Background Pro-inflammatory cytokines released from the intervertebral disc are considered key in the pathogenesis of sciatica. There is increasing interest in whether biologics such as anti-TNF therapies could be used for treatment of sciatica. Data has shown increased cytokine expression in lumbar disc and CSF samples. Fewer studies have examined whether serum cytokine levels are associated with sciatica.
Objectives To compare the levels of cytokines and other inflammatory markers in patients with sciatica with those with low back pain (LBP) alone.
Methods GP consulters aged >18 with LBP and sciatica were recruited. Participants underwent a standardised clinical assessment, lumbar spine MRI and had serum samples taken. Participants were classified as having MRI confirmed disc prolapse with nerve root compression or not and by their leg pain intensity (VAS >7, yes/no). Key cytokines, chemokines and matrix metalloproteinases (MMPs) implicated in sciatica pathogenesis including TNFα, IL-1,IL-6, MMP1,3,8, aggregan and monocyte chemoattractant protein-1 (MCP-1/CCL-2) were assayed in duplicate using commercial multiplex detection kits and measured with a Luminex suspension array system. Median levels were compared between the groups.
Results Of the 17 biomarkers tested, patients with MRI defined radiculopathy (n=53) had higher levels of MCP-1 than those without (n=63) (median MCP-1 level 301.4 vs 255.7 pg/ml, p=0.04). Patients with severe leg pain and MRI changes (n=30) also had higher levels of MCP-1 than those without (n=85) (median MCP-1 315.9 vs 256.7 pg/ml, p=0.009). None of the other cytokines including TNF, IL-6 or other pro-inflammatory markers showed significant differences between the groups (either by leg pain intensity or MRI radiculopathy).
Conclusions In this cohort, levels of the chemokine MCP-1 appeared to be higher in patients with positive MRI findings than in patients with low back pain alone. No significant differences in serum TNF or IL-6 levels was seen between patients with sciatica and those with LBP alone. Further studies are required to confirm this finding and investigate further the role of MCP-1 in sciatica pathogenesis.
Acknowledgements We acknowledge the participating patients and GP practices together with the support of the ATLAS study team and the research staff at the Haywood Hospital
Disclosure of Interest None declared