Adipocytokines are associated with radiographic joint damage in rheumatoid arthritis.
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 alpha [TNFalpha]), 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 (TNFalpha, 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 [OR] 2.38 [95% confidence interval (95% CI) 1.32-4.29], P = 0.004). Leptin concentrations showed a positive association with the BMI (rho = 0.58, P < 0.01) and showed a negative association with the Larsen score after adjustment for inflammation (OR 0.32 [95% CI 0.17-0.61], P < 0.001), but not after adjustment for BMI (OR 0.86 [95% CI 0.42-1.73], P = 0.67).


CONCLUSIONS
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.
Rho
Young Hee
YH
Vanderbilt University, Nashville, Tennessee 37232-6602, USA.
Solus
Joseph
J
Sokka
Tuulikki
T
Oeser
Annette
A
Chung
Cecilia P
CP
Gebretsadik
Tebeb
T
Shintani
Ayumi
A
Pincus
Theodore
T
Stein
C Michael
CM
D054392:Adipokines / Q000097:blood*; D052242:Adiponectin / Q000097:blood; D000328:Adult; D000368:Aged; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000000981:diagnostic imaging* / Q000473:pathology; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D005260:Female; D033023:Foot Joints / Q000000981:diagnostic imaging* / Q000473:pathology; D050823:Hand Joints / Q000000981:diagnostic imaging* / Q000473:pathology; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D020738:Leptin / Q000097:blood; D008297:Male; D008875:Middle Aged; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood; D009765:Obesity / Q000097:blood; D011859:Radiography; D052243:Resistin / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D054392:Adipokines; D052242:Adiponectin; D015850:Interleukin-6; D020738:Leptin; D052243:Resistin; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D054409:Nicotinamide Phosphoribosyltransferase