氧化应激涉及纤维肌痛症病态疼痛症状的表型调节。

Oxidative stress involves phenotype modulation of morbid soreness symptoms in fibromyalgia.

机构信息

Department of Neurology, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.

School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.

出版信息

RMD Open. 2023 Mar;9(1). doi: 10.1136/rmdopen-2022-002741.

DOI:10.1136/rmdopen-2022-002741

PMID:36918228

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10016302/

Abstract

OBJECTIVES

Muscle soreness occurs after exercise and also in musculoskeletal diseases, such as fibromyalgia (FM). However, the nosography and pathoetiology of morbid soreness in FM remain unknown. This study aimed to investigate the morbid soreness of FM, evaluate its therapeutic responses and probe its pathophysiology with metabolomics profiling.

METHODS

Patients with newly diagnosed FM were prospectively recruited and completed self-report questionnaires pertaining to musculoskeletal symptoms. The phenotypes and metabotypes were assessed with variance, classification and correlation analyses.

RESULTS

Fifty-one patients and 41 healthy controls were included. Soreness symptoms were prevalent in FM individuals (92.2%). In terms of manifestations and metabolomic features, phenotypes diverged between patients with mixed pain and soreness symptoms (FM-PS) and those with pain dominant symptoms. Conventional treatment for FM did not ameliorate soreness severity despite its efficacy on pain. Moreover, despite the salient therapeutic efficacy on pain relief in FM-PS cases, conventional treatment did not improve their general disease severity. Metabolomics analyses suggested oxidative metabolism dysregulation in FM, and high malondialdehyde level indicated excessive oxidative stress in FM individuals as compared with controls (p=0.009). Contrary to exercise-induced soreness, lactate levels were significantly lower in FM individuals than controls, especially in FM-PS. Moreover, FM-PS cases exclusively featured increased malondialdehyde level (p=0.008) and a correlative trend between malondialdehyde expression and soreness intensity (r=0.337, p=0.086).

CONCLUSIONS

Morbid soreness symptoms were prevalent in FM, with the presentation and therapeutic responses different from FM pain conditions. Oxidative stress rather than lactate accumulation involved phenotype modulation of the morbid soreness in FM.

TRIAL REGISTRATION NUMBER

NCT04832100.

摘要

目的

运动后会出现肌肉酸痛，骨关节炎等疾病也会出现肌肉酸痛，如纤维肌痛症（fibromyalgia，FM）。然而，FM 病理性疼痛的发病机制尚不清楚。本研究旨在探讨 FM 的病理性疼痛，评估其治疗反应，并通过代谢组学分析探讨其病理生理学机制。

方法

前瞻性招募新诊断的 FM 患者，并完成与肌肉骨骼症状相关的自我报告问卷。采用方差分析、分类和相关性分析评估表型和代谢型。

结果

共纳入 51 例 FM 患者和 41 例健康对照者。FM 患者普遍存在疼痛症状（92.2%）。从表现和代谢组学特征来看，疼痛伴疼痛症状（FM-PS）和疼痛为主症状患者的表型存在差异。FM 常规治疗虽然对疼痛有效，但不能改善疼痛严重程度。此外，尽管 FM-PS 患者常规治疗对缓解疼痛有显著疗效，但不能改善其整体疾病严重程度。代谢组学分析表明 FM 存在氧化代谢紊乱，与对照组相比，FM 患者的丙二醛水平升高，表明氧化应激过度（p=0.009）。与运动引起的疼痛不同，FM 患者的乳酸水平明显低于对照组，尤其是 FM-PS 患者。此外，FM-PS 患者仅表现出丙二醛水平升高（p=0.008），丙二醛表达与疼痛强度之间存在相关性趋势（r=0.337，p=0.086）。