Markedly Elevated Aspartate Aminotransferase from Non-Hepatic Causes.

Area of Science:

• Clinical Medicine
• Biochemistry
• Cardiology
• Hematology
• Neurology/Neuromuscular Diseases

Background:

• Elevated aspartate aminotransferase (AST) levels typically indicate liver injury, but non-hepatic causes are underreported.
• Understanding mortality associated with markedly elevated AST (> 400 U/L) from non-hepatic origins is crucial for patient management.

Purpose of the Study:

• To identify the primary etiologies of markedly elevated AST levels (> 400 U/L) unrelated to liver disease.
• To investigate factors, including etiology and AST magnitude, associated with 30-day mortality in this patient cohort.

Main Methods:

• Retrospective analysis of 430 patients with AST > 400 U/L from non-hepatic causes (January 2010 - December 2021).
• Etiological classification into skeletal muscle damage, cardiac muscle damage, and hematologic disorder groups.
• Binary logistic regression used to identify predictors of 30-day mortality.

Main Results:

• Skeletal muscle damage was the most frequent cause (54.2%), followed by cardiac muscle damage (39.1%) and hematologic disorders (6.7%).
• 30-day mortality rates varied significantly by etiology: skeletal muscle (14.2%), cardiac muscle (19.5%), and hematologic (65.5%).
• Higher peak AST levels and specific etiologies (cardiac, hematologic) were independently associated with increased 30-day mortality.

Conclusions:

• Markedly elevated AST levels (> 400 U/L) can arise from skeletal muscle, cardiac muscle, or hematologic conditions.
• Both the underlying etiology and the magnitude of peak AST levels are significant determinants of short-term survival.
• This study highlights the importance of considering non-hepatic causes for elevated AST and their prognostic implications.