Background Dysregulation of the immune system may play a role in chronic widespread pain (CWP)^1–3 although study findings so far are inconsistent.

Objectives This cross-sectional study examined whether basal inflammatory markers and the innate immune response are associated with the presence and severity of CWP

Methods Data are from the Netherlands Study of Depression and Anxiety including 1632 subjects. The Chronic Pain Grade questionnaire was used to determine the presence and severity of CWP. Subjects were categorized in a CWP group (n=754) and a control group (n=878). Blood levels of the basal inflammatory markers C-reactive protein (CRP), interleukin (IL)-6 and tumor necrosis factor (TNF-) alpha were determined. To obtain a measure of the innate immune response, 13 inflammatory markers were assessed after lipopolysaccharide (LPS) stimulation in a random subsample (n=707).

Results Compared to controls, subjects with CWP showed elevated levels of basal inflammatory markers. However, this association was no longer significant after adjustment for lifestyle and disease factors. For the LPS-stimulated inflammatory markers, we did find elevated levels in CWP subjects both before and after adjustment for covariates. Within CWP subjects, pain severity was not associated with inflammation.

Conclusions This study demonstrates an exaggerated innate immune response in CWP. Elevated basal inflammatory levels in CWP were driven by lifestyle and disease factors. We suggest that the innate immune response could be a potential biomarker for the onset or perpetuation of CWP.

References

1. Di FM, Iannuccelli C, Valesini G. Neuroendocrine immunology of fibromyalgia. Ann N Y Acad Sci 2010; 1193:84-90.

2. Menzies V, Lyon DE. Integrated review of the association of cytokines with fibromyalgia and fibromyalgia core symptoms. Biol Res Nurs 2010; 11(4):387-394.

3. Kwok YH, Hutchinson MR, Gentgall MG, Rolan PE. Increased responsiveness of peripheral blood mononuclear cells to in vitro TLR 2, 4 and 7 ligand stimulation in chronic pain patients. PLoS One 2012; 7(8):e44232.

Acknowledgements This manuscript is part of the PhD programme investigating neurobiological dysregulation in chronic pain, funded through The European League Against Rheumatism (EULAR). The infrastructure for the NESDA study (www.nesda.nl) is funded through the Geestkracht program of the Netherlands Organisation for Health Research and Development (Zon-Mw, grant number 10-000-1002) and is supported by participating universities and mental health care organisations (VU University Medical Center, GGZ inGeest, Arkin, Leiden University Medical Center, GGZ Rivierduinen, University Medical Center Groningen, Lentis, GGZ Friesland, GGZ Drenthe, IQ Healthcare, Netherlands Institute for Health Services Research (NIVEL) and Netherlands Institute of Mental Health and Addiction (Trimbos). Assaying of basal inflammatory markers was supported by the Neuroscience Campus Amsterdam. Assaying of LPS-stimulated inflammatory markers was supported by Hersenstichting Nederland (2011(1)-134) and Myriad RBM, Austin, TX.

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.1495