10.3389/fpsyg.2012.00132

Vollständiger Abstract

Worum geht es in dieser Arbeit?

Rheumatoid arthritis (RA) is a systemic autoimmune disorder marked by chronic synovitis, with pathological damages extending beyond joint destruction to skeletal muscle, bone and metabolic homeostasis. Sarcopenia is conventionally regarded as age-driven degeneration, yet its high prevalence in young RA patients indicates a distinct disease-specific muscle phenotype mediated by persistent inflammation and joint disuse. This review establishes an integrated "muscle-bone-fat axis" framework to interpret RA-related myopathy: systemic inflammation and cumulative glucocorticoid exposure synergistically trigger myofibrillar proteolysis, enhance bone resorption and visceral fat accumulation. At the molecular level, catabolic cytokines overactivate the ubiquitin-proteasome pathway; impaired muscle-adipose crosstalk and mitochondrial dysfunction further disrupt muscle fiber integrity. We illustrate the limitations of age-based sarcopenia criteria when applied to RA populations, as active arthritis and pain distort handgrip strength assessment. We further compare muscle-related effects of diverse anti-rheumatic therapies: biological Disease-Modifying Anti-Rheumatic Drugs (bDMARDs) reverse systemic catabolism to preserve muscle mass, while JAK inhibitors exhibit superior efficacy in recovering physical performance and muscle strength. Collectively, we propose a paradigm shift from joint-centered symptomatic care to a multidisciplinary treat-to-target strategy. Early pharmacological remission combined with pain-adjusted progressive resistance training and individualized nutritional support is recommended to sustain long-term physical function in RA patients.

Abstract: PubMed · Datensatz