Vol.21 No.6

Original Article

Past hepatitis B virus infection in rheumatoid arthritis patients receiving biological and/or nonbiological disease-modifying antirheumatic drugs

Authors

Shunsuke Mori1

  • Clinical Research Center for Rheumatic Disease, Department of Rheumatology, NHO Kumamoto Saishunsou National Hospital, 2659 Suya, Kohshi, Kumamoto, 861-1196, Japan
Received:

25 February 2011

Accepted:

7 April 2011

Published online:

29 April 2011

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Abstract

To evaluate the prevalence of past infection with hepatitis B virus (HBV) in patients with rheumatoid arthritis (RA) and the incidence of its reactivation under treatment with biological and/or nonbiological diseasemodifying antirheumatic drugs (DMARDs), 239 patients receiving DMARD therapy were consecutively enrolled and tested for HBV-DNA, using a real-time polymerase chain reaction assay, HBV serology including hepatitis B surface antigen (HBsAg) and hepatitis B core antibody (anti-HBc), and serum levels of aminotransferase. Data prior to DMARD therapy and during follow-up were examined by reviewing medical records. Two patients (0.8%) were positive for HBsAg at the start of therapy. Sixty patients (25.1%) showed HBsAg-negative and anti-HBc-positive serology indicative of past HBV infection.
Among these 60 patients, 2 patients (3.3%) experienced
reactivation of viral replication (<2.1 log copies/ml) during DMARD therapy. One had been receiving tacrolimus,
prednisolone, and methotrexate (MTX); the other had been
treated with adalimumab, prednisolone, and MTX. Their
serum aminotransferase levels remained normal, and
HBsAg was negative. Ten weeks after reactivation of viral
replication had been noted, the HBV-DNA titer in the
former patient had increased to 2.9 log copies/ml, and
HBsAg and hepatitis B e antigen had become weakly
positive. In contrast, the latter patient had become negative
for viral DNA without any antiviral prophylaxis. In conclusion, the use of biological and nonbiological DMARDs
is relatively safe in most RA patients with past HBV
infection, even when no anti-HBV prophylaxis is administered.
Considering the high prevalence of past infection in
RA patients and the high cost of prophylaxis against HBV
reactivation, universal prophylaxis is impractical. Regular
monitoring of serum viral DNA seems to be the most
rational approach to preventing the development of clinically
apparent hepatitis.

Key words

Hepatitis B virus - Rheumatoid arthritis - Disease-modifying antirheumatic drugs - Occult infection - Reactivation