Rheumatoid arthritis (RA) is an autoimmune disease characterized by proliferative synovitis, which can cause cartilage and bone damage as well as functional limitations. Disease-modifying anti-rheumatic drugs have significantly improved the… Click to show full abstract
Rheumatoid arthritis (RA) is an autoimmune disease characterized by proliferative synovitis, which can cause cartilage and bone damage as well as functional limitations. Disease-modifying anti-rheumatic drugs have significantly improved the prognosis of RA patients. However, people with RA, when combined with hepatitis B virus (HBV) infection, may experience reactivation of HBV during treatment with anti-rheumatic drugs. The outcome of HBV reactivation (HBVr) varies from liver inflammation to liver failure, while insufficient HBV screening in RA patients has been reported in various countries. Therefore, it is necessary to identify patients at high risk before starting immunosuppressive therapy. The immune response plays an important role in anti-HBV infection. However, most anti-rheumatic drugs exert an inhibitory effect on the body’s immune system, resulting in HBVr. Therefore, it is necessary to conduct a comprehensive evaluation based on host factors, viral factors, and drug factors. In this paper, we summarize the mechanism of HBVr, the risk of HBVr caused by anti-rheumatic drugs, and the appropriate diagnosis and treatment process for RA patients so that clinicians can have a more comprehensive understanding of HBVr in RA patients.
               
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