# The Relationship Between the Serum Aspartate Aminotransferase/Alanine Aminotransferase Ratio and the Occurrence and Progression of Abdominal Aortic Aneurysms: A Cross-Sectional Study

**Authors:** Hande İştar, Bugra Harmandar, Melike Korkmaz Toker, Gokhan Ilhan, Kadir Arslan, Muruvvet Funda Tetik Saruhan

PMC · DOI: 10.21470/1678-9741-2025-0157 · Brazilian Journal of Cardiovascular Surgery · 2026-02-18

## TL;DR

This study explores how the AST/ALT blood ratio relates to abdominal aortic aneurysms and their progression.

## Contribution

The AST/ALT ratio is identified as a potential marker for AAA presence but not progression.

## Key findings

- AST/ALT ratio was independently associated with AAA presence (odds ratio 2.63).
- Higher AST/ALT ratios correlated with AAA but not with rapid progression.
- ROC analysis showed moderate discrimination for rapid aneurysm enlargement.

## Abstract

This study investigated the relationship between the serum aspartate
aminotransferase to alanine aminotransferase (AST/ALT) ratio, the presence
and progression of abdominal aortic aneurysms (AAA), assessing its potential
as an accessible biochemical marker for patients at risk of rapid aneurysmal
growth.

A total of 180 patients were retrospectively analyzed: 90 with AAA and 90
ageand risk factor-matched controls. Demographic characteristics, risk
factors, laboratory parameters, and imaging data were reviewed. The AAA
group was divided into rapid and slow enlargement subgroups based on
six-month computed tomography measurements. Logistic regression, receiver
operating characteristic (ROC) analyses were used to evaluate predictive and
discriminative performance, and quartile analysis explored potential
threshold effects.

AST/ALT ratio, triglycerides, low-density lipoprotein (LDL) cholesterol, and
white blood cell (WBC) count were significantly higher in patients with AAA.
Rapid AAA enlargement group had higher AST/ALT ratios, triglycerides, LDL
cholesterol, and WBC counts. The AST/ALT ratio was independently associated
with AAA presence (odds ratio 2.63; 95% confidence interval [CI] 1.44 -
5.09; P = 0.002) but not with rapid progression (P = 0.10). ROC analysis
showed good discrimination for AAA presence (area under the curve [AUC] =
0.72; 95% CI 0.65 - 0.79) and moderate ability for rapid enlargement (AUC =
0.65; 95% CI 0.54 - 0.76). Quartile-based analysis revealed a stepwise
increase in AAA prevalence with higher AST/ALT categories.

An elevated AST/ALT ratio is associated with AAA presence but does not
independently predict progression, suggesting it reflects hepatic-vascular
inflammatory interaction rather than serving as a prognostic marker.

## Linked entities

- **Diseases:** AAA (MONDO:0009279)

## Full-text entities

- **Genes:** STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774] {aka ADMIO, ADMIO1, APRF, HIES}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, MMP9 (matrix metallopeptidase 9) [NCBI Gene 4318] {aka CLG4B, GELB, MANDP2, MMP-9}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, ELN (elastin) [NCBI Gene 2006] {aka ADCL1, SVAS, WBS, WS}, Gpt (glutamic pyruvic transaminase, soluble) [NCBI Gene 76282] {aka 1300007J06Rik, 2310022B03Rik, ALT, ALT1, Gpt-1, Gpt1}, MMP2 (matrix metallopeptidase 2) [NCBI Gene 4313] {aka CLG4, CLG4A, MMP-2, MMP-II, MONA, TBE-1}, GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, Slc17a5 (solute carrier family 17 (anion/sugar transporter), member 5) [NCBI Gene 235504] {aka 4631416G20Rik, 4732491M05, AST, ISSD, NSD, SD}, IL6ST (interleukin 6 cytokine family signal transducer) [NCBI Gene 3572] {aka CD130, CDW130, GP130, HIES4, HIES4A, HIES4B}
- **Diseases:** chronic liver disease (MESH:D008107), cardio-hepatic syndrome (MESH:D044542), Inflammatory (MESH:D007249), AAA (MESH:D017544), metabolic disturbance (MESH:D024821), hyperlipidemia (MESH:D006949), cirrhosis (MESH:D005355), hypertension (MESH:D006973), aneurysmal growth (MESH:D006130), atherogenic (MESH:D050197), viral hepatitis (MESH:D014777), aneurysm enlargement (MESH:D000783), aneurysmal dilation (MESH:D002311), non-alcoholic fatty liver disease (MESH:D065626), cardiovascular and metabolic diseases (MESH:D002318), gallstones (MESH:D042882), diabetes mellitus (MESH:D003920), endothelial dysfunction (MESH:D014652), hepatic fibrosis (MESH:D008103), abdominal pain (MESH:D015746), vascular dysfunction (MESH:D002561), endothelial injury (MESH:D057772), hepatic steatosis (MESH:D005234), peripheral artery disease (MESH:D058729), tricuspid regurgitation (MESH:D014262), heart failure (MESH:D006333), cardiac remodeling (MESH:D020257), hepatic (MESH:D056486), cardiac dysfunction (MESH:D006331), cholestatic liver disorders (MESH:D017093), systemic (MESH:D015619), coronary artery disease (MESH:D003324), ischemia (MESH:D007511), hyperbilirubinemia (MESH:D006932), renal cancer (MESH:D007680), AAAs (MESH:C536008), autoimmune hepatitis (MESH:D019693)
- **Chemicals:** bilirubin (MESH:D001663), quercetin (MESH:D011794), ethylenediaminetetraacetic acid (MESH:D004492), uric acid (MESH:D014527), triglyceride (MESH:D014280), methotrexate (MESH:D008727), lipid (MESH:D008055), alcohol (MESH:D000438), flavonoid (MESH:D005419), cholesterol (MESH:D002784), glucose (MESH:D005947)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]

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## References

22 references — full list in the complete paper: https://tomesphere.com/paper/PMC12931435/full.md

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Source: https://tomesphere.com/paper/PMC12931435