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

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 oil 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 amino-transferase (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. (First Release Oct 1 2009; J Rheumatol 2009;36:2416-20 doi: 10.3899/jrheum.081324)