Aspartate Aminotransferase (AST/SGOT)

Aspartate Aminotransferase (AST/SGOT)

CPT Test code: 84450

Specimen: Serum (preferred) or plasma
Volume: 1 mL
Minimum Volume: 0.5 mL
Container: Red-top tube, gel-barrier tube, green-top (heparin) tube, or lavender-top (EDTA) tube
Collection: Separate serum or plasma from cells within 45 minutes of collection.
Storage Instructions: Maintain specimen at room temperature.
Causes for Rejection: Gross hemolysis; improper labeling
Use: 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
Footnotes: 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, 309(3):133-9. PubMed 6866012

2. DeVivo DC, “How Common Is Reye’s Syndrome?” N Engl J Med, 1983, 309(3):179-81. PubMed 6866017

3. Winzelberg GG, Hull JD, Agar JW, et al, “Elevation of Serum Lactate Dehydrogenase Levels in Renal Infarction,” JAMA, 1979, 242(3):268-9. PubMed 448917

4. Rej R, “Aminotransferase in Disease,” Clin Lab Med, 1989, 9(4):667-87. PubMed 2686908

5. Seeff LB, Cuccherini BA, Zimmerman HJ, et al, “Acetaminophen Hepatotoxicity in Alcoholics. A Therapeutic Misadventure,” Ann Intern Med, 1986, 104(3):399-404 (review). PubMed 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, 62(8):681-7.PubMed 3600038

References: Tonks DB, “A Study of the Accuracy and Precision of Clinical Chemistry Determinations in 170 Canadian Laboratories,” Clin Chem, 1963, 9:217-63.PubMed 13985504