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Background:The mechanisms affecting anti-RA33 antibody’s involvement in RA pathogenesis is still unclear. Refining our understanding of anti-RA33’s role in RA in relation to known RA-associated genes and serological elements is needed.Objectives:We investigated the relationship between RA-associated HLA-DRB1 epitope (SE) allele and presence of anti-RA33 antibodies in different serological subsets of rheumatoid arthritis in a Malaysian population.Methods:Serum samples from 550 RA cases comprising seronegative (negative for anti-CCP2, IgG and IgM, n=250), seropositive (triple-autoantibody positive, n=150), singular anti-CCP2 positive (n=100), and double RF positive RA (n=50) were chosen from the Malaysian Epidemiological Investigations of RA (MyEIRA) case-control study. Three hundred MyEIRA population controls were used for comparison. All serum samples were assayed using a commercial anti-RA33 ELISA kit. All genetic samples were genotyped for four-digit HLA-DRB1 alleles using the PCR-SSO method on Luminex platform.Results:The proportions of anti-RA33 positive was 20.9% in all RA cases (i.e. 34% in RF only positive RA; 25% in seropositive RA; 18% in seronegative RA and 18% in anti-CCP2 only positive RA). The HLA-DRB1 shared epitope alleles were significantly associated with anti-RA33 positive in the seropositive RA subgroup (OR=6.9, 95% CI 1.4-34.8; p=0.02). We observed significant association between anti-RA33 negative and HLA-DRB1 SE alleles among the seropositive RA patients (OR=4.5, 95% CI 2.8-7.2; pConclusion:The HLA-DRB1 SE alleles increased the risk of seropositive and CCP only positive RA independent of anti-RA33 positivity.References:[1]Boeters, Debbie M et al. “The 2010 ACR/EULAR criteria are not sufficiently accurate in the early identification of autoantibody-negative rheumatoid arthritis: Results from the Leiden-EAC and ESPOIR cohorts.” Seminars in arthritis and rheumatism vol. 47,2 (2017): 170-174.[2]de Brito Rocha, Sara et al. “Clinical and pathophysiologic relevance of autoantibodies in rheumatoid arthritis.” Advances in rheumatology (London, England) vol. 59,1 2. 17 Jan. 2019.Acknowledgements:The authors would like to thank the Director General of Health, Ministry of Health Malaysia for supporting this study. The authors are also indebted to participants for their kind participation. This study was financially supported by the Ministry of Health, Malaysia (JPP-IMR 08-012).Disclosure of Interests:None declared

BackgroundAnti-citrullinated protein antibodies (ACPAs) are the hallmark of rheumatoid arthritis (RA). Protein citrullination is believed to drive autoantigen selection in RA. Nonetheless, several autoantigens in RA are targeted as native (unmodified) proteins. Here, the study of hnRNP A2/B1 (RA33) provides a framework to understand the humoral response to native and citrullinated autoantigens in RA.MethodsRA synovial fluid (SF) cells were analysed by immunoblotting and mass spectrometry. RA33 was cloned from RASF cells and splice variants expressed as recombinant proteins. Antibodies against native and citrullinated RA33 were characterised by ELISA, immunoblotting and immunoprecipitation.ResultsRA33 is citrullinated in the rheumatoid joint and targeted either as a citrullinated or native protein in distinct patient subsets with RA. A novel splice variant (hnRNP B1b) previously associated with disease initiation in experimental arthritis was identified in the RA joint and acts as the major target of the anti-RA33 response. Antibodies exclusively targeting citrullinated RA33 were positively associated with disease duration and erosive disease. In contrast, anti-(native) RA33 antibodies were detected almost exclusively in early RA and identified patients with low radiographic erosion scores. Finally, a unique subset of double-reactive patients demonstrated intermediate severity, but rapid disease progression, suggesting a transitional disease phase in the evolution of an anti-native protein antibody to ACPA response in RA.ConclusionsThese data suggest that native and citrullinated proteins targeted by autoantibodies in RA may be part of a single antibody system and challenge the paradigm of citrullination as the unifying principle underlying loss of tolerance in RA.

Background:In rheumatoid arthritis (RA), the endocardium is involved in the inflammatory process, which is caused by immunopathogenetic mechanisms involving CD4 +, T-cells and proinflammatory macrophages. Minor changes in the cardiovascular system can be successfully detected by ultrasound in patients with RA.Objectives:to improve the quality of non-invasive diagnostics of heart disease in patients with RA.Methods:57 patients with RA were under observation: 7 men and 50 women aged from 26 to 70 years; mean age 50.45 ± 10.12 years; activity (according to DAS28) was low for 3.5%, medium for 86%, and high for 10.5%. Immunological examination included determination of serum IgM-RF, CRP, antibodies to cyclic citrulline peptide (anti-CCP), antibodies to modified vimentin (anti-MCV), antibodies to antigen RA33, levels of angiopoietin-like proteins 3 (ANGPTL3) and 4 (ANGPTL4) types (classical ELISA test), as well as the detection of IgG antibodies to 5’-nucleotidase (5’-NT) and xanthine oxidase (XO) (modified ELISA test). Data from ultrasound, magnetic resonance (MRT) and computer (CT) tomography were used in assessing the state of the heart structures.Results:The pathology of cardiovascular system was diagnosed in 28 (49.1%) patients with RA. Signs of the heart damage were noted in 33.3% of cases (pericarditis and valvular heart disease were most often detected). In groups of patients with RA with elevated levels of antibodies to 5’-NT and XO (compared with RA patients with normal parameters), there was a significantly more frequent heart damage (for antibodies to 5’-NT: χ2= 3.8, p = 0.047; for antibodies to XO: χ2= 3.92, p = 0.041). It was discovered that in all patients with an increased level of antibodies to XO, one of the lesions of the heart valvular apparatus of varying severity was noted. According to ultrasound data (usually confirmed by CT and / or MRT), signs of valvular dysfunction were found in 21 (36.8%) patients with RA. The high frequency of mitral prolapse (28.6%) may be associated with the presence of a chronic inflammatory process that is able to accelerate the development of atherosclerosis and heart disease in RA patients. A tendency to an increase in the prevalence of mitral prolapse in patients with a longer duration of the disease (p = 0.062) and with high levels of serum ANGPTL4 (p = 0.058) was found.One of the main factors leading to the development of vascular pathology in RA is the accumulation of reactive oxygen intermediate. Antibodies to XO can affect the biochemical activity of the enzyme in the serum of patients with RA, stimulating the increased formation of O-form XO, which has a pronounced prooxidant effect (especially to lipids). ANGPTL4, acting as a potent inhibitor of endothelial lipoprotein lipase, can suppress the release of non-esterified fatty acids and their transfer to the heart muscle.Conclusion:To identify subclinical signs of involvement of cardiovascular system in the pathological process in the early asymptomatic stages of RA, it is advisable to use imaging techniques in combination with immunological markers of heart damage, which can be especially useful for screening, diagnostic evaluation and determining cardiovascular risk.Disclosure of Interests:None declared

Background:The majority of patients with rheumatoid arthritis (RA) produce autoantibodies against proteins that have undergone post-translational modfication, e.g. citrullination or carbamylation. There is growing evidence of their relevance and their potential utility to improve diagnosis, patient stratification, and prognosis for precision medicine. Investigating new autoantibody patterns may allow further stratification of patients and identifying subsets of patients that benefit from different treatment modalities. Following the discovery of high autoantibody reactivity against multiple modified proteins the interest in native targets decreased. Even though antibodies reacting with native proteins may also have a role in RA pathogenesis, their reactivity patterns are much less studied.Objectives:To identify novel native autoantigens in RA patients and elucidate patterns within autoantibody reactivity against native autoantigens.Methods:We investigated the reactivity of autoantibodies in plasma pools from 15 anti-CCP positive and 10 anti-CCP negative RA patients and 10 healthy donors against more than 1600 human proteins in native configuration using the Immunome high-density protein microarray.Results:We identified 86 native proteins that were recognized by IgG antibodies from anti-CCP positive RA patients and 76 native proteins recognized by IgG antibodies from anti-CCP negative RA patients, but not by antibodies from healthy donors. Examples of proteins recognized by both patient subgroups are calcium/calmodulin-dependent protein kinase type II subunits, histone deacetylases, keratin, and vimentin. Reactivity against the ribonucleic protein SSB was observed in anti-CCP negative RA patients only.Conclusion:Several human proteins in their native conformation are recognized by autoantibodies from anti-CCP positive as well as anti-CCP negative RA patients. In general, anti-CCP positive patients had higher autoantibody activity than anti-CCP negative patients and healthy donors.References:[1] Konig, M.F., Giles, J.T., Nigrovic, P.A., Andrade, F., 2016. Antibodies to native and citrullinated RA33 (hnRNP A2/B1) challenge citrullination as the inciting principle underlying loss of tolerance in rheumatoid arthritis. Ann. Rheum. Dis. 75, 2022–2028.[2] Zheng, Z., Mergaert, A.M., Fahmy, L.M., Bawadekar, M., Holmes, C.L., Ong, I.M., Bridges, A.J., Newton, M.A., Shelef, M.A., 2019. Disordered Antigens and Epitope Overlap Between Anti-Citrullinated Protein Antibodies and Rheumatoid Factor in Rheumatoid Arthritis. Arthritis Rheumatol. art.41074.[3] Sirotti, S., Generali, E., Ceribelli, A., Isailovic, N., De Santis, M., Selmi, C., 2017. Personalized medicine in rheumatology: the paradigm of serum autoantibodies. Autoimmun. Highlights 8.Acknowledgments :The Department of Clinical Immunology at Rigshospitalet Copenhagen is acknowledged for providing the healthy donor blood. The study is part of the PROCIT study financed by the Danish Council for Independent Research (grant no. DFF - 7016-00233). Moreover, the Obelske Family Foundation, the Svend Andersen Foundation, the Spar Nord Foundation and the Danish National Mass Spectrometry Platform for Functional Proteomics (PRO-MS; grant no. 5072-00007B) are acknowledged for grants to the analytical platform are acknowledged for the funding to enabling parts of this study.Disclosure of Interests:Thomas B.G. Poulsen: None declared, Dres Damgaard: None declared, Malene Møller Jørgensen: None declared, Ladislav Senolt: None declared, Jonathan Blackburn Shareholder of: Sengenics Corporation, Consultant of: Director of Sengenics Corporation, Employee of: Director of Sengenics Corporation, Claus Henrik Nielsen: None declared, Allan Stensballe: None declared

Background Rheumatoid Arthritis (RA) is an inflammatory autoimmune disease characterized by joint involvement, pain and inflammation with or without extra-articular joint commitment. Serological markers can guide early diagnosis before that clinical activity takes place, optimizing early diagnosis, less activity and functional disability. RA 33 is considered a diagnosis-marker in RA patients related to prognosis and therapeutic response compared with conventional markers. RA 33 is common in patients with negative conventional markers and with few clinical symptoms. Objectives Evaluated the frecuency of RA33 in individuals with first-degree relatives of patients with RA and patients diagnosed with early rheumatoid arthritis as a good prognosis marker Methods A transversal study was conducted evaluated rheumatologic and periodontal condition of 112 individuals with first-degree relatives of patients with RA and 46 patients diagnosed with early rheumatoid arthritis, according to classification criteria for RA (ACR-EULAR 2010). In addition, 47 healthy individuals were included. RA patients and control group were matched for age and gender. Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), rheumatoid factor RF, ACPAs, and RA 33 were performed. VAS Pain Scale, SDAI Index, HAQ and DAS28 were evaluated. Porphyromona gingivalis (Pg) by CRP, IgG1, and IgG2 were determined. The data included in the study were analyzed using STATA 11.1. Associations were determined by the statistical test Chi 2, and Comparisons between groups of rheumatologic diagnosis and median values for continuous variables was performed using Mann-Whitney Test. Approved by the Ethics Committee of the Institution. Results 112 healthy individuals with first-degree relatives of patients with RA were assessed. Of them 78.3% has periodontal disease, presence of painful joints (30.63%). 36.94% patients had Pg in subgingival plaque samples. In the control group the presence of periodontal disease was 71.74%, tender joints (19.57%), swollen joints (6.52%). Disease activity measures were not representative. Only a woman in the group of family related RA patients was positive for RA 33 (49 years old, without treatment, painful and swollen joints and the presence of periodontal disease and Pg , ESR and CRP positives but RF and ACPAs negative). No patient with RA of less than two years of diagnosis was positive for RA 33. Conclusions The diagnostic value of anti RA33 was low in this population, with regard of worst prognosis markers and higher disease severity. Ra33 should be more follow-up clinical and paraclinical to subjects with risk factors who could have positive markers, without symptoms. References Fritsch R, Eselbock D.Characterization of Autoreactive T Cells to the Autoantigens Heterogeneous Nuclear Ribonucleoprotein A2 (RA33) and Filaggrin in Patients with Rheumatoid Arthritis. The Journal of Immunology.2002; 169 (2):1068–1076. Massardo L.Artritis reumatoide temprana early rheumatoid arthritis.Rev med Chile. 2008; 136: 1468–1475 Disclosure of Interest None declared

Background Anti-Sa antibody was identified in 1994 and belongs to a class of antibodies that target citrullinated antigens. Anti-Sa antibody is highly specific for diagnosing rheumatoid arthritis (RA, but it is associated with low prevalence and sensitivity. Anti-RA33 antibody was identified in 1989 and targets RA33 complex or heterogeneous nuclear ribonucleic protein. In contrast to anti-Sa antibody, anti-RA33 antibody does not target citrullinated antigens. Both anti-Sa and anti-RA33 antibodies are considered as specific serological markers for RA. However, studies assessing the diagnostic value of these antibodies in RA have provided inconsistent results. Objectives The aim of this study is to evaluate the diagnostic performance of anti-Sa and anti-RA33 antibodies in RA. Methods PubMed, Embase, and Cochrane library databases were searched for relevant studies and 2 meta-analyses were performed to determine the diagnostic accuracy of anti-Sa and anti-RA33 antibodies in patients with RA. Results The meta-analysis included 17 studies. Of these, 9 studies, which included 1,095 patients and 1,667 controls, were on anti-Sa antibody and 8 studies, which included 905 patients and 835 controls, were on anti-RA33 antibody. Pooled sensitivity and specificity of anti-Sa antibody were 39.5% (95% confidence interval [CI], 36.5–42.4) and 96.8% (95% CI, 95.9–97.4), respectively, and those of anti-RA33 antibody were 31.8% (95% CI, 28.7–35.0) and 90.1% (95% CI, 87.8–92.1), respectively. PLR, NLR, and DOR of anti-Sa antibody were 14.11 (95% CI, 7.076–28.13), 0.607 (95% CI, 0.558–0.703, and 22.76 (95% CI, 11.10–46.69), respectively, and those of anti-RA33 antibody were 3.429 (95% CI, 2.039–5.765), 0.761 (95% CI, 0.681–0.851), and 4.597 (95% CI, 2.602–8.121), respectively. AUC and Q * index for anti-Sa antibody were 0.558 and 0.543, respectively, while those for anti-RA33 antibody were 0.501 and 0.500, respectively. Conclusions Our meta-analysis indicated that both anti-Sa and anti-RA33 antibodies were highly specific and the PLR of anti-Sa antibody was very useful for diagnosing RA, although they were not sensitive for diagnosing RA. Disclosure of Interest None declared

Background Accurate and early diagnosis of rheumatoid arthritis (RA) is vital for the timely implementation of a comprehensive treatment aimed at halting or slowing its progression (1). The sensitivity of existing biomarkers, rheumatoid factor (RF) and anti-cyclic citrullinated peptide antibodies (anti-CCP) is low (2). It requires a new diagnostic biomarker with better performance in RA. Objectives To evaluate the diagnostic value of anti-RA33 (3) test in a simple of RA patientes and controls of Bogota, Colombia, by measuring its sensitivity, specificity, positive and negative likehood ratio compared to RF and anti-CCP. Additionally, to asses the association between clinical and serological variables with the functional impairment degree in patients with RA. Methods A cross-sectional study in a sample of 80 RA patients and 20 controls without RA who attended to outpatient service in two hospitals of Bogota from 2014 until 2015 was conducted by measuring their sociodemographic characteristics, arthritis activity degree by DAS-28 index, functional ability by HAQ-DI score and serological status for anti-RA33, RF and anti-CCP. A statistic analysis with proportions, summary and dispersion measures, contingency tables for measure of sensitivity, specificity, likehood ratios, ROC curves and multiple linear regression analysis was performed. Results Sensitivity score for anti-RA33, RF and anti-CCP was 15%, 85% and 93% respectively; while specificity was 100%, 90% and 85% respectively. The positive likelihood ratio was 8.5 for RF and 6.2 for anti-CCP. Finally, negative likelihood ratio was 0.87 for anti-RA33, 0.16 for RF and 0.08 for anti-CCP. The anti-RA33 seropositive patients were greater arthritis activity and functional disability as well as higher titers of RF and anti-CCP although these differences were not statistically significant. Finally, a moderately strong positive correlation was found between DAS-28 and HAQ-DI scores (R 2 =0.51). In the multiple linear regression model, DAS-28 index was the only predictor variable that explained the changes in the HAQ-DI functional ability score. Conclusions Findings suggest that anti-RA33 test does not seem to have any clinical utility for the diagnosis of RA in Colombian population. The importance of DAS-28 activity index as a score of association with functional disability in patients with RA was confirmed. References Torpy JM, Perazza GD, Golub RM. Rheumatoid Arthritis. JAMA 2011;305(17):1824. Chang PY, Yang CT, Cheng CH, Yu KH. Diagnostic performance of anti-cyclic citrullinated peptide and rheumatoid factor in patients with rheumatoid arthritis. Int J Rheum Dis. 2015 May 4. Hassfeld W, Steiner G, Hartmuth K, Kolarz G, Scherak O, Graninger W, Thumb N, Smolen JS. Demonstration of a new antinuclear antibody (anti-RA33) that is highly specific for rheumatoid arthritis. Arthritis Rheum. 1989 Dec;32(12):1515–20 Disclosure of Interest None declared

Background Rheumatoid arthritis (RA) is a chronic inflammatory disease affecting the synovial joints, often with a progressive and destructive course, associated with the production of wide range of autoantibodies, and their detection has diagnostic and prognostic implication. Objectives This study was to estimate the diagnostic value of antibodies against cyclic citrullinated peptide (ACCP) and nuclear antigen RA33 of the IgA rheumatoid factor (RF) versus the value of routinely used profile of autoantibodies in diagnostic work-up of RA. Methods We identified 230 patients with RA prehistory of varying duration. The control group was comprised of 96 patients, including patients with seronegative spondyloarthropathies (SpA), Psoriatic Arthritis (PsA) and diffuse connective tissue diseases, as well as sex and age matched healthy controls. Serum levels of IgM and IgA RF, antibodies against cyclic citrullinated peptide (ACCP), antibodies against RA33 antigen (ARA33) and antinuclear factor (ANF) were measured in all patients and controls. Results Diagnostic sensitivity of ACCP equaled 81%, IgM RF - 76%, IgA RF - 46%, ARA33 - 36% and ANF - 29%. ACCP was significantly more commonly associated with IgM RF. Among RF seronegative patients ACCP were found in 37% cases with 26 IU/Ml detection threshold, and in 26% - with 32 IU/Ml, allowing to increase diagnostic specificity of the test up to 93% with the increment of diagnostic threshold. Incidence of ARA33 was not significantly different among the RF and ACCP positive or negative subgroups, thus making ARA33 an independent RA marker. Specificity of this marker was 83,4%, thus making it inferior to RF and ACCP by a composite of diagnostic characteristics. Conclusions The measurement of RA33 is a rational approach at the next second stage of serologic testing work-up in suspected cases of RA onset, when initial RF and ACCP tests were negative. References Emery P., Breedveld F.C., Dougados M. et al. Early referral recommendation for newly diagnosed rheumatoid arthritis: evidence based development of a clinical guide. Ann Rheum Dis 2002;61(4):290-7. Malakoutikhah M., Gomara M.J., Gomez-Puerta J.A. et al. The use of chimeric vimentin citrullinated peptides for the diagnosis of rheumatoid arthritis. J Med Chem 2011;54(21):7486-92. Schneeberger E., Citera G., Heredia M. et al. Clinical significance of anti-Ro antibodies in rheumatoid arthritis. Clin Rheumatol 2008;27(4):517-9. Pincus T., Sokka T. Laboratory tests to assess patients with rheumatoid arthritis: advantages andlimitations.Rheum Dis Clin North Am 2009;35(4):731-4. Aletaha D., Neogi T., Silman A.J. et al. Rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Ann Rheum Dis 2010;69(9):1580-8. Metz C.E. Basic principles of ROC analysis. Semin Nucl Med 1978;8(4):283-98. Nell V.P., Machold K.P., Stamm T.A. et al. Autoantibody profiling as early diagnostic and prognostic tool forrheumatoid arthritis. Ann Rheum Dis 2005;64(12):1731-6. Nell-DuxneunerV., Machold K., Stamm T. et al. Autoantibody profiling in patients with very early rheumatoid arthritis: a follow-up study. Ann Rheum Dis 2010;69(1):169-74. Acknowledgements All employees of Department of Rheumatology National Center of Cardiology and Internal Medicine, Bishkek, Kyrgyz Republic Disclosure of Interest None declared

Background Systemic sclerosis (SSc) is an autoimmune disease characterized by the occurrence of a wide range of autoantibodies (Aab) which can predict distinct clinical features of SSc. Aab to hnRNP A2 and its alternatively spliced variants B1 (anti-hnRNP B1) and B2 are generally referred to as anti-RA33 and have been extensively studied in rheumatoid arthritis (RA) [1]. However, the prevalence of anti-RA33 Aab in other autoimmune diseases, such as scleroderma, mixed connective tissue disease and systemic vasculitides, is far from determined [2–4]. Objectives To compare the frequency of anti-hnRNP B1 with other SSc-specific Aab and to determine an association thereof with the clinical phenotype in patients with SSc Methods We studied Aab prevalence in 64 patients with SSc, 29 with diffuse cutaneous SSc and 26 with limited cutaneous disease as well as 9 patients with overlap syndrome. Diagnosis of SSc in all patients was based on 1980 ACR (ARA) criteria and the disease phenotype was analyzed according to LeRoy9s classification criteria [7]. Serum samples from clinically healthy blood donors (n=174) were used as a control group. Skin involvement and disease severity was measured with Rodnan9s skin score and Valentini activity index. Vascular involvement was accessed by measurement of pulse wave velocity (PWV) and augmentation index (AI) with applanation tonometry (SphygmoCor system, AtCor Medical Pty Ltd., Sydney, Australia). Anti-hnRNP B1 IgG was assessed by an ELISA employing recombinant human hnRNP B1 expressed in E.coli (in.vent DIAGNOSTICA GmbH, Germany). SSc-specific Aab were measured with line immunoassay (Euroimmun AG, Germany) according to the manufacturer9s instructions. Results Anti-hnRNP B1 were found in 18.5% (12/64) of SSc patients and in 1.1% (2/174) of controls (p Conclusions Anti-hnRNP B1 (RA33) is an independent serological marker in SSc and is associated with vascular involvement. References Nell-Duxneuner Vet al. Ann Rheum Dis. 2010; 69(1):169-74. Tomoum HY et al. Pediatr Int. 2009;51(2):188-92. Siapka Set al. Autoimmunity. 2007;40(3):223-33. Cho SBetal.J Invest Dermatol. 2012;132:601-8. Hoffmann MH et al. J Immunol. 2007;179(11):7568-76. Steiner Get al. ClinExpRheumatol. 2002 Jul-Aug;20(4):517-24. LeRoy EC, et al. J Rheumatol 1988; 15:202-205. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.2222

OBJECTIVES—Systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) can both present with an erosive arthritis with the small joints of the hands affected. Therefore a serological marker would be useful to distinguish between these two diseases at onset. In this study anti-RA33 antibodies, which are found in patients with SLE and RA, and anti-citrullinated peptide antibodies (anti-CCP), which have recently been described as highly specific for RA, were assessed. METHODS—Two hundred and thirty one patients receiving long term follow up for SLE were evaluated for arthritis and classified as erosive and non-erosive disease. Sixty six patients were tested for anti-RA33 and anti-CCP antibodies. All the patients were tested for rheumatoid factor (RF) and HLA-DR4 status. RESULTS—Ten patients had erosive disease, six of whom were RF positive (60%), and six anti-RA33 positive (60%), whereas only two were anti-CCP positive (20%). Two hundred and twenty one patients had non-erosive disease, 40 of whom were RF positive (18%), 14 were anti-RA33 positive (6%), whereas only one patient was found to be anti-CCP positive (0.5%). CONCLUSION—The presence of anti-CCP antibodies may be useful in distinguishing RA from erosive SLE. Anti-RA33 antibodies and RF are unhelpful.