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Association Between the Plasma Levels of Mediators of Inflammation With Pain and Disability in the Elderly With Acute Low Back Pain: Data From the Back Complaints in the Elders (BACE)-Brazil Study.
Spine 2016 Februrary
STUDY DESIGN: Cross-sectional study with subsample of elderly women with acute low back pain (LBP), from Back Complaints in the Elders-Brazil (BACE-Brazil)
OBJECTIVE: To investigate the association between plasma levels of mediators of inflammation (interleukin-1 beta (IL-1β), IL-6, tumor necrosis factor alpha (TNF-α), and soluble TNF receptor 1 (sTNF-R1)) with pain and disability experienced by elderly women with acute LBP.
SUMMARY OF BACKGROUND DATA: Among the elderly, LBP is a complaint of great importance and can lead to disability. Inflammatory cytokines are elevated in painful conditions, and may promote pain.
METHODS: We included 155 community-dwelling elderly women (age ≥ 65 yr), who presented with a new (acute) episode of LBP. Enzyme-linked immunosorbent assays were used to measure TNF-α, sTNF-R1, IL-1β, and IL-6. Disability was assessed using the Roland Morris Disability Questionnaire; pain was assessed using the McGill Pain Questionnaire. Linear regression models were fit with each pain and disability outcome as dependent variables: Present Pain Intensity; Qualities of pain; Severity of pain in the last week; LBP frequency and disability.
RESULTS: Depressive symptoms and IL-6 were associated and explained 20.9% of "qualities of pain" variability. TNF-α, sTNFR1, education, body mass index, and depressive symptoms explained 8.4% of "Severity of pain in the past week" variability. TNF-α, education, BMI, depressive symptoms, present pain intensity, qualities of pain, and LBP frequency explained 48.6% of "disability." No associations between inflammatory cytokines and "present pain intensity" and "LBP frequency" were found.
CONCLUSION: Our results demonstrate associations between inflammatory markers (TNF-α and sTNFR1) and pain severity, IL-6 was associated with the qualities of pain, and TNF-α was also associated with disability. These inflammatory mediators represent new markers to be considered in the assessment and treatment of elderly patients with LBP.
LEVEL OF EVIDENCE: 5.
OBJECTIVE: To investigate the association between plasma levels of mediators of inflammation (interleukin-1 beta (IL-1β), IL-6, tumor necrosis factor alpha (TNF-α), and soluble TNF receptor 1 (sTNF-R1)) with pain and disability experienced by elderly women with acute LBP.
SUMMARY OF BACKGROUND DATA: Among the elderly, LBP is a complaint of great importance and can lead to disability. Inflammatory cytokines are elevated in painful conditions, and may promote pain.
METHODS: We included 155 community-dwelling elderly women (age ≥ 65 yr), who presented with a new (acute) episode of LBP. Enzyme-linked immunosorbent assays were used to measure TNF-α, sTNF-R1, IL-1β, and IL-6. Disability was assessed using the Roland Morris Disability Questionnaire; pain was assessed using the McGill Pain Questionnaire. Linear regression models were fit with each pain and disability outcome as dependent variables: Present Pain Intensity; Qualities of pain; Severity of pain in the last week; LBP frequency and disability.
RESULTS: Depressive symptoms and IL-6 were associated and explained 20.9% of "qualities of pain" variability. TNF-α, sTNFR1, education, body mass index, and depressive symptoms explained 8.4% of "Severity of pain in the past week" variability. TNF-α, education, BMI, depressive symptoms, present pain intensity, qualities of pain, and LBP frequency explained 48.6% of "disability." No associations between inflammatory cytokines and "present pain intensity" and "LBP frequency" were found.
CONCLUSION: Our results demonstrate associations between inflammatory markers (TNF-α and sTNFR1) and pain severity, IL-6 was associated with the qualities of pain, and TNF-α was also associated with disability. These inflammatory mediators represent new markers to be considered in the assessment and treatment of elderly patients with LBP.
LEVEL OF EVIDENCE: 5.
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