Staines Donald R
Gold Coast Public Health Unit, 10-12 Young Street, Southport, Qld 4215, Australia.
Med Hypotheses. 2004;62(5):665-9. doi: 10.1016/j.mehy.2004.01.003.
Fibromyalgia (FM) is a disorder characterised by soft tissue pain, disturbance of function an often prolonged course and variable fatigue and debility. A clearly defined aetiology has not been described. This paper proposes that immunological aberration is likely and this may prove to be associated with an expanding group of novel vasoactive neuropeptides. Vasoactive neuropeptides act as hormones, neurotransmitters, immune modulators and neurotrophes. They are readily catalysed to small peptide fragments. They and their binding sites are immunogenic and are known to be associated with a range of autoimmune conditions. They have a vital role in maintaining vascular flow in organs, and in thermoregulation, memory and concentration. They are co-transmitters for acetylcholine, are potent immune regulators with primarily anti-inflammatory activity, and have a significant role in protection of the nervous system to toxic assault and the maintenance of homeostasis. Failure of these substances has adverse consequences for homeostasis. This paper describes a biologically plausible mechanism for the development of FM based on loss of immunological tolerance to the vasoactive neuropeptides. The proposed mechanism of action is that inflammatory cytokines are provoked by tissue injury from unaccustomed exercise or physical injury. This may trigger a response by certain vasoactive neuropeptides which then undergo autoimmune dysfunction as well as affecting their receptor binding sites. The condition may potentially arise de novo perhaps in genetically susceptible individuals. FM is postulated to be an autoimmune disorder and may include dysfunction of purine nucleotide metabolism and nociception.
纤维肌痛（FM）是一种以软组织疼痛、功能障碍、病程常迁延、疲劳和身体虚弱多变为特征的疾病。尚未描述明确的病因。本文提出免疫异常很可能存在，且这可能被证明与一组不断扩大的新型血管活性神经肽有关。血管活性神经肽可作为激素、神经递质、免疫调节剂和神经营养因子。它们很容易被催化成小肽片段。它们及其结合位点具有免疫原性，并且已知与一系列自身免疫性疾病有关。它们在维持器官的血管血流以及体温调节、记忆和注意力方面起着至关重要的作用。它们是乙酰胆碱的共同递质，是主要具有抗炎活性的强效免疫调节剂，并且在保护神经系统免受毒性攻击和维持体内平衡方面具有重要作用。这些物质的功能失调会对体内平衡产生不利影响。本文描述了一种基于对血管活性神经肽免疫耐受性丧失而导致纤维肌痛发生的生物学上合理的机制。所提出的作用机制是，不习惯的运动或身体损伤引起的组织损伤会引发炎性细胞因子。这可能触发某些血管活性神经肽的反应，然后这些神经肽会发生自身免疫功能障碍并影响其受体结合位点。这种情况可能在遗传易感个体中可能会从头发生。纤维肌痛被推测是一种自身免疫性疾病，可能包括嘌呤核苷酸代谢和伤害感受功能障碍。
