Research on Liver Damage Caused by the Treatment of Rheumatoid Arthritis with Novel Biological Agents or Targeted Agents

Abstract

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by polyarticular, symmetric, and aggressive inflammation of the small joints in the hands and feet, resulting in dysfunction. With progress and development in medicine, treatment of RA is constantly evolving, making several drugs available for the treatment of RA. From the nonsteroidal anti-inflammatory drugs (NSAIDs) at the start of illness to glucocorticoids and then to conventional synthetic DMARDs (csDMARDs), biologic DMARDs (bDMARDs), and targeted synthetic DMARDs (tsDMARDs), therapeutic-use drugs for RA have been keeping pace with scientific research. However, various types of drugs have additional side effects when used over the long-term. New and emerging biological and targeted agents have been widely applied in recent years; however, the side effects have not been thoroughly investigated. In this paper, we review the research progress on liver damage caused by novel biological and targeted agents available for RA treatment. The aim is to provide a reference for rational clinical administration of such drugs.

Keywords: liver damage; novel biological agents; research progress; rheumatoid arthritis; targeted agents.

Figure 1

Biological and targeted agents in the treatment of rheumatoid arthritis. Antigen-presenting cells deliver their own antigens via major histocompatibility complexes to T cells, releasing lymphokines and activating macrophages to provide assistance to B cells. The latter may be induced to produce autoantibodies such as anti-citrullinated proteins. Autoantibodies are bound to the respective autoantigens and form immune complexes in the synovial membrane. These immune complexes bind to macrophages and other cells via Fc receptors and complement receptors, activating the secretion of pro-inflammatory cytokines and other inflammatory mediators like tumor necrosis factor, interleukins and macrophages via lymphokines, such as T-cell interferon or IL-17.