Open AccessInterferon‐β1A–induced polyarthritis in a patient with the HLA–DRB1*0404 allele
Author(s) -
Levesque Marc C.,
Ward Frances E.,
Jeffery Douglas R.,
Weinberg J. Brice
Publication year - 1999
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/1529-0131(199904)42:3<569::aid-anr23>3.0.co;2-m
Subject(s) - polyarthritis , medicine , immunology , rheumatoid arthritis , autoimmunity , arthritis , human leukocyte antigen , autoantibody , interferon , allele , inflammatory arthritis , antibody , antigen , biology , genetics , gene
Human interferon‐α (IFNα) and IFNβ are administered for treatment of several diseases, including viral infections, malignancies, and multiple sclerosis (MS). IFNα therapy has been associated with the production of autoantibodies and the development of a variety of autoimmune disorders, including polyarthritis. This report describes the development of seronegative, symmetric polyarthritis in a patient with relapsing‐remitting MS, after 8 weeks of therapy with IFNβ1a. HLA phenotyping analysis of the patient revealed the presence of HLA–DRB1*0404, an allele known to be associated with the development of rheumatoid arthritis. Therefore, IFNβ1a may have induced arthritis in a patient who was genetically predisposed to develop arthritis on the basis of HLA determinants. The English‐language literature regarding IFNα‐ and IFNβ‐induced polyarthritis is reviewed, and possible mechanisms for IFNα‐ and IFNβ‐induced autoimmunity, including the contribution of HLA determinants and nitric oxide overproduction, are discussed.