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Quantifying Anti-CCP titer: clinical utility and association with tobacco exposure in patients with rheumatoid arthritis.
  1. David M. Lee (dlee{at}rics.bwh.harvard.edu)
  1. Brigham and Women's Hospital/Harvard Medical School, United States
    1. Roxanne Phillips (phillips.ro{at}neu.edu)
    1. Brigham and Women's Hospital, United States
      1. Elizabeth M. Hagan (elizabethmaryhagan{at}gmail.com)
      1. Brigham and Women's Hospital, United States
        1. Lori B Chibnik (lchibnik{at}rics.bwh.harvard.edu)
        1. Brigham and Women's Hospital, United States
          1. Karen H Costenbader, MD, MPH (kcostenbader{at}partners.org)
          1. Brigham and Women's Hospital, United States
            1. Peter H Schur (pschur{at}partners.org)
            1. Brigham & Women's Hospital-Harvard Med School, United States

              Abstract

              Objectives: To determine the significance of quantitative levels of antibodies to cyclic citrullinated peptides (anti-CCP) in a population of patients with rheumatoid arthritis (RA).

              Methods: 241 consecutive sera from patients with RA sent from a large rheumatology clinic for laboratory testing were selected for precisely quantifying anti-CCP antibody titers with the anti-CCP2 assay. Patient charts were reviewed for demographic information, smoking history, clinical diagnosis, RF titer, radiographic information and other laboratory information (ESR and CRP). Correlations with anti-CCP titer and RF titer, disease parameters and smoking history were assessed.

              Results: We confirm previous findings that anti-CCP seropositivity is associated with a higher incidence of erosions in patients with RA (56% vs 20% CCP+ vs CCP-, kappa=0.297, P<0.0001). We also find a moderate correlation between anti-CCP titer and RF titer. However, we failed to find association between anti-CCP titer and presence of erosions, between anti-CCP titer and CRP or ESR level or between anti-CCP titer and age or disease duration. Interestingly, we did find a significantly higher anti-CCP titers in patients with a history of smoking (452 units/ml vs 229 units/ml, smoker vs. non-smoker respectively. P=0.02).

              Conclusions: Although anti-CCP titers were not associated with clinical parameters of disease, they are increased in RA patients with exposure to tobacco. In contrast, no elevation in RF was noted in patients with history of smoking. These observations are consistent with a pathogenic contribution of smoking to RA and suggest the immune stimulus for anti-CCP is distinct from that for RF.

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