Department of Clinical, Internal, Anesthesiologic and Cardiovascular Sciences, Sapienza University di Roma, 00185 Rome, Italy.
Int J Mol Sci. 2024 May 29;25(11):5922. doi: 10.3390/ijms25115922.
Fibromyalgia (FM) is a chronic disease characterized by widespread musculoskeletal pain of unknown etiology. The condition is commonly associated with other symptoms, including fatigue, sleep disturbances, cognitive impairment, and depression. For this reason, FM is also referred to as FM syndrome. The nature of the pain is defined as nociplastic according to the latest international classification and is characterized by altered nervous sensitization both centrally and peripherally. Psychosocial conditions have traditionally been considered critical in the genesis of FM. However, recent studies in animal models and humans have provided new evidence in favor of an inflammatory and/or autoimmune pathogenesis. In support of this hypothesis are epidemiological data of an increased female prevalence, similar to that of autoimmune diseases, and the frequent association with immune-mediated inflammatory disorders. In addition, the observation of an increased incidence of this condition during long COVID revived the hypothesis of an infectious pathogenesis. This narrative review will, therefore, discuss the evidence supporting the immune-mediated pathogenesis of FM in light of the most current data available in the literature.
纤维肌痛(FM)是一种以不明病因的广泛肌肉骨骼疼痛为特征的慢性疾病。这种疾病通常与其他症状有关,包括疲劳、睡眠障碍、认知障碍和抑郁。因此,FM 也被称为 FM 综合征。根据最新的国际分类,疼痛的性质被定义为神经病理性疼痛,其特征是中枢和外周的神经敏化改变。心理社会状况一直被认为是 FM 发病的关键因素。然而,最近在动物模型和人类中的研究为炎症和/或自身免疫发病机制提供了新的证据。支持这一假设的有流行病学数据表明女性患病率增加,类似于自身免疫性疾病,以及与免疫介导的炎症性疾病的频繁关联。此外,在长新冠期间观察到这种疾病的发病率增加,再次提出了感染性发病机制的假说。因此,本综述将根据文献中最新的可用数据,讨论支持 FM 免疫介导发病机制的证据。