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Research ArticleArticle

Reactivation of Hepatitis B Viral Infection in Inactive HBsAg Carriers Following Anti-Tumor Necrosis Factor-α Therapy

SOO-JIN CHUNG, JA KYUNG KIM, MIN-CHAN PARK, YONG-BEOM PARK and SOO-KON LEE
The Journal of Rheumatology November 2009, 36 (11) 2416-2420; DOI: https://doi.org/10.3899/jrheum.081324
SOO-JIN CHUNG
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JA KYUNG KIM
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MIN-CHAN PARK
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  • For correspondence: mcpark@yuhs.ac
YONG-BEOM PARK
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SOO-KON LEE
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  • Errata - January 01, 2010

Abstract

Objective. To investigate whether anti-tumor necrosis factor-α (TNF-α) therapy can influence the reactivation of hepatitis B virus (HBV) infection in inactive HBsAg carriers.

Methods. The medical records of 103 patients [59 with ankylosing spondylitis (AS), 41 with rheumatoid arthritis (RA), 2 with juvenile RA, and 1 with psoriatic arthritis] who had been treated with anti-TNF-α therapy were reviewed retrospectively. Data on seropositivity of HBV, HBV load, and serum aminotransferases prior to and after initiation of anti-TNF-α therapy were obtained.

Results. Eight patients were inactive HBsAg carriers, and all of them had normal liver function and undetectable HBV load prior to anti-TNF-α therapy. Reactivation of hepatitis B occurred in 1 patient during the course of anti-TNF-α therapy. After the third infusion of infliximab 5 mg/kg at Week 6, a blood test showed that the patient had normal liver function. When the patient returned for the fourth infusion of infliximab at Week 14, a blood test showed markedly elevated aspartate aminotransferase (AST)/alanine aminotransferase (ALT) levels (457 and 1054 IU/l, respectively) and increased viral DNA by HBV polymerase chain reaction (PCR). The fourth infliximab infusion was canceled, and entecavir 0.5 mg/day was prescribed. Then AST/ALT levels began to decrease and returned to normal range after 3 months. Followup HBV PCR showed negative results.

Conclusion. We found 1 HBV reactivation case among 8 inactive HBsAg carriers following anti-TNF-α therapy. This finding supports the prophylactic use of antiviral agents in HBV carriers, even if they have normal liver function or an undetectable viral load.

  • RHEUMATOID ARTHRITIS
  • ANKYLOSING SPONDYLITIS
  • HEPATITIS B VIRUS
  • ANTI-TUMOR NECROSIS FACTOR-α THERAPY
  • INACTIVE HBsAg CARRIERS

Footnotes

  • Supported by a faculty research grant from Yonsei University College of Medicine (6-2008-0130).

    • Accepted for publication June 22, 2009.
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The Journal of Rheumatology
Vol. 36, Issue 11
1 Nov 2009
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Reactivation of Hepatitis B Viral Infection in Inactive HBsAg Carriers Following Anti-Tumor Necrosis Factor-α Therapy
SOO-JIN CHUNG, JA KYUNG KIM, MIN-CHAN PARK, YONG-BEOM PARK, SOO-KON LEE
The Journal of Rheumatology Nov 2009, 36 (11) 2416-2420; DOI: 10.3899/jrheum.081324

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Reactivation of Hepatitis B Viral Infection in Inactive HBsAg Carriers Following Anti-Tumor Necrosis Factor-α Therapy
SOO-JIN CHUNG, JA KYUNG KIM, MIN-CHAN PARK, YONG-BEOM PARK, SOO-KON LEE
The Journal of Rheumatology Nov 2009, 36 (11) 2416-2420; DOI: 10.3899/jrheum.081324
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