Anti-apoA-1 IgG and oxidized LDL are raised in rheumatoid arthritis (RA): potential associations with cardiovascular disease and RA disease activity.
OBJECTIVE
To determine whether emerging cardiovascular risk factors such as anti-apolipoprotein A-1 (anti-apoA-1) immunoglobulin (Ig)G and oxidized low density lipoprotein (oxLDL) are associated with cardiovascular disease (CVD), carotid intima-media thickness (IMT), and disease activity in rheumatoid arthritis (RA).


METHODS
We determined the aforementioned associations in 69 RA patients with disease duration of 5 years and 46 controls matched by age, sex, and smoking status. Anti-apoA-1 IgG and oxLDL were measured by enzyme-linked immunosorbent assay (ELISA). Carotid arteries were examined by ultrasound. Disease Activity Score calculated on 28 joints (DAS28) was used to assess disease activity.


RESULTS
CVD prevalence was higher among RA patients than controls (17% vs. 2%, p = 0.01) but there was no difference in IMT (median: 0.67 vs. 0.66, p = 0.33). RA patients had a higher anti-apoA-1 IgG prevalence than controls (20% vs. 0%, p = 0.001). Anti-apoA-1 IgG and oxLDL levels were higher in cases than controls [median: 0.33 vs. 0.175 optical density (OD), p = 0.03; and 121 vs. 37.2 U/L, p = 0.0001, respectively]. Anti-apoA-1 IgG-positive patients had higher levels of oxLDL (median: 140.5 vs. 112 U/L, p = 0.01) than those tested negative. Receiver operating characteristic (ROC) curve analysis showed that only anti-apoA-1 IgG was a modest but significant predictor of CVD [area under the curve (AUC) = 0.65, p = 0.03] in RA patients. oxLDL was significantly associated with RA disease activity, whereas anti-apoA-1 IgG was not.


CONCLUSIONS
Anti-apoA-1 IgG could be a marker of CVD in RA, whereas oxLDL levels seem to reflect RA disease activity. Other causes of CVD than a general increase in atherosclerosis (as determined by IMT measurements) including plaque stability may therefore be of importance to explain the increased incidence of CVD in RA.
Vuilleumier
N
N
Department of Rheumatology, Karolinska Institutet at Karolinska University Hospital Huddinge, Stockholm, Sweden.
Bratt
J
J
Alizadeh
R
R
Jogestrand
T
T
Hafström
I
I
Frostegård
J
J
D016632:Apolipoprotein A-I / Q000276:immunology*; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000276:immunology; D001323:Autoantibodies / Q000097:blood*; D002318:Cardiovascular Diseases / Q000097:blood / Q000000981:diagnostic imaging / Q000453:epidemiology*; D002340:Carotid Artery Diseases / Q000097:blood / Q000000981:diagnostic imaging / Q000453:epidemiology; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood*; D018836:Inflammation Mediators / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood*; D008297:Male; D008875:Middle Aged; D012907:Smoking; D017539:Tunica Intima / Q000000981:diagnostic imaging; D014463:Ultrasonography
D016632:Apolipoprotein A-I; D001323:Autoantibodies; D007074:Immunoglobulin G; D018836:Inflammation Mediators; D008077:Lipoproteins, LDL; C099252:oxidized low density lipoprotein