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Rheumatology Advance Access originally published online on July 28, 2006
Rheumatology 2006 45(11):1445-1446; doi:10.1093/rheumatology/kel232
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© The Author 2006. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Is TNF{alpha} really a good therapeutic target in motoneuronal degeneration? A case of amyotrophic lateral sclerosis in a patient with RA receiving infliximab

M. Dziadzio, V. Reddy, S. Rahman, C. Mummery1 and A. Keat

Arthritis Centre and1Department of Neurology, Northwick Park Hospital, London, UK

Correspondence to: Dr Magdalena Dziadzio, Arthritis Centre, Northwick Park Hospital, Watford Road, Harrow, HA1 3UJ, London, UK. E-mail: Magdalena.Dziadzio@nwlh.nhs.uk

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SIR, Tumour necrosis factor-{alpha} (TNF-{alpha}) has been implicated in the pathogenesis of various inflammatory conditions such as rheumatoid arthritis (RA), Crohn's disease and psoriasis. In these diseases, TNF-{alpha} blockade is a successful and safe treatment option [1]. TNF-{alpha} can be neurotoxic and has also been implicated in the pathogenesis of some central nervous system diseases where inflammation has recently emerged as a significant contributor to motor neuron damage [2]. TNF-{alpha} acts as the main driver for neuroinflammation in amyotrophic lateral sclerosis (ALS). Animal studies [3–5] as well as phase II . . . [Full Text of this Article]


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