Relationship between Vitamin D and Nonspecific Low Back Pain May Be Mediated by Inflammatory Markers.

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.

Does vitamin D status influence lumbar disc degeneration and low back pain in postmenopausal women? A retrospective single-center study.

OBJECTIVE: To investigate the relationship between serum vitamin D concentration and lumbar disc degeneration (LDD) in postmenopausal women and the epidemiologic factors affecting low back pain (LBP). METHODS: Between July 2017 and December 2018, 232 participants were retrospectively enrolled. Serum concentrations of bone turnover markers were measured using electrochemiluminescence assays. Disc degeneration was evaluated using the Pfirrmann grading system. Other variables were assessed using relevant questionnaires. RESULTS: The mean age of the women was 65.6 ±â€Š10.1 and their serum 25(OH)D concentrations were 19.38 ±â€Š9.21 ng/mL. The prevalences of severe vitamin D deficiency (<10 ng/mL) and normal status (>30 ng/mL) were 12.9% and 12.5%, respectively. The severely deficient group had higher visual analog scale (VAS) scores for LBP (P = 0.002) and lower bone mineral density T scores (P = 0.004) than the other groups. Lower 25(OH)D concentration (<10 ng/mL) was significantly associated with more severe LDD in the lumbosacral region (L4-S1, L1-S1, P < 0.05), but less so in the upper lumbar region. There was an inverse relationship between vitamin D concentration and the severity of disc degeneration (L2-L3, L4-S1, L1-S1, P < 0.05). After adjustment for confounding factors, smoking, vitamin D deficiency, lack of vitamin D supplementation, high body mass index, and low bone mineral density T score were associated with higher incidence of moderate-to-severe pain in postmenopausal women (P < 0.05). CONCLUSIONS: Vitamin D deficiency is associated with LDD and LBP in postmenopausal women. Specifically, a serum vitamin D concentration < 10 ng/mL is a marker of severe LDD and LBP. Smoking, severe vitamin D deficiency, lack of vitamin D supplementation, high body mass index, and osteoporosis are associated with a higher prevalence of moderate-to-severe pain.

Preoperative vitamin D status and its effects on short-term clinical outcomes in lumbar spine surgery.

BACKGROUND: Many studies have found that vitamin D deficiency has a high incidence rate worldwide, but we found few studies on the role of vitamin D in spinal degenerative diseases. We investigated the determinants of preoperative vitamin D deficiency and its effects on postoperative outcomes among patients undergoing elective lumbar spine surgery. METHODS: 360 patients treated from July 2017 to July 2018 were retrospectively identified for inclusion. The patients' fasting serum levels of 25(OH)D, N-terminal midfragment of osteocalcin (N-MID), and ß typeⅠcollagen carboxyl terminal peptide (ß-CTX) were measured by electrochemiluminescence before the operation. The visual analogue scale (VAS), Japanese Orthopaedic Association (JOA) and Oswestry Disability Index scores (ODI) were used to evaluate the clinical outcomes. Standard demographic data and all perioperative complications occurring within 3 months follow-up after operation were recorded. RESULTS: The mean serum level of 25(OH)D was 20.81 ± 8.55 ng/mL, the rates of deficiency (<20 ng/ml) was 53.6%. The abnormal proportion of N-MID and ß-CTX were 8.61% and 34.44%, bone turnover markers serum level was higher in older age groups (p < 0.05). Female sex (p < 0.001), a high body mass index (BMI) (p = 0.012), lack of vitamin D supplementation (p = 0.018), smoking (p = 0.033), moderate (p < 0.001) to severe pain (p = 0.005) were significant predictors of vitamin D deficiency after the multivariate analysis. The VAS, JOA and ODI scores showed significantly better outcomes compared to deficient group at post-operative and final follow-up (p < 0.05). CONCLUSION: Vitamin D deficiency was common in patients undergoing elective lumbar spine surgery. Female sex, high BMI, lack of vitamin D supplementation, smoking and moderate to severe pain were risk factors for vitamin D deficiency. Moreover, preoperative hypovitaminosis D (<20 ng/ml) was correlated with worse surgical outcomes in short-term.

[Effect of pueraria crude extreact and puerarin on ethanol-induced expression of heat shock protein 70 in embryonic mouse hippocampal cultures].

OBJECTIVE: To study if the Pueraria crude extreact (CP) and standard preparation of pure puerarin (SP) possess the same neuroprotective effects on the expression of heat shock protein (HSP) 70 in the embryonic mouse hippocampal cells. METHODS: The hippocampus of 18-days-old mouse embryo was taken out and suspension of single cells was cultured. Ethanol was added to cause HSP70 mRNA expression. Solvent, ethanol of different concentrations (50, 200, and 300 mmol/L), SP + ethanol, and SP + ethanol were added respectively. Western blotting was used to detect the expression of the expression of HSP70 mRNA. RESULTS: Ethanol of different concentrations increased the expression of HSP70 mRNA and the protein in comparison with the solvent control group. SP and CP inhibited the expression of HSP70 mRNA and protein. CONCLUSION: With identical effect of anti-oxidative stress, both SP and CP inhibit the increase of expression of HSP70 mRNA and protein, thus demonstrating I vitro anti-oxidative neuroprotection.

[Potential antiviral drug Pueraria crude extract and puerarin protect against ethanol-induced cytotoxicity in embryonic mouse hippocampal cultures].

OBJECTIVE: To examine whether Chinese medical herb Pueraria crude extract (CP) and standard of pure puerarin (SP) possess the same neuroprotective effects during concomitant ethanol (EtOH) treatment. METHODS: Hippocampus cultures were prepared from mice at gestational age of 18 day. Cell viability was measured by MTT assay. RT-PCR was employed to determine mRNA expression of superoxide dismutase (SOD). RESULTS: As measured by MTT assay, supplementation with 15 mg/L CP or 10 mg/L SP afforded neuroprotection against all EtOH concentrations (50, 200 and 350 mmol/L, respectively) in embryonic hippocampal culture system. In addition, both 15 mg/L CP and 10 mg/L SP could decrease expression of SOD at mRNA level. CONCLUSION: This study suggests that CP and SP could decrease oxidative stress induced by ethanol treatment by the decreased expression of SOD at mRNA level, and demonstrates antioxidative neuroprotective effect of CP and SP against developmental ethanol exposure in vitro.