Session Information
Session Type: Abstract Submissions (ACR)
Background/Purpose: Environmental contamination with mercury (Hg) is linked to autoimmune diseases. Exposure to low-dose non-organic mercury has been reported to exacerbate murine SLE. The aim of this study is to evaluate the serum Hg levels in patients with SLE and their associated risk factors
Methods: Consecutive patients who fulfilled >=4 ACR criteria for SLE were recruited. An equal number of age and sex matched healthy controls was also recruited. Blood was taken in the morning for the assay of Hg level (atomic absorption spectrophotometry by a DMA80 direct Hg analyzer, Milestone, Italy) and other markers of disease activity (anti-dsDNA, complement C3 and C4) (for SLE patients). Disease activity of SLE patients was assessed by the SELENA-SLE disease activity index (SLEDAI) and organ damage was assessed by the SLICC/SLE damage index (SDI). Bivariate correlation between Hg level and various clinical and serological markers was studied by Pearson’s correlation test. A linear regression model was established to study the clinical risk factors associated with higher serum Hg levels in SLE patients.
Results: 246 SLE patients (93% women) were studied. All were ethnic Chinese. The mean age during venepuncture was 40.7±12.5 years and SLE duration was 7.7±7.0 years. The mean SELENA-SLEDAI and SDI score was 5.8±6.5 and 0.97±1.5, respectively. 85(35%) patients had clinically active SLE, defined as a SELENA-SLEDAI score of >=6. 107 (43%) patients had organ damage (SDI>=1). The mean serum total mercury level of the SLE patients studied was 1.34±0.69 ng/mL (NR <3.85), which was significantly higher than that of 246 age and gender matched healthy subjects (N=246) (0.72±0.34 ng/mL; p<0.001). Only 2 (0.8%) SLE patients had Hg level ³3.85ng/mL. Patients with clinically active SLE had significantly higher mercury level than those with SLEDAI<6 (1.50±0.57 vs 1.26±0.74 ng/mL; p=0.006). In addition, the levels of mercury in patients with clinically and serologically inactive disease (SLEDAI =0) were significantly higher than those with controls (1.15±0.56 vs 0.72±0.34 ng/mL; p<0.001) adjusted for age and sex (by ANCOVA test). Bivariate correlation study revealed that younger age (r -0.24; p<0.001), female sex (r 0.19; p=0.003), shorter SLE duration (r -0.16; p=0.01), anti-dsDNA titer (r 0.22; 0.001), SLEDAI score (r 0.24;<0.001) and physicians’ global assessment (PGA) of disease activity (r 0.17;p=0.007) were significantly associated with higher mercury level. SDI damage score (r -0.06; p=0.33), C3 (r -0.06; p=0.36), C4 (r -0.07; p=0.28), photosensitivity, serum creatinine and other clinical manifestations were not significantly associated with mercury levels. In a linear regression model, the SLEDAI score (beta 0.14; p=0.04) and female sex (beta 0.18; p=0.006) were independently and significantly associated with higher Hg level, after adjustment for age, SLE duration and serum creatinine level.
Conclusion: In this cross-sectional study, the total serum mercury level was significantly elevated in patients with both active and inactive SLE than matched controls. Mercury level correlated independently with clinical disease activity and the female sex in a multivariate model, suggesting mercury may be an environmental trigger for SLE.
Disclosure:
C. C. Mok,
None;
B. Fong,
None;
C. Wong,
None.
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