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. 2022 Aug;10(8):e676.
doi: 10.1002/iid3.676.

Profiling vitamin D, its mediators and proinflammatory cytokines in rheumatoid arthritis: A case-control study

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Profiling vitamin D, its mediators and proinflammatory cytokines in rheumatoid arthritis: A case-control study

Samuel A Sakyi et al. Immun Inflamm Dis. 2022 Aug.

Abstract

Introduction: The active form of vitamin D has immunomodulatory and anti-inflammatory effect. Vitamin D is implicated in pathogenesis of rheumatoid arthritis (RA) and its deficiency leads to increased inflammation. Moreover, its production is dependent on concentration of calcium, phosphorus, and parathyroid hormone (PTH). Cytokines mediates inflammation in RA synovium. This study evaluated vitamin D, its mediators and proinflammatory cytokines among RA patients.

Methods: In a case-control study, 78 RA patients from Komfo Anokye Teaching Hospital rheumatology clinic and 60 healthy blood donors were recruited. Chemistry analyzer and enzyme-linked immunosorbent assay kits were used to measure biochemical parameters and cytokines.

Results: We found significantly higher levels of interleukin (IL)-1β, interferon gamma (IFN-γ), and tumor necrosis factor-α (TNF-α) in RA patients compared with controls (p < .05). There was a significant positive correlation between intact parathyroid hormone (iPTH) and IL-10 (r = .30, p < .05) and a negative correlation between IL-6 (r = -0.28, p > .05), IL-1β (r = -0.25, p > .05), TNF-α (r = -0.26, p > .05), IFN-γ (r = -0.24, p > .05), and iPTH. There was a significant negative correlation between IL-1β (r = -0.33, p < .05), IFN- γ (r = -0.29, p < .05), and calcium.

Conclusion: Reduced PTH, calcium, and phosphorus is associated with higher levels of proinflammatory cytokines which may worsen RA disease condition. Vitamin D is therefore not an independent regulator of proinflammatory cytokines in RA.

Keywords: mediators of vitamin D; parathyroid hormone; phosphorus; proinflammatory cytokines; rheumatoid arthritis.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Levels of inflammatory cytokine between controls and RA patients. (A) IL‐1β, (B) IL‐10 (C) TNF‐α, (D) IFN‐γ, and (E) IL‐6. (ns: p > .05, *p ≤ .05, **p ≤ .01, ***p ≤ .001, ****p ≤ .0001). IFN‐γ, interferon gamma; IL, interleukin; RA, rheumatoid arthritis; TNF‐α, tumor necrosis factor‐α
Figure 2
Figure 2
Correlation between 25 VD and cytokines among RA patients: (A) IL‐1β, (B) IL‐10, (C) TNF‐α, (D) IFN‐γ, and (E) IL‐6. IFN‐γ, interferon gamma; IL, interleukin; RA, rheumatoid arthritis; TNF‐α, tumor necrosis factor‐α

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