Study design: Retrospective analysis wherein 103 patients were considered, and 76 patients were included: 49 were classified as chronic non-specific low back pain (CNSLBP) (Study group) and 27 had identifiable cases of specific chronic low back pain (LBP) (Control group).
Objective: Elucidate markers of systemic inflammation in patients with CNSLBP.
Summary of background data: Mechanisms of LBP are poorly understood. Pro-inflammatory cytokines are increased in obesity and involved with pain modulation; we previously proposed a theoretical model of their mediating role in LBP.
Methods: Demographic information was acquired via questionnaire, chart review, and blood test data. Univariate analysis identified factors associated with CNSLBP and markers of systemic inflammation. A receiver operating curve and Youden Index were used to select optimal cut-off points for elevated C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Multivariable logistic regression analysis calculated the adjusted strength of relationship between factors that were proposed in our theoretical model for CNSLBP.
Results: Unadjusted CRP was significantly correlated with ESR (R = 0.63, P < 0.0001) and body mass index (BMI) (R = 0.38, P = 0.0015). Physically inactive patients had significantly higher CRP (6.1 vs. 1.2, P = 0.0050). ESR was significantly correlated with number of comorbidities (R = 0.34, P = 0.0047), BMI (R = 0.38, P = 0.0014), and age (R = 0.36, P = 0.0026). Physically inactive patients (10.4 vs. 3.6, P = 0.0001) and females (11.2 vs. 6.4, P = 0.0422) had significantly higher ESR. Adjusted analyses indicated significant relationships between physical inactivity and markers of systemic inflammation (adjusted odds ratios for ESR and CRP: 15.9, P = 0.0380; 15.2, P = 0.0272, respectively), and between elevated CRP and CNSLBP (adjusted odds ratio: 8.0, P = 0.0126).
Conclusion: Systemic inflammation may act as a mediator for physical inactivity and obesity in the pathogenesis of CNSLBP.
Level of evidence: 2.