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. 2024;7(2):104-113.
doi: 10.26502/aimr.0169. Epub 2024 May 9.

Diabetes and Abdominal Aortic Aneurysm: Is the Protective Effect on AAA Due to Antidiabetic Medications Alone, Due to the Disease Alone, or Both?

Gaithrri Shanmuganathan  1 , Devendra K Agrawal  1
Affiliations

Diabetes and Abdominal Aortic Aneurysm: Is the Protective Effect on AAA Due to Antidiabetic Medications Alone, Due to the Disease Alone, or Both?

Gaithrri Shanmuganathan et al. Arch Intern Med Res. 2024.

Abstract

Diabetes is a metabolic disease that may result in multiple microvascular and macrovascular diseases. Interestingly, many studies have demonstrated the inverse relationship between diabetes and the development and expansion of abdominal aortic aneurysm (AAA). One hypothesis is that the aortic wall stiffness resulting from hyperglycemia and advanced glycation end products could delay the development and growth of AAA. Other studies have proposed that the concurrent use of antidiabetic medications which promote anti-inflammatory cytokines while hindering pro-inflammatory cytokines may potentially be the reason for this protective effect of diabetes on AAA. Contrastingly, the presence of diabetes has been found to have a negative effect on the outcome of AAA following its repair which may be due to elevated blood glucose negatively affecting the healing process. The current literature has also demonstrated the negative impact of the use of fluoroquinolones on AAA. This comprehensive review critically reviewed and summarized the role of diabetes, anti-diabetes medications and fluoroquinolones on AAA, and on the effect of diabetes and certain anti-diabetes medications on outcomes following its repair.

Keywords: AAA repair; Abdominal aortic aneurysm; Anti-diabetic drugs; Diabetes mellitus; Fluoroquinolones.

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Conflict of interest statement

Competing interest: Both authors have read the manuscript and declare no conflict of interest. No writing assistance was utilized in the production of this manuscript.

Figures

Figure 1:
Figure 1:
The multifactorial pathophysiology of AAA. MMP-2 is produced by smooth muscle cells and fibroblasts, and MMP-9 is produced by neutrophils and macrophages. MMPs are also produced by oxidized LDL, TNF-α, IL-1 and IL-3. MMPs, MPO, neutrophil elastase and neutrophil extracellular traps collectively lead to ECM remodeling, VSMC apoptosis and inflammation. These processes consequently lead to the formation of AAA.
Figure 2:
Figure 2:
The use of Fluoroquinolone results in increased MMP, cellular apoptosis, and DNA double break strands which cause degeneration of collagen and connective tissue in the aortic wall. This results in AAA progression.
See this image and copyright information in PMC

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