Aspartate Aminotransferase (AST/SGOT)
- Serum Glutamic Oxaloacetic Transaminase
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.