Antibodies against malondialdehyde-acetaldehyde adducts can help identify patients with abdominal aortic aneurysm

• Published in: Journal of vascular surgery Vol. 63; no. 2; pp. 477 - 485
• Main Authors: Carson, Jeffrey S., MD, Xiong, Wanfen, MD, PhD, Dale, Matthew, BS, Yu, Fang, PhD, Duryee, Michael J., MS, Anderson, Daniel R., MD, PhD, Thiele, Geoffrey M., PhD, Baxter, B. Timothy, MD
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.02.2016
• Subjects: Acetaldehyde - analogs & derivatives; Acetaldehyde - immunology; Aged; Aged, 80 and over; Animals; Aortic Aneurysm, Abdominal - blood; Aortic Aneurysm, Abdominal - chemically induced; Aortic Aneurysm, Abdominal - diagnosis; Aortic Aneurysm, Abdominal - immunology; Biomarkers - blood; Calcium Chloride; Case-Control Studies; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Female; Humans; Immunoglobulin A - blood; Immunoglobulin G - blood; Male; Malondialdehyde - analogs & derivatives; Malondialdehyde - immunology; Mice, Inbred C57BL; Predictive Value of Tests; Surgery; Up-Regulation
• ISSN: 0741-5214; 1097-6809
• DOI: 10.1016/j.jvs.2014.08.117

Objective Abdominal aortic aneurysm (AAA) is a pathologic dilation of the aorta. Inflammation of the aortic wall has been shown to be involved in AAA formation. Malondialdehyde-acetaldehyde (MAA) adducts are MAA/protein hybrids with immunogenic, proinflammatory, and profibrotic properties. Levels of MAA adducts are elevated in patients with coronary artery disease; however, the role of MAA adducts in AAA is unclear. We hypothesize that levels of circulating antibodies against MAA adducts are increased in patients with AAA. Methods Plasma samples were collected from mice and patients with AAA and control patients with atherosclerosis but not AAA. AAA was induced in mice by a standard CaCl2 protocol, with matching sham mice. Plasma levels of anti-MAA antibodies were quantified by enzyme-linked immunosorbent assay. Results Patients with AAA exhibited higher levels of immunoglobulin G and immunoglobulin A anti-MAA antibody subtypes ( P  = .049 and .026, respectively) compared with control patients. Conversely, immunoglobulin M anti-MAA antibodies in AAA patients were lower compared with control patients ( P  = .018). In CaCl2 -treated mice, immunoglobulin G anti-MAA antibodies were elevated after AAA formation ( P  = .006). Conclusions The pattern of anti-MAA antibodies is able to distinguish between patients with AAA and patients with atherosclerosis but no AAA. These results demonstrate that MAA adducts are associated with AAA and suggest that they may play a role in either initiating or propagating chronic inflammation in AAA.