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Relationship between Vitamin D and Nonspecific Low Back Pain May Be Mediated by Inflammatory Markers
Hao-Wei Xu1, Shu-Bao Zhang1, Yu-Yang Yi1
1Department of Spinal Surgery, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.
Background:
Vitamin D deficiency has been linked to nonspecific low back pain (Ns-LBP); however, the role of inflammation as a possible mediator between vitamin D levels and Ns-LBP is not well understood.
Objective:
To explore the mediating effects of inflammatory markers on the relationship between vitamin D levels and pain outcomes.
Study Design:
A retrospective study.
Setting:
Department of Spinal Surgery of a hospital affiliated to a medical university.
Methods:
In this cross-sectional study, we selected patients with non-specific acute low back pain (Ns-ALBP, n = 60) and non-specific chronic low back pain (Ns-CLBP, n = 78), as well as 60 people without Ns-LBP as controls, from January 2018 to January 2019. Serum 25(OH)D and inflammatory marker levels were examined. Regression and causal mediation analysis were used to evaluate the mediating effects of inflammatory markers on the association between vitamin D and pain.
Results:
Mean serum concentrations of vitamin D in the control, Ns-ALBP, and Ns-CLBP groups were 25.70 ± 10.04, 21.44 ± 8.46 and 18.25 ± 8.05 ng/mL, respectively (P < 0.001). After adjustment for clinical factors, vitamin D deficiency was associated with Ns-LBP (P < 0.05); however, when the interleukin 6 (IL-6) level was added to the multivariable models, the association was no longer significant in Ns-CLBP patients. Mediation analysis estimated the overall mediated effect as -0.461 (P < 0.001) in Ns-CLBP patients, and the intermediary effect of IL-6 was 0.045.
Limitations:
A retrospective study may include inevitable bias. More sensitive biomarkers were not investigated in this study. Pain intensity evaluation using the visual analogue scale is inevitably subjective.
Conclusion:
Patients with Ns-LBP had lower vitamin D and higher inflammatory marker levels. This association between hypovitaminosis D and Ns-CLBP may be mediated by IL-6. Therefore, large-scale clinical trials are warranted to investigate the clinical efficacy of vitamin D supplementation for decreasing inflammation and relieving Ns-LBP.
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