Varicella Zoster Infection Causes Severe Autoimmune Hepatitis

Main Category: Liver Disease / Hepatitis
Also Included In: Eating Disorders;  Immune System / Vaccines;  Infectious Diseases / Bacteria / Viruses
Article Date: 04 Mar 2009 - 2:00 PDT

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Autoimmune hepatitis (AIH) is a chronic liver inflammation of unknown etiology that is characterized by the presence of circulatory autoantibodies and ongoing liver tissue damage. In the past few years, the understanding of this disease has grown, and it is believed that, in a genetically predisposed individual, certain agents such as drugs and viruses can trigger this process of self-induced liver damage.

Dr. Waleed K Al-Hamoudi from Saudi Arabia presented a case of severe AIH following varicella zoster infection in a 23-year-old man. This was published on February 28, 2009 in the World Journal of Gastroenterology.

A 23-year-old man was referred to their hepatology service on September 1, 2007 with jaundice, anorexia, weight loss and malaise of 2 mo duration. The episode of jaundice was preceded by varicella zoster virus (VZV) infection (chicken pox), which he contracted from close contact with infected family members. Despite recovery from the skin eruption, he had persistent anorexia and intermittent right upper quadrant pain. One month later he developed increasing jaundice. His physical examination revealed jaundice and hepatomegaly 2 cm below the costal margin. His initial laboratory findings were as follows: hemoglobin 149 g/L, white blood cell count 9.9 - 109/L, platelets 512 - 109/L, erythrocyte sedimentation rate 39 mm/h, alanine aminotransferase (ALT) 1066 U/L, aspartate aminotransferase (AST) 755 U/L, alkaline phosphatase (ALP) 185 U/L, total bilirubin 425 μmol/L, direct bilirubin 318 μmol/L, and albumin 32 g/L. His globulins were elevated at 46 g/L and his IgG was also elevated at 20.5 g/L. The coagulation profile was normal. Anti-nuclear, anti-smooth muscle, anti-mitochondrial and antiliver/kidney microsomes (ALKM-1) autoantibodies were negative. Perinuclear antineutrophil cytoplasmic antibodies were positive. Hepatitis B surface antigen, anti-hepatitis B core antigen IgM, anti-hepatitis C virus antibodies, anticytomegalovirus (CMV) IgM, anti-Epstein-Barr virus (EBV) IgM, and anti-hepatitis A virus (HAV) IgM were all negative. Anti-VZV IgG antibodies were positive. Ceruloplasmin and iron indices were normal.

The patient refused a liver biopsy, therefore, they started him on a tapering course of prednisone for presumed AIH, at a starting dose of 60 mg. He responded to that dramatically, as he became totally asymptomatic and started gaining weight. Within 2 mo of treatment, his liver enzymes normalized. On tapering his steroids below 10 mg, his liver enzymes increased again. His prednisone dose was increased to 30 mg and 50 mg azathioprine was added, however, because of vomiting and epigastric pain, the latter was changed to mycophenolate mofetil 500 mg twice daily. Follow-up showed improvement in his liver enzymes. In August, 2008, he stopped all his medications as he was feeling well and his liver enzymes were normal.

In conclusion, VZV infection can trigger AIH that may progress to advance liver fibrosis and eventually cirrhosis in genetically predisposed individuals. Therefore, AIH should be considered in any patient with persistently altered liver enzymes following a viral infection. Similarly, patients with AIH should be screened for viral hepatitis.

Notes:

Reference: Al-Hamoudi WK. Severe autoimmune hepatitis triggered by varicella zoster infection. World J Gastroenterol 2009; 15(8): 1004-1006 http://www.wjgnet.com/1007-9327/15/1004.asp

Correspondence to: Waleed K Al-Hamoudi, MD, Gastroenterology and Hepatology Unit (59), Department of Medicine, King Saud University, PO Box 2925, Riyadh 11461, Saudi Arabia.

About World Journal of Gastroenterology

World Journal of Gastroenterology (WJG), a leading international journal in gastroenterology and hepatology, has established a reputation for publishing first class research on esophageal cancer, gastric cancer, liver cancer, viral hepatitis, colorectal cancer, and H pylori infection and provides a forum for both clinicians and scientists. WJG has been indexed and abstracted in Current Contents/Clinical Medicine, Science Citation Index Expanded (also known as SciSearch) and Journal Citation Reports/Science Edition, Index Medicus, MEDLINE and PubMed, Chemical Abstracts, EMBASE/Excerpta Medica, Abstracts Journals, Nature Clinical Practice Gastroenterology and Hepatology, CAB Abstracts and Global Health. ISI JCR 2003-2000 IF: 3.318, 2.532, 1.445 and 0.993. WJG is a weekly journal published by WJG Press. The publication dates are the 7th, 14th, 21st, and 28th day of every month. WJG is supported by The National Natural Science Foundation of China, No. 30224801 and No. 30424812, and was founded with the name of China National Journal of New Gastroenterology on October 1, 1995, and renamed WJG on January 25, 1998.

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Source: Lai-Fu Li
World Journal of Gastroenterology