Abstract
OBJECTIVE: To investigate the lipid profiles in patients with active rheumatoid arthritis (RA) and to assess the relationship of inflammatory disease activity markers, sex, and menopausal status with lipid profiles. METHODS: Three groups of patients with active RA (n = 184) were studied: men (n = 61, mean age 50.8 +/- 4.81 yrs), premenopausal women (n = 58, mean age 39.2 +/- 2.44 yrs), and postmenopausal women (n = 65, mean age 60.4 +/- 2.14 yrs), and healthy controls (n = 161): men (n = 65, mean age 50.9 +/- 3.42 yrs), premenopausal women (n = 47, mean age 40.3 +/- 1.66 yrs), and postmenopausal women (n = 49, mean age 61.3 +/- 3.16 yrs). We measured fasting plasma levels of total cholesterol (TC), triglyceride (TG), HDL-cholesterol (HDL-C), LDL-cholesterol (LDL-C), lipoprotein (a) [LP(a)], apolipoprotein A1 (apo A1), apolipoprotein B (apo B), and erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). RESULTS: Male RA patients had significantly higher apo B/apo A1 and LP(a) and lower HDL-C than male controls. Female RA patients had significantly higher TC, LDL-C, and LP(a) than female controls. Premenopausal RA patients had significantly higher LDL-C, TC/HDL-C, LDL-C/HDL-C, and apo B/apo A1 and lower TG and HDL-C than premenopausal controls. Postmenopausal RA women had significantly higher TG and LP(a) and lower TC than postmenopausal controls. Female RA patients had higher HDL-C, apo A1, and TC/HDL-C and lower apo B/apo A1 than male RA patients. Postmenopausal RA patients had significantly higher TC, TG, TC/HDL-C, apo B, LP(a), and LDL-C/HDL-C than premenopausal RA patients. CRP correlated positively with TC/HDL-C, LDL-C/HDL-C, and apo B/apo A1 and negatively with HDL-C in male RA patients. In female RA patients CRP had positive correlation with TC/HDL-C and LDL-C/HDL-C and negative correlation with HDL-C. CONCLUSION: These findings suggest that patients with active RA have altered lipid profiles and that disease activity, sex, and menopausal status affect lipid profiles, and these would be expected to change the pattern of atherosclerotic events in RA.
