Abstract

The study investigated the association between disease activity and serum 25-hydroxyvitamin D3 (25(OH)-D3), B cell activation of the tumor necrosis factor family (BAFF), or β 2 microglobulin in patients with primary Sjogren's syndrome (SS). Sixty-nine primary SS patients and 22 sicca control patients were included in the study. Disease activity was measured with EULAR Sjogren's syndrome disease activity index (ESSDAI). Serum levels of 25(OH)-D3 and β 2 microglobulin were measured by radioimmunoassay and BAFF was measured by an enzyme-linked immunosorbent assay. Serum levels of 25(OH)-D3 were significantly lower in SS patients compared to the sicca controls (p = 0.036). Serum levels of BAFF tended to be higher (p = 0.225) and those of β 2 microglobulin were significantly higher in patients with SS than in sicca controls (p = 0.023). In univariate regression analyses, ESSDAI was significantly associated with serum levels of 25(OH)-D3, BAFF, and β 2 microglobulin. After stepwise backward multivariate linear regression analyses including age and acute phase reactants, ESSDAI was associated with 25(OH)-D3 (β = −0.042, p = 0.015) and BAFF (β = 0.001, p = 0.015) in SS patients. In SS patients, ESSDAI is negatively associated with serum levels of 25(OH)-D3 and positively associated with BAFF.

Highlights

  • Sjogren’s syndrome (SS) is a chronic autoimmune disease affecting the exocrine glands that manifests as sicca symptoms including dry eyes and dry mouth

  • The extraglandular manifestations are mediated in part by the overproduction of multiple autoantibodies that are often directed against nuclear antigens such as antinuclear antibody (ANA) and anti-Ro/La antibodies, which lead to hypergammaglobulinemia due to chronic polyclonal B cell activation [1]

  • Serum levels of 25(OH)-D3 were significantly lower and those of β2 microglobulin were significantly higher in patients with SS compared with age- and sexmatched sicca controls

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Summary

Introduction

Sjogren’s syndrome (SS) is a chronic autoimmune disease affecting the exocrine glands that manifests as sicca symptoms including dry eyes and dry mouth. SS often involves extraglandular organs including joints, liver, lung, brain, and kidney. The extraglandular manifestations are mediated in part by the overproduction of multiple autoantibodies that are often directed against nuclear antigens such as antinuclear antibody (ANA) and anti-Ro/La antibodies, which lead to hypergammaglobulinemia due to chronic polyclonal B cell activation [1]. Lymphocytes or autoantibodies lead to the inflammation of the target tissues directly or due to the formation of immune complexes. Chronic B cell activation plays an important role in the pathogenesis of SS [2]. Factors associated with B cell activation were reported to correlate with SS disease activity; these include serum levels of B cell activating factor belonging to the tumor necrosis factor family (BAFF) [3], β2 microglobulin [4, 5], and free light chains of immunoglobulin [6]

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