Author(s): Chung SJ, Kim JK, Park MC, Park YB, Lee SK
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Abstract OBJECTIVE: To investigate whether anti-tumor necrosis factor-alpha (TNF-alpha) 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-alpha therapy were reviewed retrospectively. Data on seropositivity of HBV, HBV load, and serum aminotransferases prior to and after initiation of anti-TNF-alpha 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-alpha therapy. Reactivation of hepatitis B occurred in 1 patient during the course of anti-TNF-alpha 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-alpha 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.
This article was published in J Rheumatol
and referenced in Journal of Antivirals & Antiretrovirals