Effect of vitamin D on serum markers of bone turnover in SLE in a randomised controlled trial

Abstract

ObjectiveBone health in SLE is adversely affected by vitamin D deficiency, inflammatory cytokines and glucocorticoid use. We hypothesised that vitamin D supplementation would increase markers of bone formation and decrease markers of bone resorption in SLE subjects.MethodsWe studied 43 vitamin D-deficient SLE subjects who participated in a 12-week randomised controlled trial of 2000–4000 IU/day vitamin D supplementation versus placebo. Subjects had inactive SLE (SLE Disease Activity Index ≤4) and were taking <20 mg prednisone daily at baseline. We assayed baseline and week 12 serum 25-hydroxyvitamin D, N-terminal propeptide of type 1 collagen (P1NP) and C-telopeptide (CTX). We tested the effect of vitamin D versus placebo on change (Δ) in P1NP and ΔCTX in an intention-to-treat analysis. Secondary analyses evaluated whether vitamin D affected bone turnover among subjects achieving vitamin D repletion (≥30 ng/mL) or currently taking glucocorticoids.Results28 subjects were randomised to vitamin D and 15 to placebo. Mean age was 39 years and 40% were using glucocorticoids at enrolment. Repletion was achieved by 46% in the vitamin D group versus none in the placebo group. Changes in bone turnover markers were not significantly different in the vitamin D group versus placebo group (median ΔP1NP −0.2 vitamin D group vs −1.1 placebo group (p=0.83); median ΔCTX +3.5 vitamin D group vs −37.0 placebo group (p=0.50)). The effect of vitamin D did not differ based on achieving vitamin D repletion or baseline glucocorticoid use.ConclusionVitamin D supplementation did not affect the 12-week change in bone turnover markers among SLE subjects in this trial.

Effects of compound deer bone extract on osteoporosis model mice and intestinal microflora

“…In patients with primary osteoporosis, its expression level tends to rise. Therefore, it is listed as an important indicator for the detection of clinical diagnosis and differential diagnosis of primary osteoporosis and written into the diagnostic guidelines (Tedeschi et al., 2019).…”

Effect of 1.25(OH)2D3 on experimental autoimmune neuritis and its mechanism

“…Recent studies have shown that vitamin D plays a role in innate and specific immunity by regulating T lymphocytes; at the same time, studies have shown that vitamin D can not only affect the proliferation and maturation of T cells, but also reduce the expression of IL-17, promote the proliferation of Treg cells and enhance their immune tolerance [15,16] . Kevin et al [17] , Tedeschi et al [18] and Volt et al [19] detected that the downstream genes regulated by VDR are related to systemic lupus erythematosus and multiple sclerosis. Studies of Hau et al [20] , and Jeffery et al [21] showed that the therapeutic effect of 1.25(OH) 2 D 3 in rheumatoid arthritis and psoriasis was related to IL-17A.…”