Objectives Hepcidin is an acute phase reactant produced by hepatocytes that has been linked to chronic inflammation and atherosclerosis. The present study was carried out to evaluate the serum hepcidin level in patients with SLE and its relationship with disease activity, organ damage and coronary atherosclerosis.
Methods Consecutive patients who fulfilled ≥4 ACR criteria for SLE were recruited. Blood was taken from the participants at 9am in the morning for the assay of hepcidin (peptide enzyme immunoassay; Peninsula Lab, San Carlos, USA), complements (immunonephelometry; Siemens, Germany), anti-dsDNA titer (ELISA; Euro-diagnostica, Arnhem, Netherlands). SLE disease activity was assessed by the SELENA-SLEDAI and physician’s global assessment (PGA) scores. Organ damage of SLE was assessed by the ACR/SLICC damage index (SDI). Atherosclerosis of the coronary arteries was studied by a Multi-Detector CT (MDCT) scanner (BrillianceTM 16, Philips Medical Systems, Best, the Netherlands). The total calcium score (Agatston score) of left main, left anterior descending, left circumflex, and right coronary arteries was obtained and summated. An Agatston score of ≥1 was considered to be abnormal. Hepcidin level was correlated with SLEDAI score (Pearson’s correlation) and compared between patients with and without coronary calcification (Mann Whitney rank sum test).
Results 290 SLE patients were recruited but interim data on 189 patients were analyzed. There were 178 (94%) women and 11 men. The mean age at SLE onset was 32.5±13 years and the mean disease duration was 8.6±7.2 years. At the time of venepuncture, the mean SLEDAI score was 3.3±2.9 (median 2.5) and the mean PGA score was 0.55±2.9 (median 0.4). Forty-three (23%) patients had active SLE, defined as a SLEDAI score of 5 points or more. The mean serum hepcidin level was 21.6±32.5 ng/ml (median 12.7; IQR 4.4-25.8). Serum hepcidin level did not correlate with the total SLEDAI score (r=0.08, p=0.30) or PGA score (r=0.13; p=0.07), but with clinical SLEDAI score, defined as total SLEDAI score minus those contributed by active lupus serology (anti-dsDNA elevation and complement depression) (r=0.18; p=0.02). Serum hepcidin level did not correlate with anti-dsDNA titer or complement levels. Among these 189 SLE patients, 97 patients were randomly screened for coronary atherosclerosis by MDCT scan. Twenty-four patients (25%) had abnormal Agatston calcium score (≥1 point) and the mean score of these patients was 52.0±69 (median 20; IQR 3-78). The serum hepcidin level was significantly higher in those with abnormal coronary calcium score than those without (38.6±54 vs 19.6±26.3 ng/ml; p=0.048) after adjustment for age and sex. Finally, serum hepcidin level was positively correlated with the SDI score (r=0.19; p=0.009).
Conclusions In this cross-sectional study, serum hepcidin level correlates significantly with clinical SLE disease activity and damage score, but not with anti-dsDNA or complement level. SLE patients with coronary atherosclerosis have significantly higher hepcidin level than those without. The role of hepcidin in atherogenesis of SLE patients has to be further explored.
Disclosure of Interest None Declared