Adalimumab: 8 Years of Experience in Rheumatoid Arthritis
Adalimumab: 8 Years of Experience in Rheumatoid Arthritis
TNF-α is one of the inflammatory cytokines induced by RA, and is found in a high concentration in the synovial joints. It works by binding to two types of receptors (p55 and p75), and has the ability to induce other inflammatory cytokines, thereby perpetuating the inflammation cascade and resulting in joint damage. Blocking TNF-α significantly reduces such inflammation and suppresses the formation of invasive pannus. TNF-α inhibitors were introduced as a therapeutic option for RA in 1998, and currently remain the most commonly used BRM. There are five TNF-α inhibitors now licensed (Table 1) with some differences in their structure, function and administration routes. Studies have shown that they are all highly effective in reducing joint damage and disability, and improving quality of life, especially when combined with methotrexate. While TNF-α inhibitors, like the other BRMs, are mostly used when patients with active RA do not have a satisfactory response to traditional DMARDs, they can also be chosen as first-line therapy in severe cases or when traditional DMARDs are contraindicated. Adalimumab was the third TNF-α inhibitor to be introduced, and the first fully human monoclonal antibody of the group. It is currently widely used across the world for the treatment of RA. Adalimumab is also approved by the US FDA and the EMA for the treatment of ankylosing spondylitis, psoriatic arthritis, juvenile idiopathic arthritis and Crohn's disease.
To retrieve the evidence for this review, the authors searched MEDLINE (through PubMed) to identify relevant citations published in English or Spanish. Medical terms related to 'adalimumab' were combined using 'AND' with those related to 'rheumatoid arthritis'. Of 1218 potentially relevant citations, 14 publications reporting on controlled trials, 12 open-label extensions, 38 registry studies and 40 systematic reviews were summarized.
Adalimumab: A TNF-α Inhibitor
TNF-α is one of the inflammatory cytokines induced by RA, and is found in a high concentration in the synovial joints. It works by binding to two types of receptors (p55 and p75), and has the ability to induce other inflammatory cytokines, thereby perpetuating the inflammation cascade and resulting in joint damage. Blocking TNF-α significantly reduces such inflammation and suppresses the formation of invasive pannus. TNF-α inhibitors were introduced as a therapeutic option for RA in 1998, and currently remain the most commonly used BRM. There are five TNF-α inhibitors now licensed (Table 1) with some differences in their structure, function and administration routes. Studies have shown that they are all highly effective in reducing joint damage and disability, and improving quality of life, especially when combined with methotrexate. While TNF-α inhibitors, like the other BRMs, are mostly used when patients with active RA do not have a satisfactory response to traditional DMARDs, they can also be chosen as first-line therapy in severe cases or when traditional DMARDs are contraindicated. Adalimumab was the third TNF-α inhibitor to be introduced, and the first fully human monoclonal antibody of the group. It is currently widely used across the world for the treatment of RA. Adalimumab is also approved by the US FDA and the EMA for the treatment of ankylosing spondylitis, psoriatic arthritis, juvenile idiopathic arthritis and Crohn's disease.
To retrieve the evidence for this review, the authors searched MEDLINE (through PubMed) to identify relevant citations published in English or Spanish. Medical terms related to 'adalimumab' were combined using 'AND' with those related to 'rheumatoid arthritis'. Of 1218 potentially relevant citations, 14 publications reporting on controlled trials, 12 open-label extensions, 38 registry studies and 40 systematic reviews were summarized.
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