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158 Clinical and serological correlations of autoantibodies directed against RNP-C in systemic lupus erythematosus
  1. May Choi1,
  2. Ann E Clarke2,
  3. Michelle Jung3,
  4. Claire Barber2,
  5. Yvan St Pierre4,
  6. Michael Mahler5 and
  7. Marvin Fritzler3
  1. 1Cumming School of Medicine, University of Calgary
  2. 2Division of Rheumatology, Cumming School of Medicine, University of Calgary
  3. 3University of Calgary
  4. 4Department of Medicine, Division of Rheumatology, Faculty of Medicine, McGill University
  5. 5Inova Diagnostics


Background Autoantibodies to RNP-C protein, along with RNP-A, is a component of the U1RNP macromolecular complex. Antibodies to U1-RNP are typically associated with mixed connective tissue disease and other systemic autoimmune rheumatic diseases. Autoantibodies to RNP-C or their clinical significance have not been thoroughly studied in systemic lupus erythematosus (SLE). The goals of this study were to determine the frequency of anti-RNP-C autoantibodies in a SLE cohort and identify demographic, clinical, and serologic correlations.

Methods Patients fulfilling the ACR or SLICC Classification Criteria for SLE were enrolled in a local cohort. Demographic, clinical information (disease activity SLEDAI-2K; damage SLICC/ACR Damage Index (SDI)), and sera were collected at time of enrollment. Antibodies to anti-RNP-C were determined by a line immunoassay using a purified, full-length recombinant protein Euroimmun GmbH, Luebeck, Germany). Univariable and multivariable analysis were performed to determine associations between the prevalence of high positive anti-RNP-C and demographic (age, sex, race/ethnicity), clinical features (SLICC/ACR classification criteria, SLEDAI-2K and SDI total scores and subscales from SLEDAI-2K), medications, and other autoantibodies.

Results 138 SLE patients were included; 89.1% were female with a mean age of 46.1 years (SD 18.1 years) and disease duration of 13.7 years (SD 11.6 years). The prevalence of anti-RNP-C antibodies was 19.6% (27/138); 25.9% (7/27) were male. Univariable analysis demonstrated that patients fulfilling a higher total SLICC criteria (Odds Ratio, OR, 1.4 [95% Confidence interval, CI: 1.1–1.7]), particularly maculopapular rash (OR 4.0 [95% CI: 1.3–11.9]) and pericardial effusion (OR 6.3 [95% CI: 1.3–29.9]), or a higher SLEDAI score (OR 1.2 [95% CI: 1.0–1.3]) were more likely to be anti-RNP-C positive. Also, patients with higher immunological SLICC subscales (OR 1.8 [95% CI: 1.2–2.5]), anti-dsDNA (OR 7.6 [95% CI: 2.6–21.9]), anti-Sm (OR 29.7 [95% CI: 9.8–89.9]), anti-RNP (OR 44.2 [95% CI: 12.0–163.4]), anti-nucleosome (OR 9.4 [95% CI: 2.5–35.0]), anti-Ribosomal P (OR 7.4 [95% CI: 2.5–22.5]), or anti-RNP-A (OR 153.8 [95% CI: 35.8–660.5]) were associated with anti-RNP-C positivity. Patients who were female (OR 0.2 [95% CI: 0.1–0.7]), had longer disease duration (OR 0.9 [95%CI: 0.9–1.0]), or were on steroids (OR 0.3 [95% CI: 0.1–0.7]) were less likely to be anti-RNP-C positive. Multivariable analysis demonstrated that patients who were anti-RNP-A positive (OR 78.5 [95% CI: 6.5–941.2]) were more likely to be anti-RNP-C positive while those who were female (OR 0.1 [95% CI: 0.01–1.0]) were less likely to be anti-RNP-C positive.

Conclusions Anti-RNP-C antibodies were common (19.6%) in our SLE cohort. In SLE, they were associated with anti-RNP-A antibodies, a finding which is in keeping with the concept of inter-molecular epitope spreading. Most notably, anti-RNP-C antibodies were more likely seen to be seen in males with SLE. A thorough study of male SLE patients is needed.

Funding Source(s): The Arthritis Society Chair in Rheumatic Diseases at the Cumming School of Medicine, University of Calgary

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