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Terao, Chikashi

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Terao

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Chikashi

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Terao, Chikashi
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    Relationship between handedness and joint involvement in rheumatoid arthritis
    (Nature Publishing Group, 2016) Yaku, Ai; Hashimoto, Motomu; Furu, Moritoshi; Ito, Hiromu; Yamakawa, Noriyuki; Yamamoto, Wataru; Fujii, Takao; Matsuda, Fumihiko; Mimori, Tsuneyo; Terao, Chikashi
    Rheumatoid arthritis (RA) is characterized by autoimmune chronic joint inflammation, which is worsened by mechanical stress. It is still inconclusive whether joints on the right side or the dominant side get more damaged in RA since the limited number of patients analyzed in the previous study had made it difficult to separately analyze right-handed and left-handed patients. Here, we enrolled 334 RA patients, the biggest number of patients in studies to address this issue and separately analyzed right-handed and left-handed patients. As a result, we observed that joints on the dominant side got clinically and radiologically more involved in the right-handed patients (p ≤ 0.0030). Importantly, this tendency was also seen in the left-handed patients, while it was not statistically significant due to the small sample size. This tendency was observed in each component of clinical or radiological involvement. Thus, handedness influences the laterality of clinical and radiological joint involvement in RA.
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    Smoking is associated with the concurrent presence of multiple autoantibodies in rheumatoid arthritis rather than with anti-citrullinated protein antibodies per se: a multicenter cohort study
    (BioMed Central, 2016) van Wesemael, Tineke J.; Ajeganova, Sofia; Humphreys, Jennifer; Terao, Chikashi; Muhammad, Ammar; Symmons, Deborah P. M.; MacGregor, Alex J.; Hafström, Ingiäld; Trouw, Leendert A.; van der Helm-van Mil, Annette H. M.; Huizinga, Tom W. J.; Mimori, Tsuneyo; Toes, René E. M.; Matsuda, Fumihiko; Svensson, Björn; Verstappen, Suzanne M. M.; van der Woude, Diane
    Background: The contribution of smoking to rheumatoid arthritis (RA) is hypothesized to be mediated through formation of anti-citrullinated protein antibodies (ACPA). In RA, however, autoantibodies such as ACPA, rheumatoid factor (RF), and anti-carbamylated protein antibodies (anti-CarP) often occur together, and it is thus unclear whether smoking is specifically associated with some autoantibodies rather than others. We therefore investigated whether smoking is only associated with ACPA or with the presence of multiple RA-related autoantibodies. Methods: A population-based Japanese cohort (n = 9575) was used to investigate the association of smoking with RF and anti-cyclic citrullinated peptide antibodies (anti-CCP2) in individuals without RA. Furthermore, RA patients fulfilling the 1987 criteria from three early arthritis cohorts from the Netherlands (n = 678), the United Kingdom (n = 761), and Sweden (n = 795) were used. Data on smoking, RF, anti-CCP2, and anti-CarP were available. A total score of autoantibodies was calculated, and odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated by logistic regression. Results: In the population-based non-RA cohort, no association was found between smoking and one autoantibody (RF or anti-CCP2), but smoking was associated with double-autoantibody positivity (OR 2.95, 95% CI 1.32–6.58). In RA patients, there was no association between smoking and the presence of one autoantibody (OR 0.99, 95% CI 0.78–1.26), but smoking was associated with double-autoantibody positivity (OR 1.32, 95% CI 1.04–1.68) and triple-autoantibody positivity (OR 2.05, 95% CI 1.53–2.73). Conclusions: Smoking is associated with the concurrent presence of multiple RA-associated autoantibodies rather than just ACPA. This indicates that smoking is a risk factor for breaking tolerance to multiple autoantigens in RA. Electronic supplementary material The online version of this article (doi:10.1186/s13075-016-1177-9) contains supplementary material, which is available to authorized users.