TNF-Inhibition in the Treatment of Rheumatoid Arthritis by Larry W. Moreland, Paul Emery

By Larry W. Moreland, Paul Emery

The advent of tumor-necrosis-factor-alpha (TNFa) blocking off brokers is likely one of the milestones within the remedy of rheumatoid arthritis (RA). Edited by way of Larry Moreland and Paul Emery, specialists in rheumatological disorder, TNFa-Inhibition within the therapy of Rheumatoid Arthritis charts the heritage and improvement of the concept that of TNFa inhibition. The authors rfile TNFa from its discovery to its now well-documented medical functions within the remedy of sufferers with RA. They evaluate and distinction sensible administration concerns in regards to the use of those brokers either within the US and UK/Europe. The e-book is a realistic and available resource containing the latest details during this box

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Lancet 1994; 344(8930): 1125–7. Charles PJ, Smeenk RJ, De Jong J, Feldmann M, Maini RN. Assessment of antibodies to double-stranded DNA induced in rheumatoid arthritis patients following treatment with infliximab, a monoclonal antibody to tumor necrosis factor alpha: findings in open-label and randomized placebo-controlled trials. Arthritis Rheum 2000; 43(11): 2383–90. van Oosten BW, Barkhof F et al. Increased MRI activity and immune activation in two multiple sclerosis patients treated with the monoclonal antitumor necrosis factor antibody cA2.

Iyer S, Yamauchi P, Lowe NJ. Etanercept for severe psoriasis and psoriatic arthritis: observations on combination therapy. Br J Dermatol 2002; 146: 118. Yazici Y, Erkan D, Lockshin MD. A preliminary study of etanercept in the treatment of severe, resistant psoriatic arthritis. Clin Exp Rheumatol 2000; 18: 732. Sandborn WJ, Hanauer SB, Katz S et al. Etanercept for active Crohn’s disease: a randomized, double-blind, placebo-controlled trial. Gastroenterology 2001; 121: 1088. 02 25/09/2002 1 24 pm Page 23 chapter 2 Infliximab therapy Ravinder N Maini and Marc Feldmann Introduction In the past 3 years, infliximab (Remicade) has become established as a second-line treatment of moderate to severe rheumatoid arthritis (RA) for patients whose disease exhibits persistent activity despite adequate treatment with standard disease-modifying antirheumatic drugs (DMARDs).

Construction and initial characterization of a mouse-human chimeric anti-TNF antibody. Mol Immunol 1993; 30(16): 1443–53. 2. Barone D, Krantz C, Lambert D, Maggiora K, Mohler K. Comparative analysis of the ability of etanercept and infliximab to lyse TNF-expressing cell in a complement dependent fashion. Arthritis Rheum 1999; 42: S90. 3. Maini RN, Elliott MJ, Long-Fox A et al. Clinical response of rheumatoid (RA) to anti TNF␣ (cA2) monoclonal antibody (mab) is related to administered dose and persistence of circulating antibody [abstract].

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