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Autoimmune Pitfalls of Anti- TNFα Therapy Illustrated by a Case Report

Biological therapy refers to the use of medication tailored to specifically target an immune or genetic mediator of disease. It has revolutionized the treatment of chronic inflammatory diseases, such as rheumatoid arthritis (RA), ankylosing spondylitis (AS), psoriatic arthritis (PsA) and inflammatory bowel diseases (IBD) [1, 2]. Most medications are directed against tumor necrosis factor-alpha (TNFα) (infliximab, adalimumab, etanercept, golimumab, certolizumab pegol) and others against interleukin (IL)-1 (anakinra), IL-6 (tocilizumab), CD20 (rituximab), and CD28- CD80/86-mediated T cell co-stimulation (abatacept). The most extensive clinical experience was gathered from treating RA patients with anti-TNF agents. Since their introduction in 1998, over a million patients have been treated. However, increasing clinical data warn us of the potential dangers of disabling TNF-mediated immunological signaling – namely, increased incidence of infections, solid and hematological tumors, demyelinizing disease, cardiovascular incidents, and induction of autoimmunity [1, 2]. Induction of autoantibodies (antinuclear antibody, anti-dsDNA) under biological therapy iswell recognized: elevated titers were found in 11–13% of patients treated with etanercept and 3–98% treated with infliximab, depending on the indication and type of antibodies determined [1, 3]. Most of these patients had no clinical manifestations, but some of them developed autoimmune syndromes: vasculitis, systemic lupus erythematosus (SLE), interstitial lung disease, inflammatory myopathies, antiphospholipid syndrome, etc.

anti-tumor necrosis factor (anti-TNF), drug-induced lupus, etanercept, autoimmunity, antibody

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