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