A study has found that quantitative levels of antibodies to cyclic citrullinated peptides (anti-CCP) are not associated with clinical parameters of rheumatoid arthritis (RA), but are increased in patients with exposure to tobacco.
“Observations have suggested a new disease model wherein the combination of anti-CCP and inflammation-induced citrullination of tissue proteins can conspire to induce an autoimmune inflammatory arthritis,” explain David Lee, from Brigham and Women’s Hospital in Boston, Massachusetts, USA, and colleagues.
Lee et al tested sera from 241 RA patients (80.1% women, with a mean age of 48 years at RA onset) for anti-CCP quantification. The patients’ charts were reviewed for demographic information, smoking history, clinical diagnosis, rheumatoid factor (RF) titer, radiographic information, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP).
Overall, 73% of patients had a positive anti-CCP test and 42% of these had initial anti-CCP measurements higher than assay limits (equal to or more than 100 U). This confirmed the authors’ impression that a significant number of patients have anti-CCP titers that are higher than those measured in the linear range of commercial anti-CCP2 assays.
Their study also confirmed previous findings that anti-CCP and RF seropositivity predict a higher incidence of erosions in patients with RA (56% vs 20% for CCP+ and CCP- and 47% vs 28% for RF+ and RF-, respectively).
“However, we failed to find association between anti-CCP and presence of erosions, CRP or ESR level, and age or disease duration,” they state. Furthermore, the same observations were present when the authors examined the RF titer.
Of note, patients with a history of smoking had anti-CCP titers almost twice as high as those who did not (452 vs 229 U/ml).
The investigators note that these observations are consistent with a pathogenic contribution of smoking to RA, and suggest that stimuli other than tobacco exposure can drive development of anti-CCP.
“While these measurements reveal associations with potential for further mechanistic insights, the current findings do not support full anti-CCP quantification in routine clinical practice,” concludes the team.