ORIGINAL PAPER
The prevalence of ANA antibodies, anticentromere antibodies, and anti-cyclic citrullinated peptide antibodies in patients with primary Sjögren’s syndrome compared to patients with dryness symptoms without primary Sjögren’s syndrome confirmation
Submission date: 2017-06-30
Acceptance date: 2017-07-11
Online publication date: 2017-07-18
Publication date: 2017-06-30
Reumatologia 2017;55(3):113-119
KEYWORDS
TOPICS
ABSTRACT
Objectives: Our study analyses the prevalence of ANA, anti-SS-A, anti-SS-B, and ACA and ACPA antibodies in patients with pSS and with dryness symptoms without pSS confirmation, and the association of ACPA and ACA antibodies with specific clinical symptoms.
Materials and methods: 113 patients were divided into two groups: I – with diagnosed pSS (N = 75); and II – with dryness without pSS evidence (N = 38). Diagnostics: indirect immunofluorescence (IF; Hep-2 cell line) of antinuclear antibodies (ANA), anti-SS-A anti-SS-B antibodies determined with semi-quantitative method, autoantibody profile (14 antigens, ANA Profil 3 EUROLINE); basic laboratory, ophthalmic examination tests, minor salivary gland biopsy with focus score (FS), joint and lung evaluation, and ESSDAI questionnaire (pSS activity).
Results: 88% of group I had ANA antibodies (1 : 320 titre), 5.3% at 1 : 160. Anti-SS-A antibodies were present in 88% of group I, including all ANA 1 : 160. Anti-SS-A antibodies positively correlated with greater and moderate activity of ESSDAI 5 (p = 0.046) and FS. The presence of SS-B antibodies significantly affected disease activity. ACPA present: group I – 13% (associated with higher arthritis incidence; p = 0.003); group II – 8%. ACA antibodies present in 4% of group I, but not in group II. No ACA association with interstitial lung changes (small ACA + group excludes full conclusions).
Conclusions: ANA antibodies should also be considered in a titre of less than 1 : 320, but the presence of anti-SS-A antibodies is still the most important immunological marker for pSS. Anti-SS-A antibodies correlate with higher disease activity (ESSDAI ≥ 5) and higher FS. The presence of the anti-SS-B antibody was significantly affected by higher activity of the disease. The incidence of arthritis was higher in patients with ACPA+ pSS compared to ACPA– (p = 0.003). There was no relationship between ACPA and arthritis in patients with dry-type syndrome without diagnosis of pSS.
Materials and methods: 113 patients were divided into two groups: I – with diagnosed pSS (N = 75); and II – with dryness without pSS evidence (N = 38). Diagnostics: indirect immunofluorescence (IF; Hep-2 cell line) of antinuclear antibodies (ANA), anti-SS-A anti-SS-B antibodies determined with semi-quantitative method, autoantibody profile (14 antigens, ANA Profil 3 EUROLINE); basic laboratory, ophthalmic examination tests, minor salivary gland biopsy with focus score (FS), joint and lung evaluation, and ESSDAI questionnaire (pSS activity).
Results: 88% of group I had ANA antibodies (1 : 320 titre), 5.3% at 1 : 160. Anti-SS-A antibodies were present in 88% of group I, including all ANA 1 : 160. Anti-SS-A antibodies positively correlated with greater and moderate activity of ESSDAI 5 (p = 0.046) and FS. The presence of SS-B antibodies significantly affected disease activity. ACPA present: group I – 13% (associated with higher arthritis incidence; p = 0.003); group II – 8%. ACA antibodies present in 4% of group I, but not in group II. No ACA association with interstitial lung changes (small ACA + group excludes full conclusions).
Conclusions: ANA antibodies should also be considered in a titre of less than 1 : 320, but the presence of anti-SS-A antibodies is still the most important immunological marker for pSS. Anti-SS-A antibodies correlate with higher disease activity (ESSDAI ≥ 5) and higher FS. The presence of the anti-SS-B antibody was significantly affected by higher activity of the disease. The incidence of arthritis was higher in patients with ACPA+ pSS compared to ACPA– (p = 0.003). There was no relationship between ACPA and arthritis in patients with dry-type syndrome without diagnosis of pSS.
REFERENCES (25)
1.
Youinou P, Pers JO. Disturbance of cytokine networks in Sjögren’s syndrome. Arthritis Res Ther 2011; 13: 227.
2.
Maślińska M, Przygodzka M, Kwiatkowska B, Sikorska-Siudek K. Sjögren’s syndrome: still not fully understood disease. Rheumatol Int 2015; 35: 233-241.
3.
Kroese FG, Abdulahad WH, Haacke E, et al. B-cell hyperactivity in primary Sjögren’s syndrome. Exp Rev Clin Immunol 2014; 10: 483-499.
4.
Retamozo S, Brito-Zerón P, Gandía, et al. Immunological Tests in Primary Sjögren Syndrome. Ramos-Casals M, Stone JH, Moutsopoulos HM (eds.). Sjögren’s Syndrome. Springer, London 2012; 402-403.
5.
Huang YF, Cheng Q, Jiang CM, et al. The immune factors involved in the pathogenesis, diagnosis, and treatment of Sjogren’s syndrome. Clin Dev Immunol 2013; 2013: 160491.
6.
Dugar M, Cox S, Limaye V, et al. Diagnostic utility of anti-Ro52 detection in systemic autoimmunity. Postgrad Med J 2010; 86: 79-82.
7.
Yamagata H, Akizuki M, Tojo T, Homma M. Anti-Ro/SSA and -La/SSB antibodies in patients with connective tissue diseases. Scand J Rheumatol Suppl 1986; 61: 98-101.
8.
Rao L, Liu G, Li Ch, et al. Specificity of anti-SSB as a diagnostic marker for the classification of systemic lupus erythematosus. Exp Ther Med 2013; 5: 1710-1714.
9.
Bournia VK, Diamanti KD, Vlachoyiannopoulos PG, Moutsopoulos HM. Anticentromere antibody positive Sjögren’s Syndrome: a retrospective descriptive analysis. Arthritis Res Ther 2010; 12: R47.
10.
Payet J, Goulvestre C, Bialé L, et al. Anticyclic citrullinated peptide antibodies in rheumatoid and nonrheumatoid rheumatic disorders: experience with 1162 patients. J Rheumatol 2014; 41: 2395-2402.
11.
Gelber AC, Pillemer SR, Baum BJ, et al. Distinct recognition of antibodies to centromere proteins in primary Sjogren’s syndrome compared with limited scleroderma. Ann Rheum Dis 2006; 65: 1028-1032.
12.
Song G, Hu C, Zhu H, et al. New centromere autoantigens identified in systemic sclerosis using centromere protein microarrays. Rheumatology 2013; 40: 461-468.
13.
Shiboski SC, Shiboski CH, Criswell L, et al. American College of Rheumatology classification criteria for Sjögren’s syndrome: a data-driven, expert consensus approach in the Sjögren’s International Collaborative Clinical Alliance cohort. Arthritis Care Res (Hoboken) 2012; 64: 475-487.
14.
Vitali C, Bombardieri S, Jonsson R, et al. Classification criteria for Sjögren’s syndrome: a revised version of the European criteria proposed by the American-European Consensus Group. Ann Rheum Dis 2002; 61: 554-558.
15.
Kyriakidis NC, Kapsogeorgou EK, Tzioufas AG. A comprehensive review of autoantibodies in primary Sjogren’s syndrome: clinical phenotypes and regulatory mechanisms. J Autoimmun 2003; 51 C: 67-74.
16.
Nardi N, Brito-Zerón P, Ramos-Casals M, et al. Circulating auto-antibodies against nuclear and non-nuclear antigens in primary Sjögren’s syndrome: prevalence and clinical significance in 335 patients. Clin Rheum 2006; 25: 341-346.
17.
Routsias JG, Tzioufas AG. Sjögren’s syndrome – study of autoantigens and autoantibodies. Clin Rev Allergy Immunol 2007; 32: 238-251.
18.
Abrol E, González-Pulido C, Praena-Fernández JM, Isenberg DA. A retrospective study of long-term outcomes in 152 patients with primary Sjogren’s syndrome: 25-year experience. Clin Med (Lond) 2014; 14: 157-164.
19.
Shiboski CH, Shiboski SC, Seror R, et al. 2016 American College of Rheumatology/European League Against Rheumatism Classification Criteria for Primary Sjögren’s Syndrome. A Consensus and Data-Driven Methodology Involving Three International Patient Cohorts. Arthritis Rheum 2017; 69: 35-45.
20.
Baer AN, Medrano L, McAdams-DeMarco M, Gniadek TJ. Anti-centromere antibodies are associated with more severe exocrine glandular dysfunction in Sjögren’s syndrome: Analysis of the Sjögren’s International Collaborative Clinical Alliance cohort. Arthritis Care Res (Hoboken) 2016; 68: 1554-1559.
21.
Theander E, Jonsson R, Sjöström B, et al. Prediction of Sjogren’s syndrome years before diagnosis and identification of patients with early onset and severe disease course by auto-antibody profiling. Arthritis Rheum 2015; 67: 2427-2436.
22.
Salliot C, Gottenberg JE, Bengoufa D, et al. Anticentromere antibodies identify patients with Sjögren’s syndrome and autoimmune overlap syndrome. J Rheumatol 2007; 34: 2253-2258.
23.
Atzeni F, Sarzi-Puttini P, Lama N, et al. Anti-cyclic citrullinated peptide antibodies in primary Sjögren syndrome may be associated with non-erosive synovitis. Arthritis Res Ther 2008; 10: R51.
24.
He J, Ding Y, Feng M, et al. Characteristics of Sjögren’s syndrome in rheumatoid arthritis. Rheumatology (Oxford) 2013; 52: 1084-1089.
25.
Nakamura H, Kawakami A, Hayashi T. Anti-centromere antibody-seropositive Sjögren’s syndrome differs from conventional subgroup in clinical and pathological study. BMC Musculoskelet Disord 2010; 11: 140.
Copyright: © Narodowy Instytut Geriatrii, Reumatologii i Rehabilitacji w Warszawie. This is an Open Access journal, all articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License (https://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
Share
RELATED ARTICLE
| eISSN: | 2084-9834 |
| ISSN: | 0034-6233 |
We process personal data collected when visiting the website. The function of obtaining information about users and their behavior is carried out by voluntarily entered information in forms and saving cookies in end devices. Data, including cookies, are used to provide services, improve the user experience and to analyze the traffic in accordance with the Privacy policy. Data are also collected and processed by Google Analytics tool (more).
You can change cookies settings in your browser. Restricted use of cookies in the browser configuration may affect some functionalities of the website.
You can change cookies settings in your browser. Restricted use of cookies in the browser configuration may affect some functionalities of the website.
