Update: B-Cells in Rheumatic Disease

Volume 5 | January 1, 2007 - March 30, 2007

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Highest Rated Articles

Arnold DM, Dentali F, Crowther MA, et al. Systematic review: efficacy and safety of rituximab for adults with idiopathic thrombocytopenic purpura. Ann Intern Med 2007;146(1):25-33.

This is a review of the literature on the efficacy and safety of rituximab for the treatment of adults with idiopathic thrombocytopenic purpura (ITP). The authors identify 19 articles that meet their criteria on efficacy. Almost incredibly, there are no controlled studies, and no studies meet all the authors’ criteria for study quality. Overall, the number of rituximab-treated patients with ITP reported in the literature is amazingly small. The reported deaths could not be necessarily attributed to rituximab. The authors conclude that whatever enthusiasm exists for the use of rituximab in ITP is based on scanty literature and that randomized controlled trials are urgently needed.

Smolen JS, Keystone EC, Emery P, et al, for The Working Group on the Rituximab Consensus Statement. Consensus statement on the use of rituximab in patients with rheumatoid arthritis. Ann Rheum Dis 2007;66:143-150.

This is an interesting review of the use of rituximab in rheumatoid arthritis. The Working Group members are from Europe and Canada, but they are well-recognized experts in this field. They performed a systematic review of the published literature on the efficacy of rituximab in treating patients with RA that includes a careful review of indications and screening requirements.

Taylor RP, Lindorfer MA. Drug insight: the mechanism of action of rituximab in autoimmune disease—the immune complex decoy hypothesis. Nat Clin Prac Rheumatol 2007;3:86-95.

This is a very interesting, creative effort to present an alternative explanation for how rituximab may be effective in treating various forms of autoimmune disease. The authors concede that rituximab promotes rapid and long-term elimination of circulating B cells; however, they suggest that a different mechanism may underline a great deal of its efficacy. The authors hypothesize that rituximab, by binding to IgG molecules on B cells, generates an excess of cellular immune complexes that attract and bind the Fc-gamma receptors on effector cells, thereby significantly diminishing the ability of these cells to be recruited. They name this the immune complex “decoy hypothesis.” The authors suggest that this may be the means by which rituximab ultimately reduces inflammation in tissue damage.

Other Rated Articles

Molecular Immunology

Three Stars Carnahan J, Stein R, Qu Z, et al. Epratuzumab, a CD22-targeting recombinant humanized antibody with a different mode of action from rituximab. Mol Immunol 2007;44(6):1331-41.
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Copyright © 2000-2018 The Cleveland Clinic Foundation. All Rights Reserved.
Center for Continuing Education | 1950 Richmond Road, TR204, Lyndhurst, OH 44124