# Serum visfatin in multiple sclerosis: distinct profiles in healthy controls, naive patients, and treated RRMS

## TL;DR

This study found that serum visfatin levels differ between healthy people, untreated MS patients, and those on treatment, suggesting it could be a biomarker for MS treatment response.

## Contribution

The study identifies distinct visfatin profiles across MS patient subgroups and healthy controls, suggesting its potential as a biomarker for treatment response.

## Key findings

- Healthy controls had higher visfatin levels than both naive MS and treated MS patients.
- Treated MS patients with NEDA-3 status had lower visfatin levels and disability scores.
- Visfatin levels were lowest in naive MS patients compared to other groups.

## Abstract

This study aimed to evaluate serum visfatin levels in treated patients with Relapsing-Remitting Multiple Sclerosis (RRMS) (PwMS) receiving disease-modifying therapy (DMT) and in naive MS patients (nMS), and to investigate their association with clinical characteristics, treatment status, and disease activity, including NEDA-3 status.

A total of 45 PwMS under treatment at least 1 year, 20 nMS patients, and 44 age- and sex-matched healthy controls (HC) were included. Clinical and demographic data were recorded. Serum visfatin, lipid profiles, inflammatory markers, and vitamin levels were measured. Visfatin levels were compared not only between treated and naive MS patients but also within the treated group according to NEDA-3 status and treatment type (first-line vs. second-line disease-modifying therapy). Statistical analyses were performed to assess group differences and correlations.

Visfatin levels differed significantly across the three groups (Kruskal–Wallis H = 19.701, p < 0.001). Pairwise comparisons revealed significant differences between all groups: the control group had higher visfatin levels than both the nMS (p < 0.001) and PwMS (p = 0.006). The treated group also showed higher visfatin levels compared to the naive MS group (p = 0.014). Among PwMS visfatin levels were lower than in healthy controls (p = 0.006). Among PwMS patients, those meeting the NEDA-3 criteria had lower visfatin levels and EDSS scores compared with non-NEDA patients (p = 0.008 and p = 0.006, respectively). No significant correlation was found between visfatin and relapse count or EDSS. LDL and total cholesterol levels were significantly higher in patients receiving fingolimod.

Across the three groups, visfatin levels differed significantly, with healthy controls showing the highest levels, followed by PwwMS, and the lowest levels observed in nMS patients. Lower serum visfatin levels in stable treated MS patients may reflect reduced inflammatory burden and effective immunomodulation. These findings suggest that visfatin could serve as a potential biomarker for treatment response in MS. Nevertheless, longitudinal studies including larger cohorts of naive patients are needed to clarify visfatin’s regulatory role in MS pathophysiology and its interaction with disease-modifying therapies.