Role of resistin as a marker of inflammation in systemic lupus erythematosus.
BACKGROUND
Resistin is a cystein-rich secretory adipokine. It is proposed to have proinflammatory properties in humans. The aim of this study was to determine associations between serum levels of resistin and markers of inflammation and bone mineral density (BMD) in female patients with systemic lupus erythematosus (SLE).


METHODS
One hundred sixty-three female patients with SLE (20 to 82 years old) were examined in a cross-sectional study. Venous blood samples were analyzed for resistin, erythrocyte sedimentation rate (ESR), C-reactive protein, creatinine, fasting lipids, complements, tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6, sIL-6R (soluble IL-6 receptor), ICTP (C-terminal telopeptide of type I collagen), and PINP (N-terminal propeptide of type I procollagen). Simple and multiple regression analyses as well as logistic regression analyses were performed. Resistin in serum was compared with 42 healthy female controls with respect to age.


RESULTS
Serum resistin levels in controls were similar to those of patients with SLE. Markers of inflammation and current dose of glucocorticosteroids correlated positively to resistin in serum. Markers of renal function, number of prevalent vertebral fractures, and BMD were also significantly associated with resistin. In a multiple regression model, ESR, creatinine, C3, current glucocorticosteroid dose, high-density lipoprotein, and BMD radius remained significantly associated with resistin. In logistic regression analyses with resistin as the independent variable, a significant association was found with ESR (normal or elevated) but not with S-creatinine or z score for hip and radius total.


CONCLUSIONS
Although resistin measurements did not differ between patients and controls, resistin was clearly associated with general inflammation, renal disease, treatment with glucocorticosteroids, and bone loss. We hypothesize that resistin has proinflammatory and disease-promoting properties in SLE. Further studies are needed to elucidate the mechanism behind these associations.
Almehed
Katarina
K
Department of Rheumatology and Inflammation Research, Sahlgrenska Academy at Göteborg University Guldhedsgatan 10, S-413 46 Göteborg, Sweden. katarina.almehed@vgregion.se
d'Elia
Helena Forsblad
HF
Bokarewa
Maria
M
Carlsten
Hans
H
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood / Q000378:metabolism*; D001799:Blood Sedimentation; D015519:Bone Density; D005260:Female; D005919:Glomerular Filtration Rate; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000209:etiology*; D018836:Inflammation Mediators / Q000097:blood; D007668:Kidney / Q000503:physiopathology; D007674:Kidney Diseases / Q000097:blood / Q000503:physiopathology; D008075:Lipoproteins, HDL / Q000097:blood; D016015:Logistic Models; D008180:Lupus Erythematosus, Systemic / Q000150:complications* / Q000188:drug therapy / Q000378:metabolism*; D008875:Middle Aged; D015995:Prevalence; D052243:Resistin / Q000097:blood*; D016103:Spinal Fractures / Q000453:epidemiology
D015415:Biomarkers; D005938:Glucocorticoids; D018836:Inflammation Mediators; D008075:Lipoproteins, HDL; D052243:Resistin