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AB0193 Antibodies to Hnrnp B1 (RA33) in Patients with Systemic Sclerosis
  1. A. Maslyanskiy1,
  2. D. Roggenbuck2,
  3. S. Lapin3,
  4. A. Mazing3,
  5. N. Lazareva3,
  6. E. Ilivanova4,
  7. E. Kolesova5,
  8. V. Mazurov6
  1. 1Rheumatology, Almazov Medical Research Centre, Saint-Petersburg, Russian Federation
  2. 2Brandenburg Technical University Cottbus-Senftenberg, Berlin, Germany
  3. 3Laboratory of Autoimmune Diagnostics, St. Petersburg Pavlov State Medical University
  4. 4Rheumatology, Leningrad Regional Clinical Hospital
  5. 5Cardiology, Almazov Medical Research Centre
  6. 6Rheumatology, North-Western State Medical University named after I.I. Mechnicov, Saint-Petersburg, Russian Federation

Abstract

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 LeRoy's 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 Rodnan's 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 manufacturer's instructions.

Results Anti-hnRNP B1 were found in 18.5% (12/64) of SSc patients and in 1.1% (2/174) of controls (p<0.001). Median concentrations were also significantly higher in SSc patients (p<0.001). There were no significant associations of anti-hnRNP B1 level with any other particular SSc-specific Aab, clinical form of the SSc, degree of skin involvement, and clinical activity. We found that anti-hnRNP B1 antibodies directly correlated with the presence (r=0.33 p=0.009) of arterial hypertension and vessel-wall stiffness parameters like PWV (r=0.39, p=0.004) and AI (r=0.35, p<0.001).

Conclusions Anti-hnRNP B1 (RA33) is an independent serological marker in SSc and is associated with vascular involvement.

References

  1. Nell-Duxneuner Vet al. Ann Rheum Dis. 2010; 69(1):169-74.

  2. Tomoum HY et al. Pediatr Int. 2009;51(2):188-92.

  3. Siapka Set al. Autoimmunity. 2007;40(3):223-33.

  4. Cho SBetal.J Invest Dermatol. 2012;132:601-8.

  5. Hoffmann MH et al. J Immunol. 2007;179(11):7568-76.

  6. Steiner Get al. ClinExpRheumatol. 2002 Jul-Aug;20(4):517-24.

  7. LeRoy EC, et al. J Rheumatol 1988; 15:202-205.

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.2222

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