NEUROLOGY 2004;63:2396-2398
© 2004 American Academy of Neurology
Brief Communications
Associations with autoimmune disorders and HLA class I and II antigens in inclusion body myositis
U. A. Badrising, MD, PhD,
G. M.Th. Schreuder, PhD,
M. J. Giphart, MD, PhD,
K. Geleijns, MD,
J. J.G.M. Verschuuren, MD, PhD,
A. R. Wintzen, MD, PhD and
the Dutch IBM Study Group*
From the Departments of Neurology (Drs. Badrising, Geleijns, Verschuuren, and Wintzen) and Immunohematology and Blood Transfusion (Drs. Schreuder and Giphart), Leiden University Medical Center, the Netherlands.
Address correspondence and reprint requests to Dr. U.A. Badrising, Department of Neurology, K5Q, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, the Netherlands; e-mail: ubadrising{at}lumc.nl
Whether autoimmune mechanisms play a role in the pathogenesis of inclusion body myositis (IBM) is unknown. Human leukocyte antigen (HLA) analysis in 52 patients, including 17 with autoimmune disorders (AIDs), showed that patients were more likely to have antigens from the autoimmune-prone HLA-B8-DR3 ancestral haplotype than healthy control subjects, irrespective of the presence of AIDs. Patients lacked the apparently protective HLA-DR53 antigen. The results provide further support for an autoimmune basis in IBM.
Received November 19, 2003.
Accepted in final form August 10, 2004.
Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the December 28 issue to find the title link for this article.
*See the Appendix on page 2398 for a list of Group members.
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