[Association between systemic inflammation and autoimmunity parameters and plasma lipid in patients with rheumatoid arthritis].
OBJECTIVE
The purpose of this study was to observe the association between inflammation status/autoimmune antibodies and plasma lipid in patients with rheumatoid arthritis (RA).


METHODS
A total of 402 RA patients were admitted into our hospital during January 2008 to March 2009 and 225 RA patients who met the inclusion criteria were selected to perform a full lipid profile examination including total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and triglyceride (TG). Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), rheumatoid factor (RF), anti-cyclic citrullinated peptide (anti-CCP), anti-keratin antibody (AKA), anti-perinuclear factor autoantibody (APF) and complement (C) were also evaluated. Atherogenic index of plasma (AIP) was calculate by the formula Log (TG/HDL-C).


RESULTS
(1) There were 12.9%, 10.2% and 14.2% patients with elevated TC, LDL-C and TC respectively, patients with reduced HDL-C accounted for 43.6%. (2) C(3) was higher in elevated TC group than normal TC group (P < 0.05). ESR and CRP were significantly higher in decreased HDL-C group than in normal HDL-C group (P < 0.05). CRP, C(3) and C(4) were significantly higher in elevated LDL-C group than in normal LDL-C group (P < 0.05). (3) Multiple stepwise regression analysis showed that C(3) was positively correlated with TC (R(2) = 0.067, P < 0.05). Both ESR and CRP were negative correlated with HDL-C (R(2) = 0.202, P < 0.05). CRP and anti-CCP were positively correlated with LDL-C (R(2) = 0.129, P < 0.05). ESR and C(4) were positively correlated with AIP (R(2) = 0.046, P < 0.05).


CONCLUSIONS
This study showed that rheumatoid arthritis is associated with an abnormal lipid profile, especially in patients with increased inflammation markers and autoimmune antibodies. Moreover, ESR and C(4) were predictors of increased AIP in this cohort.
Department of Cardiology, People's Hospital of Peking University, Beijing 100044, China.
Chao
C
Xue
Wen-ling
WL
Liu
Yi-hong
YH
Sun
Rong-jing
RJ
Ding
Da-yi
DY
Hu
D000368:Aged; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000276:immunology* / Q000503:physiopathology; D001323:Autoantibodies / Q000097:blood*; D015551:Autoimmunity; D002097:C-Reactive Protein / Q000032:analysis; D008076:Cholesterol, HDL / Q000097:blood*; D008078:Cholesterol, LDL / Q000097:blood*; D003165:Complement System Proteins; D006801:Humans; D007249:Inflammation; D008055:Lipids / Q000097:blood; D008075:Lipoproteins, HDL / Q000097:blood; D014280:Triglycerides / Q000097:blood
D001323:Autoantibodies; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; C034396:HDL-triglyceride; D008055:Lipids; D008075:Lipoproteins, HDL; D014280:Triglycerides; D003165:Complement System Proteins; D002097:C-Reactive Protein