Blood Sciences Test


Aspartate Aminotransferase

Specimen

Serum

Units

u/L

Reference Range

M 18- 37
F 7-31

Test Usage

Aspartate aminotransferase (AST) is an enzyme involved in the transfer of an amino group from aspartate to alpha ketoglutarate to produce oxaloacetic acid and glutamate. AST is present in most organs. The highest concentrations, listed in descending order, are found in liver, heart, skeletal muscle, kidney, brain, pancreas, lung, leukocytes, and erythrocytes. Because of its wide tissue distribution, elevated AST levels have low specificity for any single disease. AST activities in liver are 7000 times higher than serum activities. Historically, AST has been used clinically to diagnose hepatitis, myocardial infarction, and skeletal muscle disease. AST increase in the absence of ALT increase indicates cardiac or skeletal muscle disease. ALT is a better indicator of liver disease, because of its more limited tissue distribution.

AST tends to run slightly higher in males than females due to differences in body mass and varies with age. AST is slightly higher than ALT until the age of 15 to 20 years. Thereafter, AST activity tends to be lower than ALT. At age 60, AST and ALT activities become roughly equal. AST levels are about 15% higher in Africans than Caucasian men. Obese men may have mildly elevated AST levels. AST levels can fluctuate between 5 and 10% from one day to the next in the same individual. Moderate exercise increases AST levels for as long as 24 hours, usually less than 3 times the upper limit of normal. The half-life of AST in the circulation is 17 +/- 5 hours.

The ratio of AST to ALT is sometimes useful to diagnose specific liver diseases. AST is distributed both in cytoplasm and mitochrondria of hepatocytes, while ALT is distributed mainly in the cytoplasm. Normal serum levels of AST are derived from the cytoplasmic fraction. Mild cell injury results in release of cytoplasmic enzyme, while severe injury releases both cytoplasmic and mitochondrial AST. In most types of liver disease, AST activity is lower than ALT; exceptions include alcoholic hepatitis and Reye syndrome. In alcoholic hepatitis, damage is primarily to the mitochondria and more AST is released than ALT. Also, alcoholic liver disease causes pyridoxine deficiency, which depresses ALT activity, because pyridoxine is an important enzyme cofactor. In alcoholic hepatitis, the AST:ALT ratio is greater than 2.0 and the AST increase is seldom more than 300 U/L. In contrast, viral hepatitis primarily damages the cell membrane, releasing more ALT than AST. The AST:ALT ratio is less than 1. The AST: ALT ratio is less useful in distinguishing alcoholic from other causes of hepatocellular injury in patients with cirrhosis, because the ratio is usually >1.

Disease Peak ALT
x ULN
AST:ALT
Ratio
Peak Bilirubin Protime
Prolongation
Viral hepatitis 10 – 40 <1 <15 <3
Alcoholic hepatitis 2 – 8 >2 <15 1 – 3
Toxic injury >40 >1 early <5 >5 transient
Ischemic injury >40 >1 early <5 >5 transient

The chronology and extent of AST elevation provides some insight into the etiology of the underlying liver disease. The highest serum levels occur in viral and toxic hepatitis and ischemic necrosis.

     Liver Disease AST Pattern
Choledocholithiasis Early increase to peak of <5 times ULN and return to normal within 72 hours
Cholangitis Increase up to 10 times ULN
Viral hepatitis Steady increase to peak level in low thousands at 7 – 14 days
Alcoholic hepatitis Increase to <300
Ischemic injury Abrupt increase within 24 hours to peak >10,000
Acetaminophen toxicity Increase over 48 hours to peak >10,000

Turnaround time

1 day

Availability

Local test
Can be added on to an existing request up to 4 days following sample receipt

Specimen Labelling Procedure