PMID- 18270431
OWN - NLM
STAT- MEDLINE
DCOM- 20080416
LR  - 20220310
IS  - 1348-4540 (Electronic)
IS  - 0918-8959 (Linking)
VI  - 55
IP  - 1
DP  - 2008 Mar
TI  - Induction of hyperadiponectinemia following long-term treatment of patients with 
      rheumatoid arthritis with infliximab (IFX), an anti-TNF-alpha antibody.
PG  - 213-6
AB  - 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.
FAU - Nishida, Keiko
AU  - Nishida K
AD  - First Department of Internal Medicine, University of Occupational and 
      Environmental Health, School of Medicine, Kitakyushu, Japan.
FAU - Okada, Yosuke
AU  - Okada Y
FAU - Nawata, Masao
AU  - Nawata M
FAU - Saito, Kazuyoshi
AU  - Saito K
FAU - Tanaka, Yoshiya
AU  - Tanaka Y
LA  - eng
PT  - Clinical Trial
PT  - Journal Article
DEP - 20080213
PL  - Japan
TA  - Endocr J
JT  - Endocrine journal
JID - 9313485
RN  - 0 (ADIPOQ protein, human)
RN  - 0 (Adiponectin)
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - B72HH48FLU (Infliximab)
SB  - IM
CIN - Endocr J. 2008 Oct;55(5):947; author reply 949. PMID: 18497451
MH  - Adiponectin/blood
MH  - Adult
MH  - Aged
MH  - Antibodies, Monoclonal/adverse effects/*therapeutic use
MH  - Antirheumatic Agents/adverse effects/therapeutic use
MH  - Arthritis, Rheumatoid/physiopathology/*therapy
MH  - Blood Pressure
MH  - C-Reactive Protein/analysis
MH  - Coronary Artery Disease/blood/etiology
MH  - Female
MH  - Humans
MH  - Immunotherapy
MH  - Infliximab
MH  - Male
MH  - Middle Aged
MH  - Risk Factors
MH  - Time Factors
MH  - Tumor Necrosis Factor-alpha/*immunology
MH  - Up-Regulation/drug effects
EDAT- 2008/02/14 09:00
MHDA- 2008/04/17 09:00
CRDT- 2008/02/14 09:00
PHST- 2008/02/14 09:00 [pubmed]
PHST- 2008/04/17 09:00 [medline]
PHST- 2008/02/14 09:00 [entrez]
AID - JST.JSTAGE/endocrj/K07E-043 [pii]
AID - 10.1507/endocrj.k07e-043 [doi]
PST - ppublish
SO  - Endocr J. 2008 Mar;55(1):213-6. doi: 10.1507/endocrj.k07e-043. Epub 2008 Feb 13.