Effects of spinal manipulative therapy on inflammatory mediators in patients with non-specific low back pain: a non-randomized controlled clinical trial.

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  • Additional Information
    • Source:
      Publisher: BioMed Central Country of Publication: England NLM ID: 101551481 Publication Model: Electronic Cited Medium: Internet ISSN: 2045-709X (Electronic) Linking ISSN: 2045709X NLM ISO Abbreviation: Chiropr Man Therap Subsets: MEDLINE
    • Publication Information:
      Original Publication: London : BioMed Central
    • Subject Terms:
      Inflammation Mediators/*metabolism ; Low Back Pain/*therapy ; Manipulation, Spinal/*methods; Adult ; Female ; Humans ; Interferons/metabolism ; Interleukin 1 Receptor Antagonist Protein/metabolism ; Interleukins/metabolism ; Male ; Tumor Necrosis Factor-alpha/metabolism ; Young Adult
    • Abstract:
      Background: The inflammatory profiles of patients with acute and chronic nonspecific low back pain (LBP) patients are distinct. Spinal manipulative therapy (SMT) has been shown to modulate the production of nociceptive chemokines differently in these patient cohorts. The present study further investigates the effect(s) of SMT on other inflammatory mediators in the same LBP patient cohorts.
      Methods: Acute (n = 22) and chronic (n = 25) LBP patients with minimum pain scores of 3 on a 10-point numeric scale, and asymptomatic controls (n = 24) were recruited according to stringent exclusion criteria. Blood samples were obtained at baseline and after 2 weeks during which patients received 6 SMTs in the lumbar or lumbosacral region. The in vitro production of tumor necrosis factor (TNFα), interleukin-1 β (IL-1β), IL-6, IL-2, interferon ɣ (IFNɣ), IL-1 receptor antagonist (IL-1RA), TNF soluble receptor type 2 (sTNFR2) and IL-10 was determined by specific immunoassays. Parametric as well as non-parametric statistics (PAST 3.18 beta software) was used to determine significance of differences between and within study groups prior and post-SMT. Effect size (ES) estimates were obtained using Cohen's d.
      Results: Compared with asymptomatic controls, SMT-related change scores were significant (P = 0.03-0.01) in reducing the production levels of TNFα in both patient cohorts and those of IL-6, IFNɣ and sTNFR2 (P = 0.001-0.02) in patients with chronic LBP. Above-moderate to large ES (d > 0.6-1.4) was observed for these mediators. Compared with respective baselines, a significant post-SMT reduction (P = 0.01) of IL-6 production was detected only in patients with chronic LBP while a significant increase of IL-2 production (P = 0.001 vs. control, and P = 0.004 vs. chronic LBP group) and a large ES (d = 0.87) were observed in patients with acute LBP. Pain and disability scores declined significantly (P < 0.001) in all LBP patients, and were positively correlated (P = 0.03) with IFNɣ and IL-2 levels in the acute LBP cohort.
      Conclusion: The short course of SMT treatments of non-specific LBP patients resulted in significant albeit limited and diverse alterations in the production of several of the mediators investigated in this study. This exploratory study highlights the potential of SMT to modulate the production of inflammatory components in acute and chronic non-specific LBP patients and suggests a need for further, randomized controlled clinical trials in this area.
      Trial Registration: This study was prospectively registered April 2012 with Clinical Trials.gov ( #NCT01766141 ). https://register.clinicaltrials.gov/prs/app/action/SelectProtocol?sid=S0003ZIL&selectaction=Edit&uid=U0001V74&ts=2&cx=-axvqtg.
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    • Contributed Indexing:
      Keywords: Cytokine; Inflammatory mediators; Low back pain; Spinal manipulation
    • Molecular Sequence:
      ClinicalTrials.gov NCT01766141
    • Accession Number:
      0 (Inflammation Mediators)
      0 (Interleukin 1 Receptor Antagonist Protein)
      0 (Interleukins)
      0 (Tumor Necrosis Factor-alpha)
      9008-11-1 (Interferons)
    • Publication Date:
      Date Created: 20210108 Date Completed: 20210812 Latest Revision: 20210812
    • Publication Date:
      20221213
    • Accession Number:
      PMC7792327
    • Accession Number:
      10.1186/s12998-020-00357-y
    • Accession Number:
      33413508