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Fibromyalgia (FM) prevalence is much higher in patients with other rheumatic diseases than in the general population. This leads to increase in the perceived disease activity scores and prevents patients from reaching remission. Elucidating the pathogenesis of such “secondary” FM can help alleviate some unmet needs in these diseases. Methods: MEDLINE and Scopus databases were searched for a scoping review for hypothesis generation regarding the genesis of secondary FM. Results: FM has been postulated to be due to cytokine dysfunction, neurogenic neuroinflammation, stress, including social defeat, sleep disturbances, sympathetic overactivity, and small fibre neuropathy. These factors increase in most autoimmune and autoinflammatory diseases. Further the evidence for the role of these factors in the pathogenesis of FM is seems strong. Metabolic syndrome and mitochondrial dysfunction are also associated with FM, but it is difficult to distinguish between cause and effect. Conclusion: FM is the common phenotype arising from the amalgamation of various aetiologies. Recruitment or amplification of the above 6 factors by various rheumatic diseases may thus lead precipitation of secondary FM in susceptible individuals.

PATHOGENESIS OF FIBROMYALGIA IN PATIENTS WITH AUTOIMMUNE DISEASES: SCOPING REVIEW FOR HYPOTHESIS GENERATION