Rheumatoid Arthritis (RA) is a systemic, chronic inflammatory disease characterized by inflammation of synovial joints and production of autoantibodies such as Rheumatoid Factor and antibodies directed against modified proteins - i.e. anti-citrullinated peptides antibody (ACPA). Carbamylation, as a post translational modification, has been recently associated to RA since anti-carbamylated protein antibodies (anti-CarP) have been detected in the sera of RA patients. The effect of treatment on anti-CarP level has been never addressed before.
Through this study we aimed to investigate the short term effect of anti-TNF treatment with Etanercept on anti-CarP.
We enrolled consecutive RA patients before starting treatment with Etanercept. Clinical data and serum samples were gathered from each patient at baseline and after 3 months of treatment. Disease activity was assessed at baseline and after 3 months by using the C-reactive protein - Disease Activity Score (DAS) 28. Sixty-three age and sex matched healthy donors served as controls. Anti-Car-P antibodies were investigated by immune-enzymatic assay.
We enrolled 17 RA patients (F:M 15:2, mean age 44.1 ± 10.7 years, mean disease duration 7.9 ± 5.8 years). Six patients (35.3%) were positive for anti-CarP antibodies at baseline while three months after only 4 patients (23.5%) remained positive. Mean serum level of anti-CarP antibodies at baseline and after 3 months were: 253.0 ± 139.8AU/ml and 271.0 ± 132.4AU/ml respectively. Considering the persistently anti-CarP positive patients, the mean antibody titre increases from 386.2 ± 49.3AU/ml at baseline to 421.8 ± 144.0AU/ml at follow up.
The effect of anti-TNF treatment on autoantibody status is still controversial; in particular, data on ACPA variation during treatment are discordant. In our cohort of long standing RA patients, a short term course of Etanercept did not affect the anti-CarP status.
In conclusion, this pilot study demonstrated a slight reduction in the percentage of anti-CarP positive patients but an overall increase of antibody titres unrelated to the clinical response to TNF blockade was observed
