4.6 Article

Relationship between systemic inflammation and recovery over 12 months after an acute episode of low back pain

Journal

SPINE JOURNAL
Volume 22, Issue 2, Pages 214-225

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.spinee.2021.09.006

Keywords

Depression; Low back pain (LBP); Recovery; Sleep; Systemic inflammation; Transition to chronicity

Funding

  1. National Health and Medical Research Council (NHMRC) of Australia [ID631369, APP1091302]
  2. NHMRC Investigator Grant Leadership 3 Fellowship [APP1194937]
  3. U.S. Department of Defense through the FY19 Chronic Pain Management Research Program [W81XWH2010909]
  4. U.S. Department of Defense (DOD) [W81XWH2010909] Funding Source: U.S. Department of Defense (DOD)

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Individual characteristics may influence the recovery and systemic inflammation of individuals with early-acute low back pain. Different subgroups of patients with specific biopsychosocial features exhibited distinct trajectories of recovery and inflammation.
BACKGROUND CONTEXT: Individual characteristics can influence outcomes after injury. Our previous work in individuals with early-acute low back pain (LBP) identified subgroups (clusters) with specific biopsychosocial features that recovered poorly or well by 6 months. PURPOSE: This study extends on that work by revealing the short- and long-term trajectories of recovery and systemic inflammation of these participant clusters: (1) inflammatory & poor sleep (Cluster 1), high TNF & depression (Cluster 2), high pain & high pain-related fear (Cluster 3), and low pain & low pain-related fear (Cluster 4). STUDY DESIGN/SETTING: Longitudinal cohort study. PATIENT SAMPLE: Eighty-three individuals within 2 weeks of an acute episode of LBP - grouped into their a priori-defined cluster. OUTCOME MEASURES: General participant characteristics (sex, age, body mass index, smoking history, previous LBP history); self-reported LBP (0-10 numerical rating scale, LBP-related disability (Roland-Morris Disability Questionnaire), depression (Center for Epidemiological Studies Depression Scale, pain catastrophizing (Pain Catastrophizing Scale), fear avoidance (Fear Avoidance Beliefs Questionnaire), pain self-efficacy (Pain Self-Efficacy Questionnaire), and sleep (Pittsburgh Sleep Quality Index); systemic inflammatory biomarkers (C-reactive protein [CRP], interleukin-6 [IL-6], interleukin-1 beta, tumor necrosis factor [TNF]). METHODS: Participants provided blood for the measurement of CRP/cytokines, and completed questionnaires related to their pain/disability, psychological and sleep status. Blood measures were repeated 3-monthly for 9 months, and pain/disability were self-reported fortnightly for 12 months. Recovery (change in pain) and CRP/cytokines were longitudinally compared between clusters using mixed-models. Associations between baseline factors and follow-up CRP/cytokines levels were assessed with multiple regression. RESULTS: Clusters 1 and 2 were associated, but oppositely, with recovery over the 12-months. Cluster 1 reported most recovery at every 3-monthly interval, whereas Cluster 2 reported least recovery. Cluster 1 had elevated CRP (and IL-6) at baseline that continued to decrease from 3 to 9 months. TNF was elevated early and persistently in Cluster 2. Baseline factors other than inflammation generally failed to predict follow-up inflammation. CONCLUSIONS: Findings support the early role of CRP (and perhaps IL-6) in control of inflammation and recovery, and a pathological role of persistent TNF overexpression, which may be perpetuated by depressive-like behaviors. (C) 2021 Elsevier Inc. All rights reserved.

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