Infliximab: 12 years of experience
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REVIEW
Infliximab: 12 years of experience Josef S Smolen1,2* and Paul Emery3
Abstract Rheumatoid arthritis (RA), ankylosing spondylitis (AS) and psoriatic arthritis (PsA) are immune-mediated conditions that share an inflammatory mechanism fuelled by excessive cytokines, particularly TNF. Control of inflammation and rapid suppression of cytokines are important in treating these diseases. With this understanding and the corresponding advent of TNF inhibitors, RA patients, AS patients and PsA patients have found more choices than ever before and have greater hope of sustained relief. As a widely used TNF inhibitor, infliximab has a deep and established record of efficacy and safety data. Extensive evidence – from randomised controlled clinical trials, large registries and postmarketing surveillance studies – shows that infliximab effectively treats the signs and symptoms, provides rapid and prolonged suppression of inflammation, prevents radiologically observable disease progression and offers an acceptable safety profile in RA, AS and PsA. In very recent studies, investigators have observed drug-free remission in some patients. Additionally, infliximab may interfere with rapidly progressing disease in RA by early addition to methotrexate in patients with signs of an aggressive course. Finally, infliximab has been shown to reduce PsA clinical manifestations such as nail involvement. With our current understanding, substantial data and increasing confidence regarding use in practice, infliximab can be considered a wellknown drug in our continued campaign against inflammatory rheumatic diseases.
Insights into mechanisms Rheumatoid arthritis (RA), ankylosing spondylitis (AS) and psoriatic arthritis (PsA) are all associated with a probably distinct immune-mediated pathogenesis that is *Correspondence: [email protected]; [email protected] 1 Division of Rheumatology, Department of Medicine III, Medical University of Vienna 2 2nd Department of Medicine, Hietzing Hospital, Waehringer Guertel 18-20, A-1090 Vienna, Austria Full list of author information is available at the end of the article
© 2010 BioMed Central Ltd
© 2011 BioMed Central Ltd
central to the pathophysiology of each disease but ultimately leads to a chronic inflammatory response as a final common pathway. This fundamental inflammatory response is characterised by an overproduction of proinflammatory cytokines, particularly TNF, IL-1 and IL-6 [1]. TNF is a dominant proinflammatory cytokine in RA, AS and PsA. The cytokine has both a direct effect and an indirect effect on the inflammatory events in these conditions [2-4]. TNF induces macrophages and other cells to secrete other proinflammatory cytokines (for example, IL-1, IL-6, IL-8), leads to T-cell activation and induces endothelial cells to express both adhesion molecules that increase T-cell infiltration and vascular growth factors that promote angiogenesis and keratinocyte proliferation. TNF is also involved in the differentiation and maturation of osteoclasts, the pivotal cells engaged in bone
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