Abstract

Vitamin D (VitD) insufficiency is common in multiple sclerosis (MS). VitD has possible anti-inflammatory effects on the immune system. The ratio between VitD metabolites in MS patients and the severity of the disease are suggested to be related. However, the exact effect of the bone-derived hormone fibroblast-growth-factor-23 (FGF23) and VitD binding protein (VDBP) on this ratio is not fully elucidated yet. Therefore, the aim is to study differences in total, free, and bioavailable VD metabolites and FGF23 between MS patients and healthy controls (HCs). FGF23, vitD (25(OH)D), active vitD (1,25(OH)2D), inactive 24,25(OH)D, and VDBP were measured in 91 MS patients and 92 HCs. Bioavailable and free concentrations were calculated. No difference in FGF23 (p = 0.65) and 25(OH)D/24.25(OH)2D ratio (p = 0.21) between MS patients and HCs was observed. Bioavailable 25(OH)D and bioavailable 1.25(OH)2D were lower (p < 0.01), while VDBP concentrations were higher in MS patients (p = 0.02) compared with HCs, specifically in male MS patients (p = 0.01). In conclusion, FGF23 and 25(OH)D/24.25(OH)2D did not differ between MS patients and HCs, yet bioavailable VitD concentrations are of potential clinical relevance in MS patients. The possible immunomodulating role of VDBP and gender-related differences in the VD-FGF23 axis in MS need further study.

Highlights

  • Multiple sclerosis (MS) is a chronic, progressive disease of the central nervous system characterized by an inflammatory, demyelinating, and neurodegenerative process, which can result in varying levels of disability

  • Previous research showed a higher plasma vitamin D binding protein (VDBP) concentration in MS patients compared with healthy controls (HCs) [21]

  • We found gender differences in vitamin D metabolism: serum concentrations of total 25(OH)D, 25(OH)D3, 24.25(OH)2 D, free 25(OH)D, and free 1.25(OH)2 D were lower in female MS

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Summary

Introduction

Multiple sclerosis (MS) is a chronic, progressive disease of the central nervous system characterized by an inflammatory, demyelinating, and neurodegenerative process, which can result in varying levels of disability. VDBP is known to play an important role in the intracellular actin scavenging system by removing actin derived from damaged tissue and promotes inflammation [22,23,24,25,26]. Polymorphisms of both VDBP and of the vitamin D receptor (VDR) can result in a changed equilibrium between active and inactive vitamin D metabolites [24,27,28]

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