Is Fibromyalgia an Autoimmune Disease?
Fibromyalgia is not an autoimmune disease. It is a chronic pain syndrome characterized by abnormal central pain processing and central sensitization, not by immune-mediated tissue damage or inflammation. 1, 2
Pathophysiological Classification
Fibromyalgia is classified as a "nociplastic" pain condition, which is fundamentally distinct from autoimmune or inflammatory disorders. 2 The key distinguishing features include:
No organic tissue damage or inflammation is present in fibromyalgia, and normal laboratory results (including inflammatory markers) support rather than exclude the diagnosis. 2
The primary pathophysiology involves peripheral and central hyperexcitability at spinal or brainstem level, altered pain perception, and inadequate filtering of nociceptive signals by descending antinociceptive pathways (central sensitization). 1
There is no evidence that inflammatory, infectious, or autoimmune disorders are etiological events in the development of fibromyalgia, despite these mechanisms being frequently proposed. 3
Clinical Implications of This Distinction
This classification has critical treatment implications:
Corticosteroids are not recommended for fibromyalgia management, as they lack efficacy in conditions without inflammatory or autoimmune mechanisms. 1, 2
The absence of autoimmune pathology means that immunosuppressive therapies have no role in fibromyalgia treatment. 3
Treatment should focus on central pain modulation through medications like amitriptyline, duloxetine, and pregabalin, which enhance descending pain inhibition or reduce excitatory neurotransmitter release. 2
Common Diagnostic Pitfall
A critical error occurs when clinicians pursue extensive autoimmune workup in patients with fibromyalgia. Normal laboratory results, including negative autoimmune markers, support the diagnosis of fibromyalgia rather than suggesting an alternative diagnosis. 2 The diagnosis is clinical, based on widespread pain in all four quadrants for at least 3 months plus pain on palpation in at least 11 of 18 specific tender points. 2
Evidence Quality Note
While some recent research has investigated inflammatory and immune mechanisms that may develop concurrently with central sensitization in fibromyalgia 4, and neuroinflammation with stress peptides has been proposed 5, these represent secondary phenomena rather than primary autoimmune pathology. The highest quality guidelines from EULAR consistently characterize fibromyalgia as a condition of abnormal pain processing without immune-mediated tissue damage. 1, 2