Abstract
Earlier studies suggest that lumbar radicular pain following disc herniation may be associated with a local or systemic inflammatory process. In the present study, we investigated the serum inflammatory protein profile of such patients. All 45 patients were recruited from Oslo University Hospital, Ullevål, Norway, during the period 2007–2009. The new multiplex proximity extension assay (PEA) technology was used to analyze the levels of 92 proteins. Interestingly, the present data showed that patients with radicular pain 12 months after disc herniation may be different from other patients with regard to many measurable serum cytokines. Given a false discovery rate (FDR) of 0.10 and 0.05, we identified 41 and 13 proteins, respectively, which were significantly upregulated in the patients with severe pain one year after disc herniation. On the top of the list ranked by estimated increase we found C-X-C motif chemokine 5 (CXCM5; 217% increase), epidermal growth factor (EGF; 142% increase), and monocyte chemotactic protein 4 (MCP-4; 70% increase). Moreover, a clear overall difference in the serum cytokine profile between the chronic and the recovered patients was demonstrated. Thus, the present results may be important for future protein serum profiling of lumbar radicular pain patients with regard to prognosis and choice of treatment. We conclude that serum proteins may be measurable molecular markers of persistent pain after disc herniation.
Highlights
Lumbar radicular pain, referred to as “sciatica,” is characterized by radiating pain that typically follows the dermatome of the affected nerve-root
Our results indicate that the proximity extension assay (PEA) technology may be important for future protein serum profiling of lumbar radicular pain patients with regard to prognosis and choice of treatment
Among these 76 proteins, we identified 41 with false discovery rate (FDR) < 0.10 and 13 with FDR < 0.05, which were considered upregulated in the patients with severe pain one year after disc herniation (Table 2)
Summary
Referred to as “sciatica,” is characterized by radiating pain that typically follows the dermatome of the affected nerve-root. Earlier studies suggest that leakage of nucleus pulposus into the spinal canal after disc herniation may initiate immunological and inflammatory responses close to the nerve-roots [5, 6] that increase the activity in nociceptive pathways [7,8,9,10,11]. This inflammatory influence has been attributed to an upregulation of interleukins (ILs), tumor necrosis factor (TNF), matrix metalloproteinases (MMPs), nitric oxide (NO), and prostaglandins (PGs) in or around the herniated disc [12,13,14]
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