%0 Journal Article
%T Correlation of antinuclear antibody and anti-double-stranded DNA antibody with clinical response to infliximab in patients with rheumatoid arthritis: a retrospective clinical study
%A Naoichiro Yukawa
%A Takao Fujii
%A Seiko Kondo-Ishikawa
%A Hajime Yoshifuji
%A Daisuke Kawabata
%A Takaki Nojima
%A Koichiro Ohmura
%A Takashi Usui
%A Tsuneyo Mimori
%J Arthritis Research & Therapy
%D 2011
%I BioMed Central
%R 10.1186/ar3546
%X One hundred eleven RA patients who had received IFX were studied. ANA (indirect immunofluorescence with HEp-2 cells) and anti-ds-DNA Abs (Farr assay) results were examined before and after IFX therapy.The overall clinical response assessed by EULAR response criteria was as follows: good response in 55%, including remission in 38%; moderate response in 18%; and no response (NOR) in 27%. The positivity of ANA (¡Ý 1:160) and anti-ds-DNA Abs significantly increased from 25% to 40% (P = 0.03) and from 3% to 26% (P < 0.001) after IFX, respectively. EULAR response differed significantly according to the ANA titer before IFX (P = 0.001), and the efficacy of IFX became worse as the ANA titer before starting IFX increased. Furthermore, the differences in the clinical response of the ANA titer before IFX ¡Ü 1:80 and ¡Ý 1:160 were significant (good, moderate, and no response were 66%, 9%, and 25% in ¡Ü 1:80 group versus 26%, 33%, 41% in ¡Ý 1:160 group, respectively; P < 0.001). In 13 patients whose ANA had increased after IFX, 10 showed NOR, only one showed a good response, and none reached remission. These clinical responses were significantly different from ANA no-change patients. In 21 patients with positive anti-ds-DNA Abs after IFX, 16 showed NOR, only two showed a good response, and none reached remission.The present study suggests that the ANA titer before starting IFX predicts the clinical response to IFX. The increased titers of ANA or anti-ds-DNA Abs after IFX may be useful markers of NOR.Rheumatoid arthritis (RA) is a chronic, inflammatory disease with the potential to cause substantial joint damage and disability. Tumor necrosis factor (TNF)-¦Á plays a central role in the pathogenesis of RA, as demonstrated by the clinical benefit of anti-TNF-¦Á therapy [1-6]. Infliximab (IFX), a chimeric anti-human TNF-¦Á monoclonal antibody, has enabled great advances in the treatment strategy for RA, resulting in a paradigm shift of RA treatment. Although IFX therapy concomitant with met
%U http://arthritis-research.com/content/13/6/R213