Clinical and Serological Features of Sjogren Syndrome in Patients with Rheumatoid Arthritis

Background: It is uncertain whether the Sjogren Syndrome (SS) associated with Rheumatoid Arthritis (RA) represents a clinical entity similar to primary SS (pSS) or merely a manifestation in the clinical spectrum of RA. In the present study, we sought to determine the clinic and serologic features of SS associated with RA in comparison to the RA features using well defined SS classification criteria.
Methods: RA patients successively referred for a biologic infusion were questioned on oral and ocular dryness. Schirmer’s test and unstimulated salivary flow were performed in each patient. Patients with subjective oral or ocular dryness and/or 1 abnormal objective test underwent a minor salivary gland biopsy. The diagnosis of secondary SS was based on the criteria of European-American consensus group criteria for SS. Clinical and biological parameters of SS and RA (with measure of disease activity and health status of RA, search for Raynaud’s phenomenon, anti-CCP, RF anti-SSA-positivity and beta2-microglobulin level) were then compared between patients with/without sSS.
Results: Among the 76 patients prospectively assessed, 11(14.1%) fulfilled the European-American consensus group criteria for secondary SS. Median age and RA disease duration were similar in patients with sSS as in patients with RA only (63.0 v 59.2, p=0;33; 18.2 vs 13.9, p= 0.12). Median DAS28-ESR and HAQ were not significantly different between patients with sSS and patient with RA only (4.0 vs 4.1, p= 0.8; 0.84 vs 0.81, p=0.7). Patients with sSS had more frequently a Raynaud’s phenomenon (27.2 vs 1.5%, p=0.01). RF and anti-CCP-positivity were similar in the 2 groups. The prevalence of anti-SSA antibodies was comparable in the 2 groups (p=1). Median beta2-microglobulin levels were higher in sSS than RA only (2.4 vs 1.9 mg/l, p= 0.02).
Conclusion: 14% of patients with RA had secondary SS in the present study. Conversely to previous reports, secondary SS did not modify the clinical and biologic pattern of RA.