Literature DB >> 15833077

Infliximab for the treatment of early rheumatoid arthritis.

Robin C Geletka1, E William St Clair.   

Abstract

Rheumatoid arthritis (RA) is a systemic, chronic inflammatory disease characterised predominately by polyarthritis with frequent progression to permanent joint damage and disability. Evidence shows that starting treatment with disease-modifying antirheumatic drug (DMARD) therapy early in the course of disease can slow radiographic progression of RA compared with a more delayed approach. Moreover, in the early stages of RA, treatment with a combination of methotrexate (MTX), a traditional DMARD, and a biologic with tumour necrosis factor (TNF)-alpha blocking activity has proven to be more effective than using MTX alone. Among the approved TNF-alpha inhibitors, infliximab is a chimeric monoclonal antibody with high affinity and specificity for its target cytokine. It binds to soluble TNF monomers and trimers, as well as membrane-bound TNF-alpha, forming a stable complex which prevents TNF-alpha from binding to its receptor and triggering a biological response. The combination of MTX and infliximab therapy has shown superior clinical outcomes compared with MTX monotherapy in early RA, as well as greater protection against joint damage and physical disability. Although infliximab therapy has been associated with side effects, including serious infections, this drug can be administered with an acceptable margin of safety for several years by appropriate selection of patients, screening for latent and active tuberculosis, and monitoring of patients for infection and other toxicities. The knowledge of the benefits of infliximab therapy for early RA affords groundwork for developing more effective treatment strategies that can minimise disease progression over the long term.

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Year:  2005        PMID: 15833077     DOI: 10.1517/14712598.5.3.405

Source DB:  PubMed          Journal:  Expert Opin Biol Ther        ISSN: 1471-2598            Impact factor:   4.388


  1 in total

1.  Identification of the most active interleukin-32 isoform.

Authors:  Ji-Da Choi; Su-Young Bae; Jae-Woo Hong; Tania Azam; Charles A Dinarello; Erk Her; Whan-Soo Choi; Bo-Kyung Kim; Chang-Kwon Lee; Do-Young Yoon; Sun-Jong Kim; Soo-Hyun Kim
Journal:  Immunology       Date:  2008-09-02       Impact factor: 7.397

  1 in total

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