Laurence Ollier, MD; Nathalie Tieulie, MD; Frédérick Sanderson, MD; Philippe Heudier, MD; Valérie Giordanengo, MD, PhD; Jean-Gabriel Fuzibet, MD, PhD; Elisabeth Nicand, MD
Acknowledgment: The authors thank the personnel of the Laboratoire d'Anatomie-Pathologique du CHU de Nice for technical assistance and Dr. Fanny Vandebos for examination of the liver biopsy.
Potential Financial Conflicts of Interest: None disclosed.
Ollier L., Tieulie N., Sanderson F., Heudier P., Giordanengo V., Fuzibet J., Nicand E.; Chronic Hepatitis After Hepatitis E Virus Infection in a Patient With Non-Hodgkin Lymphoma Taking Rituximab. Ann Intern Med. 2009;150:430-431. doi: 10.7326/0003-4819-150-6-200903170-00026
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Published: Ann Intern Med. 2009;150(6):430-431.
Background: Hepatitis E virus (HEV) is endemic in developing countries, and infection typically causes acute hepatitis.
Objective: To report a case of chronic hepatitis after HEV infection in a man receiving rituximab for non-Hodgkin lymphoma.
Case Report: In August 2007, a 77-year-old man with low-grade non-Hodgkin lymphoma presented with jaundice after a few days of gastrointestinal pain. He had been receiving bimonthly rituximab for 1 year after several years of treatment with sequential chlorambucil and fludarabine. Laboratory tests showed increased levels of alanine aminotransferase and aspartate aminotransferase (more than 30-fold), γ-glutamyltransferase, bilirubin, and alkaline phosphatase. Abdominal ultrasonography excluded biliary tract complications and showed normal liver parenchyma. Test results for hepatitis B and C virus infection were negative, and hepatitis A, cytomegalovirus, and Epstein–Barr virus serologies were in accordance with past immunization. The patient's history excluded toxic and drug-related causes of elevated liver enzyme levels, and testing for other infectious causes (legionellosis, rickettsiosis, Lyme disease, leptospirosis) and autoimmune causes (antinuclear autoantibodies, anti–smooth-muscle cell antibodies, antimitochondrial antibodies, anti–liver-kidney microsomal antibodies) was negative. The patient had no clinical risk factors for nonalcoholic steatohepatitis, such as overweight, diabetes, or dyslipidemia. We did not test for α1-antitrypsin deficiency.
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