In the originally published version of this article, the first author, Chikashi Tereo, had footnotes indicating affiliations with the first seven institutions. The correct affiliations are the first six plus footnote 17, indicating equal contribution.

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Objective Multiple studies have found a relationship between alcohol consumption and disease activity in rheumatoid arthritis (RA), although reverse causation has been suggested to explain the association. We aimed to study the relationship between alcohol consumption and disease activity, disease progression, and health‐related quality of life in patients with RA. Methods We followed up 1,228 patients with newly diagnosed RA from a population‐based case–control study, Epidemiological Investigation of Rheumatoid Arthritis (EIRA). Drinkers and non‐drinkers were compared to evaluate risk of unfavorable outcomes regarding disease activity and health‐related quality of life. Odds ratios with 95% confidence intervals were calculated using logistic regression models. Results Non‐drinkers at baseline had higher disease activity and estimated their pain as more severe compared to drinkers. At 1 year of follow‐up, non‐drinkers reported higher swollen and tender joint counts and experienced more pain and fatigue, lower global health scores, and lower health‐related quality of life. The inverse relationship between alcohol consumption and RA‐specific outcomes was also observed when comparing drinkers and non‐drinkers who had not changed their alcohol consumption habits at or after the year of disease onset. Those who stopped drinking postbaseline experienced higher disease activity, more pain, and lower health‐related quality of life at 1 year of follow‐up, compared to drinkers, although there was no difference in disease activity at baseline between drinkers who continued versus discontinued drinking. Our findings argue against bias due to reverse causation. Conclusion Alcohol consumption was associated with lower disease activity and higher health‐related quality of life in RA patients in a dose‐dependent manner.

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Background In rheumatoid arthritis (RA), several genetic risk factors and smoking are strongly associated with the presence of anti-citrullinated protein antibodies (ACPA), while much less is known about risk factors for ACPA-negative RA. Antibodies against carbamylated proteins (anti-CarP) have been described in both ACPA-positive and ACPA-negative RA patients. Objectives In this study we have analysed the relationships between anti-CarP antibodies, ACPA, genetic risk factors (HLA-DRB1 alleles and PTPN22) and smoking in RA. Methods Presence of antibodies to carbamylated fetal calf serum (CarP-FCS) and fibrinogen (CarP-Fib) was determined by in-house ELISAs in the Leiden Early Arthritis Cohort (EAC) and in the Swedish Epidemiological Investigation of RA (EIRA) cohort. Odds ratios for associations with different HLA-DRB1 alleles, PTPN22 genotypes and smoking were calculated separately for each cohort as well as in the combined meta-analysis, in RA subsets defined by anti-CarP and anti-cyclic citrullinated peptide (CCP) antibody status. Results In both cohorts, anti-CarP antibodies were mainly detected in the anti-CCP-positive population, but also in the anti-CCP-negative population. No associations between anti-CarP antibodies and HLA-DRB1 shared epitope alleles could be identified, while a consistent signal for an association between anti-CarP-FCS and HLA-DRB1*03 was observed. Further analyses did not reveal any specific associations of anti-CarP antibodies with other HLA-DRB1 alleles, PTPN22 genotypes or smoking. Conclusions Anti-CarP antibodies were present in both ACPA-positive and ACPA-negative RA. Except for a modest association with HLA-DRB1*03, there were no strong associations between anti-CarP antibodies and HLA-DRB1 alleles, PTPN22 or smoking. These data suggest that different biological mechanisms may underlie anti-CarP versus anti-CCP antibody formation. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.4653