Session Type: Poster Session (Tuesday)
Session Time: 9:00AM-11:00AM
Background/Purpose: Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by devastating end-organ manifestations. Cardiovascular disease (CVD) is a leading cause for premature death in SLE patients across different ethnicities. While the traditional Framingham risk factors likely contribute to CVD in SLE, they cannot fully account for the highly increased risk of CVD in SLE. Malondialdehyde-acetaldehyde (MAA) protein adduct (a byproduct of oxidative stress) and antibodies to MAA have been suggested to mediate early inflammation in atherosclerotic disease. The purpose of this study is to determine whether SLE patients develop anti-MAA antibodies and whether anti-MAA antibodies identify SLE patients with cardiovascular manifestations.
Methods: 201 SLE patients who fulfilled the 1997 revised American College of Rheumatology criteria for the classification of SLE and 205 non-diseased healthy controls (matched in age, sex, and ethnicity) were recruited from the Dominican Republic for the study. Enzyme-linked immunosorbent assay (ELISA) was performed to determine the serum levels of anti-MAA IgG antibodies. Data were analyzed using Mann Whitney test. A p value of < 0.05 was considered significant.
Results: The mean anti-MAA IgG levels in SLE patients was 0.13 (in optical density units; SD 0.27, 95% CI 0.09-0.17), which is significantly higher than that in healthy controls (mean: 0.06; SD 0.07, 95% CI 0.05-0.07; p=0.041). SLE patients with pericarditis or myocarditis have higher levels of anti-MAA IgG antibodies than SLE patients without pericarditis or myocarditis (mean: 0.24 versus 0.07; p=0.018). SLE patients with vasculitis have significantly higher levels of anti-MAA IgG antibodies than SLE patients without vasculitis (mean: 0.22 versus 0.08; p=0.019).
Conclusion: SLE patients with CVD (such as pericarditis, myocarditis, or vasculitis) have significantly higher anti-MAA IgG antibodies than SLE patients without CVD. These results suggest that anti-MAA antibodies may be a biomarker for CVD in SLE. Future studies will determine if MAA and/or anti-MAA antibodies play a role in the pathogenesis of CVD in SLE.
To cite this abstract in AMA style:Yu Y, Hearth-Holmes M, Wang T, Lopez P, Tineo C, Paulino G, Duryee M, Thiele G, Mikuls T, Loyo E, Su K. Antibodies to Malondialdehyde-acetaldehyde (MAA) Protein Adduct as a Biomarker for Cardiovascular Manifestations in Systemic Lupus Erythematosus [abstract]. Arthritis Rheumatol. 2019; 71 (suppl 10). https://acrabstracts.org/abstract/antibodies-to-malondialdehyde-acetaldehyde-maa-protein-adduct-as-a-biomarker-for-cardiovascular-manifestations-in-systemic-lupus-erythematosus/. Accessed November 28, 2020.
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ACR Meeting Abstracts - https://acrabstracts.org/abstract/antibodies-to-malondialdehyde-acetaldehyde-maa-protein-adduct-as-a-biomarker-for-cardiovascular-manifestations-in-systemic-lupus-erythematosus/