Abstract

IntroductionFatigue is prevalent in primary Sjögren's syndrome (pSS), and contributes to the considerably reduced health related quality of life in this disease. The symptom is included in proposed disease activity and outcome measures for pSS. Several studies indicate that there is an inflammatory component of fatigue in pSS and other chronic inflammatory rheumatic diseases. The purpose of this study was to investigate fatigue change in pSS in a longitudinal study, and explore whether any clinical or laboratory variables at baseline, including serum cytokines, were associated with a change in fatigue scores over time.MethodsA clinical and laboratory investigation of 141 patients fulfilling the American-European consensus criteria of pSS was undertaken in the period May 2004 to April 2005. Median time since diagnosis was 5.5 years. Examinations included the fatigue questionnaires: fatigue severity scale (FSS), fatigue visual analogue scale (VAS), functional assessment of chronic illness therapy - fatigue (FACIT-F) and medical outcome study short form-36 (SF-36) vitality, which were repeated in a follow-up investigation in January and February 2010.ResultsA total of 122 patients (87%) responded at both time-points. Thirty-five percent of patients experienced a clinically significant FSS increase. On the group level, fatigue measures did not change except that there was a slight deterioration in SF-36 vitality score. High serum anti-Sjögren's syndrome A antigen (anti-SSA) showed weak associations with high baseline fatigue, and patients with increasing fatigue had lower baseline unstimulated whole salivary volume. Weak associations between increasing fatigue and serum immunoglobulin G (IgG), and the pro-inflammatory cytokine interleukin-17 (IL-17), were observed. Baseline sicca symptoms correlated with higher fatigue both at baseline and with increasing fatigue over time. Linear regression analysis did not identify any predictive ability of clinical or laboratory measures on fatigue change over time.ConclusionsFatigue remained mainly unchanged over time. Using multivariate models did not reveal any clinical or laboratory predictors of fatigue change over time.

Highlights

  • Fatigue is prevalent in primary Sjögren’s syndrome, and contributes to the considerably reduced health related quality of life in this disease

  • The assay comprises analyses of 25 cytokines: IL-1b, IL-1 receptor antagonist (IL-1Ra), IL-2, IL-2 receptor, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-13, IL-15, IL-17, tumour necrosis factor (TNF), IL-12p40, interferon (IFN)-g, IFN-a, granulocyte macrophage colony-stimulating factor (GM-CSF), monokine induced by IFN-g (MIG), monocyte chemotactic protein-1 (MCP-1), IFN-ginduced protein 10 kDa (IP-10), macrophage inflammatory protein (MIP)-1a, MIP-1b, eotaxin and Regulated upon Activation, Normal T-cell Expressed, and Secreted (RANTES)

  • In 122 primary Sjögren’s syndrome (pSS) patients, fatigue measured by fatigue severity scale (FSS), FACIT-F, vitality and fatigue visual analogue scale (VAS) showed no significant change during a mean follow-up time of 5.2 years, except a weak vitality worsening

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Summary

Introduction

Fatigue is prevalent in primary Sjögren’s syndrome (pSS), and contributes to the considerably reduced health related quality of life in this disease. Several studies indicate that there is an inflammatory component of fatigue in pSS and other chronic inflammatory rheumatic diseases. Primary Sjögren’s syndrome (pSS) is a systemic rheumatic autoimmune disease targeting, in particular, exocrine glands, with eye and mouth dryness as classic symptoms. In rheumatic diseases, it is debated whether fatigue is independently associated with disease activity. Rituximab treatment was associated with fatigue improvement in two small double-blind, randomised studies, the most extensive of which included 20 pSS patients receiving rituximab and 10 receiving a placebo [10,11]. Cerebrospinal IL-1 receptor antagonist (IL-1Ra) levels showed an association with fatigue in a pSS study [13]

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