Association of Anticentromere Antibodies With More Severe Exocrine Glandular Dysfunction in Sjögren's Syndrome: Analysis of the Sjögren's International Collaborative Clinical Alliance Cohort

Objective Anticentromere antibodies (ACAs) define a subset of primary Sjögren's syndrome (SS) with a unique phenotype, including features of limited cutaneous systemic sclerosis and a lower frequency of anti‐SSA/SSB antibodies. We sought to determine whether ACAs are associated with more severe...

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Published inArthritis care & research (2010) Vol. 68; no. 10; pp. 1554 - 1559
Main Authors Baer, Alan N., Medrano, Leah, McAdams‐DeMarco, Mara, Gniadek, Thomas J.
Format Journal Article
LanguageEnglish
Published United States 01.10.2016
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Summary:Objective Anticentromere antibodies (ACAs) define a subset of primary Sjögren's syndrome (SS) with a unique phenotype, including features of limited cutaneous systemic sclerosis and a lower frequency of anti‐SSA/SSB antibodies. We sought to determine whether ACAs are associated with more severe exocrine glandular dysfunction in a large cohort of primary SS subjects. Methods We performed a cross‐sectional analysis of 1,361 subjects with primary SS from the Sjögren's International Collaborative Clinical Alliance Registry, stratified by the presence or absence of ACAs. ACAs were assayed by immunofluorescence staining on HEp‐2 cells. Results ACAs were present in 82 of the 1,361 SS subjects (6%) and were associated with older age, female sex, and lower frequencies of anti‐SSA/SSB, rheumatoid factor, and hyperglobulinemia. Among ACA‐positive versus ACA‐negative subjects, there was a higher frequency of a focus score ≥2 (71% versus 53%; P = 0.002), a higher median focus score (2.8 versus 2.5; P = 0.0440), and greater exocrine gland dysfunction: Schirmer's test value: median 4 versus 5 mm/5 minutes; P = 0.0003, and unstimulated whole saliva (UWS) flow rate: median 0.08 versus 0.37 ml/5 minutes; P < 0.0001. ACA‐positive subjects had an increased risk of UWS <0.1 ml/minute (odds ratio [OR] 12.24 [95% confidence interval (95% CI) 4.91–41.02]) and Schirmer's test value <5 mm/5 minutes (OR 2.52 [95% CI 1.50–4.36]) after correcting for age, sex, anti‐SSA/SSB, and focus score. Labial gland fibrosis was not different between the 2 groups. Conclusion In a large international registry of SS, ACA had an independent association with more severe exocrine glandular dysfunction. This dysfunction was associated with more pronounced labial salivary glandular inflammation but not fibrosis.
Bibliography:Supported by a contract from the NIH/National Institute of Dental and Craniofacial Research (NO1‐DE‐32636) and the Jerome L. Greene Foundation. Dr. Baer's work was supported by the NIH (grant R01‐DE‐12354‐15A1). Dr. McAdams‐DeMarco's work was supported by the NIH (grant K01‐AG‐043501). Data and specimens used in this manuscript are from the Sjögren's International Collaborative Clinical Alliance Biorepository, funded under contract HHSN26S201300057C by the National Institute of Dental and Craniofacial Research.
This manuscript was prepared using a publicly available Sjögren's International Collaborative Clinical Alliance (SICCA) data set and does not necessarily reflect the opinions or views of the SICCA investigators, the NIH, or the National Institute of Dental and Craniofacial Research.
Dr. Baer has received consulting fees from Glenmark and Bristol Myers Squibb (less than $10,000 each).
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ISSN:2151-464X
2151-4658
DOI:10.1002/acr.22859