title: Induction of hyperadiponectinemia following long-term treatment of patients with rheumatoid arthritis with infliximab (IFX), an anti-TNF-alpha antibody.
abstract: Tumor necrosis factor-alpha (TNF-alpha) plays an important role in forming atherosclerosis based on chronic inflammatory condition in vivo and animal models. In human system, it is not clear the involvement of TNF-alpha to atherosclerosis. To clarify the relevance of TNF-alpha to atherosclerotic factors in human, We performed a prospective cohort study to investigate the inhibition of TNF-alpha with anti-TNF-alpha antibody infliximab may contribute to increase serum adiponectin levels, adipocyte-derived hormone with antiatherogenic properties, in patients with RA. 97 patients with active RA had been treated every 8 weeks for 1 year(13 men and 84 women, 54.2 +/- 12.6 years, disease duration; 8.5 +/- 1.5 years). They received a fixed dose of infliximab of 3 mg/kg every 8 weeks for 52 weeks. We evaluated changes of inflammatory markers, high molecular weight form of adiponectin levels and blood lipid levels. We also studied the association between increment rate of serum adiponectin and improvement of disease activity and inflammatory markers. Infliximab were strikingly dropped inflammatory markers (p<0.01), increased total cholesterol (TC) and high-density lipoprotein cholesterol (HDL-C) (p<0.05). Besides, serum adiponectin significantly increased, independent of RA activity and clinical backgrounds, suggesting that TNF-alpha and adiponectin exhibit opposite effects in human body. TNF-alpha blockade may interfere in the atherosclerosis directly or indirectly, by increasing serum adiponectin levels, therefore TNF-alpha blockade may improve cardiovascular morbidity and mortality in chronic inflammatory disease such as RA.
authors.affiliation: First Department of Internal Medicine, University of Occupational and Environmental Health, School of Medicine, Kitakyushu, Japan.
authors.forename: Keiko
authors.initials: K
authors.lastname: Nishida
authors.forename: Yosuke
authors.initials: Y
authors.lastname: Okada
authors.forename: Masao
authors.initials: M
authors.lastname: Nawata
authors.forename: Kazuyoshi
authors.initials: K
authors.lastname: Saito
authors.forename: Yoshiya
authors.initials: Y
authors.lastname: Tanaka
mesh_terms: D052242:Adiponectin / Q000097:blood; D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000009:adverse effects / Q000627:therapeutic use*; D018501:Antirheumatic Agents / Q000009:adverse effects / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000503:physiopathology / Q000628:therapy*; D001794:Blood Pressure; D002097:C-Reactive Protein / Q000032:analysis; D003324:Coronary Artery Disease / Q000097:blood / Q000209:etiology; D005260:Female; D006801:Humans; D007167:Immunotherapy; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology*; D015854:Up-Regulation / Q000187:drug effects
chemical_list: C499918:ADIPOQ protein, human; D052242:Adiponectin; D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D000069285:Infliximab