Fibromyalgia (FM) is characterized by chronic widespread musculoskeletal pain along with a broad spectrum of associated psychosomatic manifestations, such as fatigue, sleep disturbances, generalized stiffness, depression, anxiety, and cognitive impairment. The underlying mechanism of FM is central sensitization, which is thought to arise from both congenital and acquired neuroendocrine dysfunctions, as well as autoimmune processes. FM is among the most common comorbidities in patients with rheumatoid arthritis (RA). While the general population prevalence of FM is 2–4%, it reaches 15–30% in patients with RA (averaging about 20%). Given that the prevalence of FM in early RA is much lower (4–9%), it is likely that FM develops progressively as RA advances. This increased prevalence may be driven by a shared mechanism of chronic pain related to nociceptive system dysfunction. FM significantly worsens the clinical picture in RA patients: these patients report more intense pain, greater fatigue, worse functional capacity, a higher number of tender joints, and poorer patient global assessments – factors that inflate disease activity scores such as DAS28, CDAI, and SDAI. FM is also a major contributor to suboptimal responses to biologic DMARDs and Janus kinase inhibitors (JAKi) in RA patients. The coexistence of RA and FM may define a specific phenotype known as non-inflammatory refractory rheumatoid arthritis (NIRRA), distinguished among difficult-to-treat RA variants. Timely diagnosis of FM is essential for personalizing RA treatment and avoiding unnecessary switching of biologics and JAKi. However, management of RA patients with coexisting FM remains poorly developed. Promising strategies include the use of IL-6 inhibitors and JAKi, which have demonstrated good analgesic potential and the ability to reduce nociceptive dysfunction. FM treatment should also involve antidepressants, anticonvulsants, and non-pharmacological interventions.
Каратеев et al. (Thu,) studied this question.