Primary Sources of AST (SGOT) in the Body
AST is present in multiple tissues throughout the body, with the highest concentrations found in the liver, cardiac muscle, skeletal muscle, kidneys, brain, and red blood cells, making it a non-specific marker compared to ALT. 1
Tissue Distribution of AST
Major Sources
Liver tissue contains high concentrations of AST in both cytoplasmic (c-AST) and mitochondrial (m-AST) forms, making hepatic injury a primary source of serum AST elevation 2
Cardiac muscle is a significant source of AST, with myocardial infarction causing measurable AST elevations, though cardiac troponin is now the preferred biomarker for cardiac injury 3, 1
Skeletal muscle contains substantial AST, with muscle injury or rhabdomyolysis causing significant elevations that can be mistaken for liver disease 1, 4
Red blood cells (erythrocytes) contain AST, making hemolysis a potential source of elevated serum levels 1, 5
Kidneys and brain tissue also contain AST, though these are less commonly recognized sources of serum elevation 1
Clinical Implications of Non-Specificity
Distinguishing Hepatic from Non-Hepatic Sources
ALT is highly liver-specific due to minimal presence in other tissues, whereas AST elevation requires consideration of multiple organ systems 6, 5
Muscle injury confirmation requires checking creatine kinase (CK) levels, which will be markedly elevated in rhabdomyolysis or significant muscle damage 1
Intensive exercise, particularly weight lifting, can cause acute AST elevations from muscle damage that may be mistaken for liver injury 1
The AST:ALT ratio helps differentiate sources: ratios >2:1 suggest alcoholic liver disease, while ratios <1 suggest nonalcoholic fatty liver disease (NAFLD) 3, 1
AST Isoenzymes
Two distinct isoenzymes exist: cytoplasmic AST (c-AST) and mitochondrial AST (m-AST), with striated muscle, myocardium, and liver being the main tissue sources 2
Mitochondrial AST elevation may indicate more severe hepatocellular necrosis and can assist in determining prognosis in liver disease 2
Common Clinical Pitfalls
Do not assume AST elevation equals liver disease without considering recent exercise, muscle trauma, cardiac events, or hemolysis 1, 4
Transient biliary obstruction from choledocholithiasis can cause marked AST elevations (>600 units) that rise and fall rapidly within 24-72 hours, mimicking acute hepatocellular injury 7
Always correlate AST with ALT levels: isolated or disproportionate AST elevation should prompt investigation of non-hepatic sources 5, 4