RT Journal Article
SR Electronic
T1 180 Plasma myeloperoxidase is inversely associated with future atherosclerosis progression and inflammatory hdl function in sle
JF Lupus Science & Medicine
JO Lupus Sci & Med
FD Lupus Foundation of America
SP A84
OP A84
DO 10.1136/lupus-2017-000215.180
VO 4
IS Suppl 1
A1 McMahon, M
A1 Grossman, J
A1 Hahn, B
A1 Skaggs, B
YR 2017
UL http://lupus.bmj.com/content/4/Suppl_1/A84.2.abstract
AB Background and aims Women with SLE have increased atherosclerosis (ATH) that is not adequately explained by traditional risk factors. We previously discovered that a “high risk” score on a panel of biomarkers, PREDICTS, confers 28-fold increased odds for carotid plaque in SLE women. The biomarkers included in PREDICTS are sTWEAK, pro-inflammatory HDL (piHDL), homocysteine, leptin, age ≥48, and DMII. It is unknown, however, whether other biomarkers of oxidative stress also predict progression of ATH in SLE. The enzyme myeloperoxidase (MPO) catalyses formation of reactive oxygen species and generates piHDL. The aim of this study was to determine whether MPO levels might predict future progression of ATH in SLE.Methods B-mode and Doppler scanning of carotid arteries was performed at baseline and 24–36 months. Baseline plasma MPO levels were measured using ELISA.Results Repeat carotid ultrasounds and MPO measurements were completed on 202 SLE women. Plaque progression (defined as new or increased plaque) was seen in 42 subjects (21%). Baseline MPO levels were significantly lower in SLE patients with plaque progression vs. those without (p<0.001). Baseline MPO levels were also inversely correlated with piHDL function at follow-up (r=−0.33, p<0.001). Using logistic regression, the variables associated with plaque progression in SLE included high PREDICTS (OR 27.0 p<0.001), MPO levels in the lowest half (OR 4.2, p=0.005), and non-Caucasian ethnicity (OR 4.5, p=0.003).Conclusions Plasma MPO levels are inversely associated with plaque progression in SLE. Lower baseline MPO levels are also associated with future formation of inflammatory piHDL, suggesting that this could be one mechanism to explain the association.