Markers of inflammation are negatively correlated with serum leptin in rheumatoid arthritis

Background: Leptin regulates food intake and modulates immunity and inflammation. A positive feedback mechanism has been described between tumour necrosis factor (TNF) and leptin, and it has been suggested that leptin potentiates inflammation in patients with rheumatoid arthritis (RA). Objective: To...

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Bibliographic Details
Published in:	Annals of the rheumatic diseases Vol. 64; no. 8; pp. 1195 - 1198
Main Authors:	Popa, C, Netea, M G, Radstake, T R D S, van Riel, P L, Barrera, P, van der Meer, J W M
Format:	Journal Article
Language:	English
Published:	London BMJ Publishing Group Ltd and European League Against Rheumatism 01-08-2005 BMJ BMJ Publishing Group LTD
Subjects:	Adalimumab anti-tumour necrosis factor treatment Antibodies, Monoclonal - therapeutic use Antibodies, Monoclonal, Humanized Antirheumatic Agents - therapeutic use Arthritis, Rheumatoid - blood Arthritis, Rheumatoid - drug therapy Biological and medical sciences Biomarkers - blood BMI body mass index C reactive protein C-Reactive Protein - metabolism CRP disease modifying antirheumatic drugs Diseases of the osteoarticular system DMARDs Double-Blind Method Extended Report Female Hibernation Humans inflammation Inflammation - blood Inflammation Mediators - blood Inflammatory joint diseases interleukin Interleukin-6 - blood leptin Leptin - blood Male Medical sciences Middle Aged Rheumatoid arthritis Rodents Studies TNFα Tumor Necrosis Factor-alpha - antagonists & inhibitors tumour necrosis factor α Chronic Leptin Rheumatoid arthritis Diseases of the osteoarticular system Autoimmune disease Serum Inflammatory joint disease Inflammation
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Summary:	Background: Leptin regulates food intake and modulates immunity and inflammation. A positive feedback mechanism has been described between tumour necrosis factor (TNF) and leptin, and it has been suggested that leptin potentiates inflammation in patients with rheumatoid arthritis (RA). Objective: To assess whether inflammation correlates with leptin concentrations in patients with RA, and whether anti-TNF treatment modulates leptin concentrations in these patients. Methods: Leptin, IL6 and CRP were measured (at baseline and after 2 weeks of treatment) in the blood of 31 patients with RA starting either anti-TNF treatment or placebo, and in 18 healthy controls. Results: In patients with RA, plasma leptin concentrations at baseline correlated inversely with the degree of inflammation as assessed by C reactive protein (CRP; rs2 = 0.21, p<0.01) or interleukin (IL) 6 concentrations (rs2 = 0.22, p<0.008). Mean (SD) leptin concentrations did not differ between patients with RA and controls (6.0 (4.6) v 4.2 (2.8) ng/ml in men; 15.1 (7.9) v 13.4 (5.2) ng/ml in women). Short course anti-TNF treatment for 2 weeks did not modify leptin concentrations, despite significant reduction of CRP and IL6. Conclusion: A significant inverse correlation between inflammation and leptin concentrations was found in patients with active RA, although plasma leptin concentrations did not significantly differ from those in healthy controls. This suggests that active chronic inflammation may lower plasma leptin concentrations. Two weeks’ treatment with anti-TNF did not change plasma leptin concentrations and longer treatment may be needed to see an effect on leptin.
Bibliography:	ark:/67375/NVC-1XLF1P4G-V local:0641195 istex:CF2019A0D58D6E9A814110B0A3BF928CB2B052B6 Correspondence to:  Professor J W M van der Meer  Department of Internal Medicine (541), UMC St Radboud, PO Box 9101, 6500HB Nijmegen, The Netherlands; j.vandermeer@aig.umcn.nl PMID:15731289 href:annrheumdis-64-1195.pdf ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23
ISSN:	0003-4967 1468-2060
DOI:	10.1136/ard.2004.032243