Adipocytokines are associated with radiographic joint damage in rheumatoid arthritis

Abstract

Objective. Obesity protects against radiographic joint damage in rheumatoid arthritis (RA) through poorly defined mechanisms. Adipocytokines are produced in adipose tissue and modulate inflammatory responses and radiographic joint damage in animal models. The purpose of this study was to examine the hypothesis that adipocytokines modulate inflammation and radiographic joint damage in patients with RA.Methods. We compared serum concentrations of leptin, resistin, adiponectin, and visfatin in 167 RA patients and 91 control subjects. The independent association between adipocytokines and body mass index (BMI), measures of inflammation (C-reactive protein [CRP], interleukin-6 [IL-6], and tumor necrosis factor ␣ [TNF␣]), and radiographic joint damage (Larsen score; n ‫؍‬ 93 patients) was examined in RA patients by multivariable regression analysis first controlling for age, race, and sex, and then for obesity (BMI) and inflammation (TNF␣, IL-6, and CRP).Results. Concentrations of all adipocytokines were significantly higher in RA patients than in controls; for visfatin and adiponectin, this association remained significant after adjusting for BMI, inflammation, or both. Visfatin concentrations were associated with higher Larsen scores, and this association remained significant after adjustment for age, race, sex, disease duration, BMI, and inflammation (odds ratio Conclusion. Concentrations of adipocytokines are increased in patients with RA and may modulate radiographic joint damage. Visfatin is associated with increased, and leptin with reduced, levels of radiographic joint damage.[

Serum Resistin in Lean Rheumatoid Arthritis Patients: Does it correlate with disease activity and radiological joint damage?

“…On the contrary to our results, the studies conducted by Forsblad et al 19 , Kassem et al 15 and Rho et al 23 found a significant positive correlation between serum resistin levels and Larsen score for radiological joint damage in RA patients (p< 0.05). While Canoru et al 16 recorded that there was no significant correlation between resistin and ESR, and CRP.…”

“…While Rho et al 23 reported that the concentrations of resistin did not differ significantly among patients with seropositive and seronegative RA. They also reported that disease duration, DAS 28, Larsen score, and CRP were not correlated with resistin.…”

Adipokines and Systemic Rheumatic Diseases: Linking Inflammation, Immunity and Metabolism

“…It is widely accepted that leptin levels are elevated in patients with RA and that there is a correlation between serum leptin and synovial fluid/serum leptin ratio and disease duration and parameters of RA activity (Olama et al, 2010). Generally, leptin is considered to be pro-inflammatory, but this hormone has been also reported to reduce radiographic joint damage (Rho et al, 2009). This effect could be related to some leptin anabolic effects, such as the stimulation of the synthesis of insulin-like growth factor-1 (IGF-1) and transforming growth factor-(TGF-) at both the messenger RNA (mRNA) and protein levels (Dumond et al, 2003) The actions of leptin in RA are not only targeted to articular tissues, this adipokine also exerts direct modulatory effects on activation, proliferation, maturation and production of inflammatory mediators in a variety of immune cells, including lymphocytes, NK cells, monocytes/macrophages, dendritic cells, neutrophils and eosinophils (Lam & Lu, 2007).…”

“…In fact, patients with SLE have increased concentrations of leptin and these concentrations are associated with insulin resistance, BMI (Body Mass Index) and CRP (C-reactive protein) in these patients (Chung et al, 2009). …”

Cardiometabolic comorbidities and rheumatic diseases: Focus on the role of fat mass and adipokines

“…Adiponectin has been found to be higher in RA patients than in healthy controls (34,(77)(78)(79)(80)(81). Moreover, adiponectin levels are increased in early RA patients that had never taken disease-modifying antirheumatic drugs and in chronic RA patients (82).…”