Chemistry
Cardiac related
Aspartate aminotransferase (AST)

Author: Larry H. Bernstein, M.D. (see Authors page)

Revised: 28 January 2016, last major update December 2009

Copyright: (c) 2002-2016, PathologyOutlines.com, Inc.

PubMed Search: Aspartate aminotransferase [title]
Terminology
  • Previously known as Serum Glutamic Oxaloacetic Transaminase (SGOT)
  • Transaminase classification EC 2.6 (L-aspartate: 2-oxoglutarate aminotransferase, EC 2.6.1.1)
  • Distinct from ALanine aminoTransferase (ALT), another hepatic aminotransferase previously known as serum glutamic pyruvic transaminase (SGPT)
Pathophysiology
  • Ubiquitously distributed in tissues
  • Has different specific activity (rate of NADH oxidation per gram of protein) in red cells, heart, liver, muscle, brain, kidneys and placenta
  • After myocardial infarction, is released into the circulation and becomes elevated at 6 to 10 hours, peaks at 24-36 hours (at serum levels of 2 to 10 times upper limit of reference range)
Laboratory
Function
  • Catalyzes the transfer of an amino group to the keto acid in the conversion of conversion of aspartate and alpha-ketoglutarate to oxaloacetate and glutamate, with pyridoxal phosphate (Vitamin B6) as a cofactor
  • Found in hepatocyte cytoplasm and mitochondria as two isoenzymes, but this has no clinical significance

Methodology
  • May be assayed spectrophotometrically in a coupled reaction with malate dehydrogenase in the presence of NADH (Karmen 1955 J Clin Invest 1955;34:126, Amador and Wacker 1962 Clin Chem 1962;8:343)
  • One unit oxidizes one micromole of NADH per minute at 25°C and pH 7.4 under the specified conditions
  • Laboratory methods for aminotransferases should be supplemented with pyridoxal phosphate, to avoid falsely decreased activities in samples obtained from malnourished individuals with low endogenous vitamin B6 concentrations
Interpretation
Indications for testing (serum)
  • For acute myocardial infarction, use has been superseded by cardiac troponins
  • Screening test for liver disease, although ALT is more specific
    • Increases in AST and ALT are higher when hepatocytes are damaged by viruses or toxic substances than in biliary obstruction
    • In elderly, AST elevation is associated with obesity and consuming >3 alcoholic drinks / day (Aliment Pharmacol Ther 2009;30:1137)
  • To assess prognosis after liver transplantation (Transplant Proc 2009;41:1727)
  • To assess prognosis in autoimmune hepatitis (Clin Gastroenterol Hepatol 2008;6:1389)
  • To assess effectiveness of treatment for liver disease (decline in levels may be due to disease resolution, or severe disease with minimal enzyme left for release)
  • AST/ALT ratio is useful:
  • AST/platelet ratio index is useful:
  • Levels in vaginal washing fluid may predict preterm premature rupture of membranes (Fetal Diagn Ther 2008;24:425)
  • A more sensitive marker of muscle damage than ALT, but less sensitive than CK, aldolase and myoglobin (Clinical Chemistry 2009;55:1573)

Limitations
  • For acute myocardial infarction, AST elevation is nonspecific in the absence of crushing chest pain and ECG changes of ST elevation, ST depression or T-wave inversion
  • High AST levels are associated with acute pancreatitis, celiac disease, exercise, hemolysis, hypothyroidism, liver disease (see above), muscle disease (see above), post-delivery, post-intramuscular injection, post-surgery, premature rupture of membranes, renal infract, sepsis (General Practice Notebook)
  • In leukemia patients, falsely elevated levels may be due to pneumatic transport of specimen (Ann Clin Biochem 2010;47:94)
  • Children may have isolated elevated levels, often due to macroenzyme form of AST (Am J Gastroenter 2005; 100;243), but phenomenon appears to be benign (J Pediatr 2009;154:744)

Reference ranges
  • Female: 6 - 34 IU/L
  • Male: 8 - 40 IU/L (may vary between laboratories)
  • High value: needs to be interpreted in the context of chest pain and ECG findings