Abstract

Patients with autoimmune disorders often have low levels of 25-hydroxyvitamin D [25(OH)D3], which correlates with disability or disease activity. Vitamin D may play a role in neuromyelitis optica (NMO) or NMO spectrum disorder (NMOSD), as an important factor involved in immunological pathways. We investigated the relationship between vitamin D levels and disease related disability and clinical activity in patients with NMOSD. Blood samples from 51 patients with NMOSD who were positive for anti-aquaporin4-antibody (AQP4-ab) and 204 healthy controls were collected for 25(OH)D3 measurement. Clinical parameters, including expanded disability status scale (EDSS) score, annualized relapse rate (ARR) and time of blood sampling relative to attack, were determined in patients with NMOSD. We found that 25(OH)D3 levels were significantly lower in patients with NMOSD compared to healthy controls. There was no difference between 25(OH)D3 levels in blood samples taken at relapse or remission, and no association between 25(OH)D3 levels and ARR, but there was an inverse correlation between 25(OH)D3 levels and EDSS scores in patients with NMOSD. It remains to be determined whether low vitamin D levels predispose to NMO and/or modify disease severity, or are secondary to neurological disability. In either case the results could also be of relevance to other neurological diseases such as multiple sclerosis as well as NMO.

Highlights

  • Vitamin D3 is a prohormone produced by the action of ultraviolet (UV) on 7-dehydrocholesterol in the skin

  • Comparison of vitamin D levels between patients with neuromyelitis optica (NMO) spectrum disorder (NMOSD) and healthy controls We found that 25(OH)D3 levels were significantly lower in patients with NMOSD compared to age, sex- and seasonmatched healthy controls (p,0.001) (Figure 1A)

  • In the analysis according to the season, vitamin D levels sampled in the spring, summer, fall, and winter were all significantly lower in patients with NMOSD than those in healthy controls (p,0.001, p = 0.006, p = 0.033, and p,0.001 respectively) (Figure 1B)

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Summary

Introduction

Vitamin D3 is a prohormone produced by the action of ultraviolet (UV) on 7-dehydrocholesterol in the skin. Vitamin D suppresses B cell proliferation and differentiation to decrease immunoglobulin secretion and affects T cell proliferation and maturation to decrease the numbers of T cells with Th1 and Th17 phenotypes [1,2] It induces T regulatory (Treg) cells to decrease the production of inflammatory cytokines, such as interleukin (IL)-17 and IL-21[3]. These effects of vitamin D were evidenced in in vivo studies, where vitamin D suppressed disease in animal models of autoimmune diseases, such as multiple sclerosis (MS), systemic lupus erythematosus (SLE), and type 1 diabetes [4,5,6]. Vitamin D levels have been reported to be associated with disease disability or activity in these disorders [8,9,10]

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