Information
Refer to: Babb RR: Clinical significance of the SGOT test (Infor-
mation). Calif Med 118:89-91, May 1973
The Clinical Significance
of the SGOT Test
RICHARD R. BABB, MD
Palo Alto
ALTHOUGH THE HISTORY and physical examina-
tion performed with patience and care remain the
cornerstone of successful medical practice, the
modern physician must also rely on laboratory
tests for confirmation of clinical impressions and
monitoring of therapeutic endeavors. Advances in
laboratory technology now allow for a battery of
tests to be done on one specimen of blood and
often provide us with unanticipated abnormal re-
sults that must either be ignored or somehow
explained. We are anxious about "missing some-
thing," and yet we hope to avoid what Rang' has
labeled the Ulysses syndrome-the mental and
physical disorders which befall a patient as his
physician attempts to track down the cause of a
falsely positive laboratory result.
In these circumstances it seems timely to discuss
the clinical significance of the serum glutamic
oxalacetic transaminase (SGOT) test, a common
component of most biochemical screening panels.
In three recent studies of large patient popula-
tions,24 the SGOT was abnormal in 1 to 4 percent.
Friedman et al3 reviewed the results of a 20-test
screening panel drawn on 8,446 persons having a
"multiphasic health checkup" in the context of the
Kaiser-Permanente program in Oakland and San
Francisco. Of 7,512 SGOT tests 202 (3 percent)
were abnormally high. In a study of 547 patients
seen in the General Medical Clinic of the Stanford
University Medical Center, Schneiderman et a12
found seven, or about 1 percent, to have abnormal
From the Section of Gastroenterology, Palo Alto Medical Clinic.
Reprint requests to: R. R. Babb, MD, Palo Alto Medical Clinic,
300 Homer Avenue, Palo Alto, Ca. 94301.
SGOT tests. Finally, Bates and Yellin4 analyzed all
results from a large multiphasic screening unit in
the Rochester, N.Y., area and noted 4 percent of
the SGOT values to be elevated. My own experience
has been similar and will be discussed below.
As has been pointed out by other investiga-
tors,2'5 the statistical "normal" of any given test
refers to values lying within two standard devia-
tions from the mean; that is, between the 2.5 and
97.5 percentile points "of the distribution of values
for healthy persons." It follows, then, that occa-
sionally, or one time out of 20, the test in question
will fall outside the normal range without indicat-
ing a true abnormality. The normal range for a
test will vary according to the control popula-
tion and specific laboratory method used for its
determination.
Method
Several exhaustive reviews have been published
regarding the nature of the GOT enzyme and the
methods for determining how much of it is pres-
ent.6'2 For the purposes of this brief clinical re-
view, it need only be remembered that this enzyme
catalyzes the transfer of an amino group from an
alpha amino acid to an alpha keto acid-that is,
a transamination reaction:
glutamic
aspartic + ketoglutaric SGOT oxalacetic
acid acid = acid acid
The enzyme is found throughout the body, espe-
cially in the heart, liver and muscle tissues.6-'2 Its
concentration in the serum depends on the amount
originally in the normal or injured tissue, the rate
of cellular release, and the rate of removal from
circulation.8 Injected glutamic oxalacetic transami-
nase distributes throughout body fluid and very
little is lost in the bile or urine.'3 Presumably the
enzyme is metabolized and degraded within the
body.
Measurement of serum enzyme activity can be
done by chromatographic,6 spectrophotometric7
or colorimetric methods." Most automated screen-
ing panels have used diazonium salts to give the
colorimetric reaction, and it is now clear that in-
terfering substances in the patient's blood such as
acetone or drugs may give falsely elevated re-
sults.'4-'6 Determinations based on the manual
CALIFORNIA MEDICINE 89
The Western Journal of Medicine
spectrophotometric method of Karmen7 which in-
volve the oxidation-reduction of nicotinamide ade-
nine dinucleotide (NAD) are less likely to give
spurious results, and are being incorporated into
the screening panel methods of some laboratories.
Clinical Significance of SGOT
As noted above, 1 to 4 percent of serum speci-
mens from several outpatient populations showed
elevated SGOT. My own experience has been simi-
lar. Twenty-five of 350 consecutive patients (7
percent) seen over a recent 12-month period for
annual examinations had elevated SGOT on the
sequential multiple analysis (SMA) 12/60 multi-
phasic panel which uses a colorimetric procedure
with "normal" being up to 50 units. None had
values higher than 150 units and most were under
100. Two of the 25 patients could not be traced
for further evaluation. In the remaining 23 pa-
tients, however, repeat SGOT determinations done
manually by the Karmen method were normal in
18 and still abnormal in five. Of the latter, one
proved to have chronic hepatitis on liver biopsy,
and the other four had a return to normal values
after stopping all alcohol ingestion for one month.
When confronted with an abnormal SGOT on a
screening panel, one should first repeat the test,
using the specific NAD-linked method if at all pos-
sible. More often than not, the repeat value will
be normal. Elking and Kabat14 listed 34 drugs
which they feel can falsely elevate SGOT test values.
Other observers have described spurious eleva-
tions of the SGOT when measured by the colori-
metric method in patients taking erythromycin"5
or para-aminosalicylic acid.16
Repeated intramuscular injections of drugs, by
damaging muscle, may also elevate the SWOT."
Knirsch and Gralla found elevations to levels of
115 units after three days of parenteral carbenicil-
lin. I have seen several similar cases. Values return
to normal within a week or two of stopping the in-
jections, and the CPK (creatine phosphokinase),
an enzyme not elevated in liver disease, also rises
at the same time.
To this point, discussion has revolved around
the presumably healthy person with an unantici-
pated elevation in their SGOT. What is the ap-
proach when the patient is obviously ill? There
should be little difficulty in evaluating an elevated
SGOT in patients with acute tissue damage from
myocardial infarction, viral or drug-induced hepa-
titis, or muscle inflammation. In my experience,
90 MAY 1973 * 118 * 5
the clinical picture in these common causes of
SGOT elevation is usually clear, and the diagnosis
can be readily confirmed by utilization of other
appropriate laboratory tests.'8-23
Certain other diseases, or medical events, how-
ever, which can occur in sick patients may elevate
the SGOT and cause considerable confusion unless
recognized.
It is common to administer opiates to patients
with abdominal pain. Shuster et al24 showed that
codeine, meperidine, or morphine did not elevate
the SGOT when given to healthy students. It is quite
clear, however, that if these drugs are given to
patients with either a nonfunctioning or absent
gallbladder, the SGOT will be elevated to levels
ten to twenty times normal.'5-" The rise starts
within two to four hours of the injection and is
usually back to normal by 24 hours. Presumably
these opiates increase biliary pressure by inducing
spasm at the sphincter of Oddi. The lack of a
normal gallbladder reservoir allows the increased
pressure to be exerted on liver cells with subse-
quent injury and leakage of the enzyme. Thus,
serum should be drawn for later laboratory tests
before opiates are administered to a patient with
abdominal pain.
The SGOT is often very helpful in deciding
whether a patient with jaundice has intrahepatic
or extrahepatic disease. Nonetheless, occasionally
extrahepatic obstruction will markedly elevate the
SGOT and cause diagnostic confusion. Abbruzzese
and Jeffery28 reported three patients with common
duct stones who showed SGOT values of 1,320,
1,250 and 960 units soon after admission. Gins-
berg29 likewise noted three similar patients with
SGOT values of 1,710, 2,450, and greater than
1,250 units secondary to extrahepatic biliary tract
obstruction. In reviewing the literature, he found
the incidence of an SGOT value greater than 300
units in extrahepatic obstruction to be about 3
percent (6 of 176 cases). Thus not all jaundiced
patients with an SGOT value higher than 500 units
will have hepatitis. Clues to the elevation's being
secondary to extrahepatic disease are the rapid
fall toward normal (below 300 units by day 3 to
4) and the accompanying pronounced elevation
in the lactic dehydrogenase (LDH) values.
Acute pancreatitis may raise the SGOT also.
Foulk and Fleisher30 found 22 of 32 patients with
pancreatitis to have elevated serum levels depend-
ing on the severity of associated biliary tract
inflammation. There was no correlation with the
severity of the pancreatitis per se. Seven of the
22 had levels higher than five times normal, and
one measured approximately 700 Karmen units.
SGOT values higher than 1,000 units are usually
due to viral or drug-induced hepatitis. As men-
tioned above, another cause may be extrahepatic
obstruction. Shock and congestive heart failure
may also lead to extremely high levels of SGOT. I
have seen several patients in severe heart failure
with values higher than 2,000 units. Fragge et a131
reported in 1960 that one-third of their patients
with heart failure had elevated SGOT values. They
noted levels of SGOT in a literature review ranging
from 45 to 750 units, with a few cases greater
than 2,000. Logan et a132 reported three cases of
severe heart failure with SGOT values of 1,180,
1,780, and 1,300 units. They felt the cause might
be two-fold: liver congestion, and also anoxia
from decreased oxygen concentration and blood
flow in the hepatic artery.
One may be asked to see a patient with ele-
vated SGOT in the immediate postoperative period.
Besides the numerous causes already alluded to,
question arises as to the role of surgical operation
per se. Ayres and Williard33 studied 266 patients
after operation. They found 20 percent to have
a slight elevation of SGOT over the first four days.
Levels were usually less than 120 units, with a
few as high as 250 units, and all were back to
normal by day 5.
In conclusion, the advent of biochemical screen-
ing panels has confronted the clinician with an
array of unexpected abnormalities in presumably
healthy patients. Because of the presence of SGOT
in tissues, often effected by serious disease, and
the inclusion of the test on most panels, the results
of the test must be reckoned with. One should
first ascertain if the reported value is truly or
spuriously elevated. In my experience, if the pa-
tient is asymptomatic and the results of physical
examination are within normal limits, the com-
monest cause of elevation is alcohol abuse or drug
ingestion. If the patient is ill, diseases of the heart,
liver or muscle are usually the cause of the in-
creased values, but one must remember that sub-
stantial elevations of the SGOT can occur in pa-
tients wvho have been given opiates, or who are
ill with extrahepatic obstruction, congestive heart
failure, or shock.
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