ArticleJournal of clinical medicine2022
Markedly Elevated Aspartate Aminotransferase from Non-Hepatic Causes.
Article in Journal of clinical medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 3 of them syntheses that pooled it.
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Who cites it
27 citing papers in PubMed, 3 syntheses or guidelines pooled it, 32 citations in OpenAlex.
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- Exertional Rhabdomyolysis With Moderate Creatine Kinase Elevation and Marked Transaminase Elevation but Preserved Synthetic Function: A Case Report.The American journal of case reports · 2026Article
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- Aspartate Aminotransferase-to-Platelet Ratio Index (APRI) as a Predictor of Mortality in Patients with Femoral Fracture: A Retrospective Cohort Analysis.Therapeutics and clinical risk management · 2026Article
- Statin-Associated Immune-Mediated Necrotizing Myopathy Presenting as Persistent Hypertransaminasemia.Cureus · 2026Article
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- Association between liver function at hospital admission and mortality in pediatric patients receiving postcardiotomy venoarterial extracorporeal membrane oxygenation support.World journal of emergency medicine · 2025Article
- Association of hepatic biomarkers with incident diabetes: a mediation analysis of the triglyceride-glucose index in a large Chinese cohort.Lipids in health and disease · 2025Article
- The prognostic role of albumin-bilirubin grade in the mortality of extrahepatic cholangiocarcinoma patients.BMC gastroenterology · 2025Article
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Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There have been no reports on mortality in patients with markedly elevated aspartate aminotransferase (AST) levels from non-hepatic causes to date. This study aimed to determine the etiologies of markedly elevated AST levels > 400 U/L due to non-hepatic causes and to investigate the factors associated with mortality in these cases. This retrospective study included 430 patients with AST levels > 400 U/L unrelated to liver disease at two centers between January 2010 and December 2021. Patients were classified into three groups according to etiology: skeletal muscle damage, cardiac muscle damage, and hematologic disorder. Binary logistic regression analysis was performed to evaluate the factors associated with 30-day mortality. The most common etiology for markedly elevated AST levels was skeletal muscle damage (54.2%), followed by cardiac muscle damage (39.1%) and hematologic disorder (6.7%). The 30-day mortality rates for the skeletal muscle damage, cardiac muscle damage, and hematologic disorder groups were 14.2%, 19.5%, and 65.5%, respectively. The magnitude of the peak AST level significantly correlated with 30-day mortality, with rates of 12.8%, 26.7%, and 50.0% for peak AST levels < 1000 U/L, <3000 U/L, and ≥3000 U/L, respectively. In the multivariate analysis, cardiac muscle damage (odds ratio [OR] = 2.76, 95% confidence interval [CI] = 1.31−5.80), hematologic disorder (OR = 9.47, 95% CI = 2.95−30.39), peak AST < 3000 U/L (OR = 2.94, 95% CI = 1.36−6.35), and peak AST ≥ 3000 U/L (OR = 9.61, 95% CI = 3.54−26.08) were associated with increased 30-day mortality. Our study revealed three etiologies of markedly elevated AST unrelated to liver disease and showed that etiology and peak AST level significantly affected the survival rate.
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