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Test Code 8335 Aspartate Aminotransferase (AST/SGOT)

Important Note

Available individually or as part of a CMP or Hepatic Panel. 

Purpose

A wide range of disease entities alters AST (SGOT), with origin from many organs. When an increased AST is from the liver, it is more likely to relate to disease of the hepatocyte. Other enzymes, including alkaline phosphatase and GT, are more sensitive indicators of biliary obstruction. Causes of low AST: uremia, vitamin B6 deficiency (this can be corrected), metronidazole, trifluoperazine. Causes of high AST: chronic alcohol ingestion, not limited to overt chronic alcoholism; cirrhosis. In alcoholic hepatitis, AST values usually are <300 units/L. In hepatitis, look for a high AST:LD (LDH) ratio, >3, and very high AST peaking at 500−3000 units/L in acute viral hepatitis (ie, in clinical acute viral hepatitis the transaminases may be increased 10 times or more above their upper limits of normal). AST increases are found in other types of liver disease, including earlier stages of hemochromatosis; chemical injury (eg, necrosis related to toxins such as carbon tetrachloride). Some instances of cholecystitis cause increased AST. AST and ALT (SGPT) are increased in Reye syndrome. In infectious mononucleosis, LD (LDH) is commonly considerably higher than AST. Trauma (including head trauma and including surgery) and other striated muscle diseases, including dystrophy, dermatomyositis, trichinosis, polymyositis, and gangrene cause AST increases. Both AST and ALT elevations are found with Duchenne muscular dystrophy. Look for high CK in myositis, high LD5 (or isomorphic pattern in some instances of polymyositis) on LD isoenzymes. In myocardial infarction AST peaks about 24 hours after infarct and returns to normal three to seven days later. In acute MI without shock or heart failure, ALT is not apt to increase significantly. AST increases in congestive failure with centrilobular liver congestion, in which high LD5 on LD isoenzymes is found, and in pericarditis, myocarditis, pancreatitis, and other inflammatory states including Legionnaires' disease. In renal infarction LD is usually high, out of proportion to AST. Lung infarction and other disease entities leading to necrosis including large, necrotic tumors cause increased AST; LD is commonly also increased in such instances. Shock (LD also usually increased); hypothyroidism (LD and/or CK not infrequently increased in myxedema); hemolytic anemias (LD high with increased LD1) and certain CNS diseases may increase AST. Very high AST levels usually are caused by liver disease and/or by shock.

 

Performing Laboratory

Copley Hospital

 

Methodology

Bichromatic Rate

 

Specimen Requirements

Specimen Type: Blood (Plasma or Serum)

Preferred: Light-Green Top

Acceptable: Gold Top

Specimen Volume: Full Tube

Specimen Minimum Volume: 2 mL

Reject: Slight Hemolysis

 

Collection Instructions:

1. Label specimen with patient’s full name, date of birth,

    date & time of collection, and person collecting.

2. If delay in specimen transport > 1 hour, centrifuge tube.

3. Refrigerate specimen during transport.

 

Reference Values

Normal: 15 - 37 U / L

 

Stability

Refrigerated: 7 Days

 

Day(s) Performed

Daily

Available STAT

Analytical Time: 1 Day

 

Aliases

Aspartate Aminotransferase

GOT

SGOT

Transaminase, SGOT

AST

 

Test Classification & CPT Coding

84450