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Primary Sjögren’s syndrome (pSS) is an autoimmune late onset disease characterised mainly by sicca symptoms. Lymphocytic infiltrate of the minor salivary glands and the presence of autoantibodies are the hallmarks of disease.1 The spectrum of pSS extends from an organ-specific autoimmune disorder (autoimmune exocrinopathy) to a systemic process that may involve the musculoskeletal system, leading to arthralgias and arthritis. In the latter case differential diagnosis with other autoimmune diseases like rheumatoid arthritis (RA) is a challenge.
In these situations, specific antibodies may be useful for making a correct diagnosis and, consequently, guide treatment. Anti-cyclic citrullinated peptide (anti-CCP) antibodies have been shown to be a specific marker for the diagnosis of RA.2 They bind to determinants rich in the unusual amino acid, citrulline, generated by deamination of arginine.3 We have read the recent article by Gottenberg et al,4 in which a 7.5% prevalence of anti-CCP antibodies in 134 French patients with pSS was reported. Here, we describe a similar experience in Colombian patients with pSS.
We evaluated 53 patients who fulfilled the classification criteria of the American-European Consensus Group for pSS,5 and 79 patients with RA fulfilling the American College of Rheumatology classification criteria,6 of whom nine had secondary SS to RA. All patients with SS had a minor salivary gland biopsy disclosing a lymphocytic infiltrate with a focus score >1. Demographics and cumulative clinical and laboratory manifestations over the course of disease for the patients with SS were obtained and classified according to the terminology proposed by Oxholm et al.7 No patient with pSS met the RA classification criteria.
Anti-CCP antibodies were determined by enzyme linked immunosorbent assay (ELISA) using the anti-CCP2 kit QUANTA lite (INOVA Diagnostics Inc, San Diego, CA, USA). Levels above 60 IU were considered positive. Five (9%) patients with pSS tested positive for anti-CCP antibodies, and table 1 shows their main characteristics. Demographic and clinical characteristics of these five patients were not significantly different from those with pSS who were negative for anti-CCP antibodies, including articular involvement (arthralgias and/or arthritis). It should be noted that their long duration of disease (12.6 (7) years) together with a lack of erosions on x ray examination do not support a diagnosis of RA. Sixty six (84%) patients with RA were positive for anti-CCP antibodies (p<0.001); clinical and immunogenetic characteristics of these patients are described elsewhere.8 Six of nine (67%) patients with secondary SS to RA tested positive for anti-CCP antibodies.
Our results indicate a low prevalence of anti-CCP antibodies in pSS. However, an anti-CCP positive test in patients with suggestive SS does not rule out the diagnosis of pSS, even in the presence of articular involvement. In addition, a positive anti-CCP test in patients with pSS is not necessarily a risk for articular involvement or development of RA. Further studies are warranted to elucidate the role of anti-CCP antibodies in pSS.
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