Aspartate Aminotraferase (AST)

Diagnostic Use

Assesses liver and muscle damage; elevated in hepatitis, myocardial infarction, or muscle injury.

Interpretation

AST has a number of sources, including hepatocytes, cardiac and skeletal muscle, erythrocytes, kidneys, brain and pancreas. As such AST is less specific than ALT for parenchymal liver conditions.

Hepatic causes of raised AST:

Marked increase (up to 10 – 100x) can occur in acute viral hepatitis, toxic hepatitis or ischaemic/hypoxic liver injury. Occasionally early-stage extrahepatic biliary obstruction can induce a transient significant ALT/AST rise.

As well as the above, mild to moderate increase can be observed in e.g. cirrhosis, liver tumours, congestive heart failure, autoimmune hepatitis and alcoholic liver disease.

AST rise in general is less than or at most equal to that of ALT (alanine transaminase) rise. Exceptions to this include or ischaemic hepatitis, alcoholic hepatitis and chronic hepatitis/cirrhosis.

The activity level is not necessarily a reliable index of the severity of hepatocyte necrosis or of patient prognosis. Low levels may be seen with severe hepatic necrosis, when there are few cells left for the enzyme to leak from.

Non-hepatic causes of raised AST:

Moderate increase in AST can be seen associated with inflammation, trauma, or infarction of skeletal muscle or myocardial muscle. Severe haemolytic episodes cause elevated levels.

Although AST can be raised in conditions like skeletal myopathies, myocardial cell injury or intravascular haemolysis, it is not specific enough for use in their diagnosis or monitoring. Other much better biomarkers like creatine kinase, high sensitivity troponin T and haptoglobin/plasma Hb are easily available and should be used instead.