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Long-term use of adalimumab in the treatment of rheumatic diseases - PubMed

  • ️Thu Jan 01 2009

Review

Long-term use of adalimumab in the treatment of rheumatic diseases

Charalampos Papagoras et al. Open Access Rheumatol. 2009.

Abstract

Adalimumab, a fully humanized monoclonal antibody against tumor necrosis factor-alpha (TNFα), has been evaluated in various randomized placebo-controlled trials in rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis and juvenile idiopathic arthritis. In the short time frame of these trials adalimumab has been shown to be effective in reducing disease activity, slowing radiographic disease progression and improving patients' quality of life, while at the same time demonstrating an acceptable safety profile. Furthermore, release of adalimumab on the market, prospective observational studies, as well as open-label extensions of the original double-blind trials have provided experience and data about the long-term efficacy and safety of the drug. Initial effectiveness, in terms of reducing disease activity, is sustained, while in most cases patients treated with adalimumab experienced a slower radiographic progression and consequently less disability and improved health-related quality-of-life outcomes. Moreover, long-standing treatment of thousands of patients with adalimumab outside the controlled context of clinical trials was not related to new safety signals, with the most common adverse events being respiratory infections. The most common serious adverse events seem to be tuberculosis reactivation, while a putative association with malignant lymphoma development is not yet proven. Besides, both of these adverse reactions pertain to the whole TNFα blocker group. In conclusion, adalimumab is a safe and effective option for the treatment of patients with rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis and juvenile idiopathic arthritis.

Keywords: adalimumab; ankylosing spondylitis; juvenile idiopathic arthritis; psoriatic arthritis; rheumatoid arthritis; tumor necrosis factor-alpha.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1

Putative pathways whereby adalimumab exerts its actions. Adalimumab binds to soluble TNFα trimers forming immune complexes (A) thus preventing sTNFα from binding to TNF receptor (TNFR). Alternatively it may bind to mTNFα expressed on cell surface preventing its own binding to TNFR (not shown); or it induces antibody-dependent cell-mediated cytotoxicity (ADCC) via binding to FcγR expressed on the surface of effector cells (B); moreover adalimumab may directly activate complement classical pathway inducing complement-dependent cytotoxicity (CDC), (C); finally, cross-linking of mTNFα may cause reverse signaling leading to cytokine suppression and/or cellular apoptosis (D).

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