Systemic inflammatory profiles and their relationships with demographic, behavioural and clinical features in acute low back pain

- Findings point to systemic IL-6 and CRP as important contributors to inflammation in acute back pain.
- Physiological reactivity (such as pain) to IL-6 may require a threshold concentration.
- Demographic, behavioural and psychosocial factors have a likely role in shaping these responses.
- Inflammatory profiles in acute low back pain differ from those in chronic low back pain.

Systemic inflammation is linked with development and persistence of many pathological pain states. Although chronic phase inflammatory responses are well reported, the acute phase has received limited attention. Here we investigated circulating pro-inflammatory cytokines and C-reactive protein (CRP), and explored their relationships with symptom severity and other factors in acute low back pain (LBP). Ninety-nine individuals within two weeks of onset of acute LBP and 55 pain-free controls completed questionnaires related to their pain (visual analogue scale, VAS) and disability, behaviour, sleep quality and psychological status. CRP, interleukin-6 (IL-6), tumor necrosis factor (TNF) and interleukin-1β (IL-1β) were measured from serum samples. Biomarkers were compared between LBP and control participants, and in a separate analysis, for those with “high-pain” (VAS ⩾4) and “low-pain” (VAS <4). The relationships between biomarkers and all other variables, including other cytokines/CRP were assessed. CRP was higher in LBP than controls and in those with high- than low-pain (p < 0.01). IL-6 was higher in those with high- than low-pain (p < 0.05), but not controls. Various pain and non-pain factors were associated with each biomarker differently. These findings suggest systemic CRP and IL-6 are important contributors to inflammation in the early post-onset phase of LBP and that various factors can shape these responses.