Skip Navigation


Rheumatology Advance Access originally published online on May 4, 2009
Rheumatology 2009 48(7):716-720; doi:10.1093/rheumatology/kep080
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
48/7/716    most recent
kep080v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Williams, E. L.
Right arrow Articles by Edwards, C. J.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Williams, E. L.
Right arrow Articles by Edwards, C. J.
Related Collections
Right arrow Pharmacology
Right arrow Systemic Lupus Erythematosus and Autoimmunity
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2009. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

REVIEWS

Anti-TNF-induced lupus

Emma L. Williams1, Stephan Gadola1,2 and Christopher J. Edwards1

1Department of Rheumatology, Southampton University Hospitals NHS Trust and 2Division of Infection, Inflammation and Repair, School of Medicine, Southampton University, Southampton, UK.

Correspondence to: Christopher J. Edwards, Department of Rheumatology, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, UK. E-mail: cedwards{at}soton.ac.uk


  Abstract

The use of protein-based anti-TNF-{alpha} therapies such as antibodies and soluble TNF-{alpha} receptors is commonly associated with the induction of autoantibodies, whereas anti-TNF-induced lupus (ATIL) is rare. ATIL can occur with any of the available TNF inhibitors, but the frequency and clinical characteristics of ATIL vary between different drugs. Cutaneous, renal and cerebral involvement as well as dsDNA antibodies are more common in ATIL compared to classical drug-induced lupus (DIL), suggesting different pathogenic mechanisms of ATIL and DIL. True ATIL must be clinically differentiated from mixed CTD, SLE or overlap syndromes unmasked, but not induced, by anti-TNF-{alpha} treatment of unclassified polyarthritis. The pathogenesis of ATIL is still unknown. Concomitant immunosuppression can reduce autoantibody formation in ATIL, and withdrawal of anti-TNF-{alpha} therapy usually leads to resolution of symptoms. Steroids and/or immunosuppressive therapy may be required in severe cases.

KEY WORDS: Drug-induced, Lupus, Anti-TNF, Arthritis

Submitted 31 December 2008; revised version accepted 16 March 2009.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.