and was followed as an outpatient.

Transaminase levels were elevated (AST 1000 IU/l, ALT 2000 IU/l). Total bilirubin was 328.32 μmol/l, direct bilirubin 241.11 μmol/l, and alkaline phosphatase 450 IU/l. Markers for HAV, HCV, HBV, HGV, CMV, and EBV were negative; she was positive for anti-HEV IgM and negative for anti-HEV IgG. Three weeks later jaundice subsided and transaminases returned to near normal. Six weeks later she was anti-HEV IgG positive, and her liver function tests were normal.

As in the McCrudden series, neither of our two patients presented risk factors for HEV. The increased prevalence of this infection among haemodialysis patients in developed countries4 and the association observed in Italy between HEV and hepatitis C clearly show that the orofaecal route is not the only means of transmission.2 ,5 In light of the acute sporadic HEV cases reported in non-endemic countries with high hygienic standards, it is important that clinicians consider the possibility of HEV infection in patients with clinical and biochemical features of acute non-toxic hepatitis without evidence of exposure to the major hepatitis viruses, even if there are no known risk factors for HEV.