Aspartate Aminotransferase (AST/SGOT)

CPT: 84450
Print Share


  • Serum Glutamic Oxaloacetic Transaminase
  • SGOT
  • Transaminases

Expected Turnaround Time

Within 1 day

Related Documents

For more information, please view the literature below.

Hereditary Hemochromatosis

Specimen Requirements


Serum (preferred) or plasma


1 mL

Minimum Volume

0.7 mL (Note: This volume does not allow for repeat testing.)


Red-top tube, gel-barrier tube, or green-top (lithium heparin) tube. Do not use oxalate, EDTA, or citrate plasma.


Separate serum or plasma from cells within 45 minutes of collection.

Storage Instructions

Maintain specimen at room temperature.

Stability Requirements



Room temperature

7 days


14 days


14 days

Freeze/thaw cycles

Stable x3

Causes for Rejection

Gross hemolysis; improper labeling

Test Details


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.1,2 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.3 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.

Drugs: A large number of commonly used drugs have been reported to elevate AST: isoniazid, phenothiazines, erythromycin, progesterone, anabolic-androgenic steroids, halothane, methyldopa, opiates, indomethacin, salicylates in children, and other drugs. Hepatotoxicity from drugs may cause high aminotransferase activity with elevation of AST:ALT ratio.4

Acetaminophen hepatotoxicity deserves special mention. In alcoholics, apparently moderate doses of the analgesic have caused severe hepatotoxicity. Doses of 2.6−16.5 g/24 hours are reported with total bilirubin 1.3−23.9 mg/dL, AST 1960−29,700 units/L, and ALT 12,000−12,550 units/L. The characteristic pattern included mild to severe coagulopathy and AST greater than ALT by a considerable margin.5

Macroenzyme causing unexplained increase of AST is described with normal levels of CK and ALT.6



Additional Information

AST has origin from heart, liver, skeletal muscle, kidney, pancreas, spleen, and lung. Very high values, >500 units/L, usually suggest hepatitis or other kinds of hepatocellular necrosis but can also be found with large necrotic tumors, other types of necrosis or extensive hypoxia, congestive failure, and shock. Unexplained AST elevations should first be investigated with ALT and GT. Mitochondrial AST (m-AST) may be useful in the diagnosis of alcoholic liver disease; it is reviewed by Rej.4


1. Lichtenstein PK, Heubi JE, Daugherty CC, et al. Grade I Reye's syndrome. A frequent cause of vomiting and liver dysfunction after varicella and upper respiratory tract infection. N Engl J Med. 1983 Jul 21; 309(3):133-139. 6866012
2. DeVivo DC. How common is Reye's syndrome? N Engl J Med. 1983 Jul 21; 309(3):179-181. 6866017
3. Winzelberg GG, Hull JD, Agar JW, Rose BD, Pletka PG. Elevation of serum lactate dehydrogenase levels in renal infarction. JAMA. 1979 Jul 20; 242(3):268-269. 448917
4. Rej R. Aminotransferase in disease. Clin Lab Med. 1989 Dec; 9(4):667-687. 2686908
5. Seeff LB, Cuccherini BA, Zimmerman HJ, Adler E, Benjamin SB. Acetaminophen hepatotoxicity in alcoholics. A therapeutic misadventure. Ann Intern Med. 1986 Mar; 104(3):399-404 (review). 3511825
6. Litin SC, O'Brien JF, Pruett S, et al. Macroenzyme as a cause of unexplained elevation of aspartate aminotransferase. Mayo Clin Proc. 1987 Aug; 62(8):681-687. 3600038


Tonks DB. A study of the accuracy and precision of clinical chemistry determinations in 170 Canadian laboratories. Clin Chem. 1963 Apr; 9:217-233. 13985504


Order Code Order Code Name Order Loinc Result Code Result Code Name UofM Result LOINC
001123 AST (SGOT) 1920-8 001123 AST (SGOT) IU/L 1920-8

For Providers

Please login to order a test

Order a Test

© 2023 Laboratory Corporation of America® Holdings and Lexi-Comp Inc. All Rights Reserved.

CPT Statement/Profile Statement

The LOINC® codes are copyright © 1994-2023, Regenstrief Institute, Inc. and the Logical Observation Identifiers Names and Codes (LOINC) Committee. Permission is granted in perpetuity, without payment of license fees or royalties, to use, copy, or distribute the LOINC® codes for any commercial or non-commercial purpose, subject to the terms under the license agreement found at Additional information regarding LOINC® codes can be found at, including the LOINC Manual, which can be downloaded at