AMERICAN JOURNAL OF CLINICAL PATHOLOGY
Vol. 33, No. 2, February, 1960, pp. 97-108
Printed in U.S.A.
AN EVALUATION OF SERUM TRANSAMINASE IN
T H E JAUNDICE STATES
HARRY J. SACKS, M.D., AND GERARD P. LANCHANTIN, P H . D .
Division of Laboratories, Cedars of Lebanon Hospital, Los Angeles, California
Since the observation of LaDue and
Wroblewski13 that the serum glutamic
oxalacetic transaminase (SGOT) became
elevated after myocardial infarction, a
large number of reports have been published
dealing with abnormal elevation of this
enzyme in diseases of the heart and other
organ systems. Generally, elevated SGOT
has been observed in 6 chief groups of illnesses. These include injury to skeletal
muscle, hepatobiliary disease, extensive
damage to the brain, hemolytic anemia,
certain chemical and drug intoxications, and,
in some instances, pulmonary infarction.1-8 •
analyzed by means of the spectrophotometric procedure of Karmen. 9 The Beckman model DU spectrophotometer was
used and the units of SGOT were equated to
a unit drop in optical density per minute
under the conditions defined.9 It should be
pointed out, however, that although the
analysis was originally standardized at
room temperature, presumably 25 C., the
cell compartment of the Beckman spectrophotometer has an ambient temperature
range of some 30 to 32 C. It was, therefore,
assumed that this temperature differential
also existed in the original method of Karmen. Our experience in using this technic as
an adjunct to the clinical diagnosis of myocardial infarction has been reported previously.19 With this method, we observed the
normal range to be 10 to 40 units with a
mean of 23 units, as also reported by
others. 8,29
Colorimetric assay of SGOT. Because of
the technical ease which permits the routine
performance of multiple analyses of SGOT,
the colorimetric procedure of Reitman and
Frankel20 was used throughout the major
portion of this investigation. The technic
and reagents used were supplied by the
Sigma Chemical Company. Although Sigma
states that the resultant values for SGOT
are said to be equivalent to spectrophotometric results, parallel analysis in our
laboratory by means of both methods with
more than 60 specimens (normal and elevated SGOT included) demonstrated that
the colorimetric procedure consistently resulted in values lower than those obtained
with the technic of Karmen.
Parenthetically, these lower findings are
confirmed by the reports that the mean
value for normal serums is 16 units by the
colorimetric method 2,20 in contrast to 22.1
units by the spectrophotometric method. 3,2 *
When our results, obtained by the 2 methods, were plotted against each other, the
factor 1.38 was derived. The colorimetric
result was then multiplied by 1.38 in each
10-12, 14-19, 2 1 , 22, 24, 26-34
Apart from the characteristically transient
elevation of SGOT after myocardial infarction, there have been no established unified
criteria for the evaluation of abnormal levels
of SGOT in these other pathologic conditions.
This paper deals with a study of the level
of serum transaminase in patients with
jaundice of varying etiology. These cases,
for the most part, were followed by serial
determinations of SGOT and, to a limited
extent, by analyses of serum glutamic
pyruvic transaminase (SGPT).
METHODS AND
MATERIALS
Laboratory Methods
Spectrophotometric assay of SGOT. During
the early phase of this study, the SGOT was
Received, June 26, 1959; revision received,
September 8; accepted for publication November 3.
Dr. Sacks is Associate Director, Division of
Laboratories, Cedars of Lebanon Hospital, and
Assistant Clinical Professor of Pathology, University of Southern California. Dr. Lanchantin is
Chief of Biochemistry, Division of Laboratories,
Cedars of Lebanon Hospital, and Adjunct Assistant Professor of Biochemistry and Nutrition,
University of Southern California.
This paper was presented at the Thirty-Seventh
Annual Meeting of the American Society of
Clinical Pathologists, Chicago, Illinois, November
3 to 7, 1958.
97
98
SACKS AND
analysis in order to calculate the approximate spectrophotometric equivalent. Using
this factor, the mean level of SGOT obtained for a group of 20 young people (10
males and 10 females) in good health was
24.2 units per ml. with a range (95 per cent
limits) of 6 to 42 units per ml. Use of this
factor thus permitted continuity in our
study with the earlier results for SGOT obtained in our laboratory by means of spectrophotometric assay. Furthermore, the
use of this factor was justified by the fact
that the Karmen assay not only was the
established reference technic, but the normal and abnormal ranges of SGOT had been
disseminated throughout the world in terms
of the spectrophotometric method. Thus,
results in terms of Karmen units would be
comparable to previous work. For those
wishing to compare colorimetric results, the
figures for SGOT as listed in this report can
be divided by the 1.38 factor in order to
yield the results that would be obtained by
means of following the Sigma colorimetric
technic.
The reproducibility of the method for 10
replicate analyses of single specimens at
various levels of SGOT were (95 per cent
limits): 8 per cent at 24 units per ml., 5 per
cent at 170 units per ml., and 3.4 per cent
at 1700 units per ml.
Analysis of SGPT. The procedure used in
this study was that of Reitman and Frankel.20 The mean level for SGPT obtained
for a group of 20 young people in good
health was 21.3 units per ml. with a range
(95 per cent limits) of 5 to 35 units per ml.
The above normal ranges were comparable
to colorimetric values reported in the
literature. 20 •27 It should be noted that mean
spectrophotometric values for normal persons have been reported as 16 with a range
of 5 to 35 units,32 but that in the abnormal
ranges 1 colorimetric unit is equal to approximately 2 spectrophotometric units.27 A
correction was not attempted, inasmuch as
the staff in this laboratory did not use the
latter technic and, consequently, we were
not in a position to confirm or deny the
factor of 2 reported in the abnormal ranges.27
For those who would want to compare
SGOT and SGPT in terms of Karmen
Vol. 33
LANCHANTIN
(spectrophotometric) units, however, the
results of the colorimetric SGPT as observed
in this study can be multiplied by the factor
of 2, assuming the above report27 is correct.
Clinical Material
The data presented in this study were
obtained from 120 jaundiced patients admitted to Cedars of Lebanon Hospital and
Clinic from November 1956 to January
1959. Diagnosis was occasionally by biopsy
but chiefly clinical in the medical cases of
jaundice. In the duct obstruction cases, it
was generally made at surgery or autopsy.
RESULTS
Figure 1 presents the maximal values for
SGOT obtained in 114 persons with jaundice
of varying etiology.
Of 30 cases of viral hepatitis, the level of
SGOT exceeded 500 units in 21 instances.
There was no statistical difference between
the levels of enzyme in serum hepatitis (11
cases) and infectious hepatitis (19 cases),
and, consequently both groups were treated
as one. There were 2 with less than 300 units,
but, inasmuch as these were convalescing
patients at the time of study, the peak
SGOT may have been missed. The highest
value in this series was 10,000 units (not
diagrammed).
Figures 2 and 3 illustrate the course of 2
patients with serum hepatitis, which course,
incidentally, is essentially the same as in
infectious hepatitis. In Figure 2, the early
classic striking rise of SGOT is observed
prior to the onset of icterus. The relation, in
this instance, of the values for SGOT in the
first few days of icterus can not be correlated with values for bilirubin, inasmuch as
the latter were not available. In Figure 2
the first values for transaminase were obtained as the level of bilirubin was beginning
to fall, and, in parallel, the values for
SGOT and SGPT decreased precipitously,
so that by the seventeenth day a value
in the range of 450 units for each enzyme
was noted. Parenthetically, it should be
pointed out that an SGOT below the 500
units is nondiagnostic and illustrates the
importance of obtaining the value for SGOT
at the ascendency of the illness and, prefer-
Feb. 1960
99
TRANSAMINASE IN JAUNDICE
VIRAL
BILE DUCT
3 Q Q Q HEPATITIS ^ STASIS
DRUG
HEPATITIS rlBaur,o,o
JAUNDICE (CHOUMWOLITIC) CIRRHOSIS
CARCINOMA PANCREApp U V E R
TIT IS
2000
.1000
! 900
• 800
700
Z
600
3
500
O
o
400
V)
300
200
1000
s
•••
• •
30
37
10
5
18
1L
NUMBER OF CASES STUDIED
3000,
2000
serum hepatitis,
1000
68 yr. female
ANOREXIA
750
" FATIGUE^
SL. FEVER
COMA
NO CLINICAL
ICTERUS
500
250
FIG. 1 (upper). Highest levels of SGOT in 114 jaundiced patients. £>—Marsilid;
©—Methyltestosterone; and 9—thorazine.
FIG. 2. (lower). Preicteric elevation of SGOT in hepatitis.
ably, prior to the peak of the jaundice. The
subsequent course of both patients is also
typical in that as the bilirubin continued to
decrease in concentration, the SGOT and
SGPT fell in parallel manner. In a number
of the patients who have been followed to
the completion of the illness, it is noted
that the SGOT has returned practically to
100
Vol. 38
SACKS AND LANCHANTIN
serum hepatitis
64 yr., MALE
X
10
20
30
40
50
60
DAYS
FIG. 3. Transaminase and bilirubin relationships in hepatitis.
normal limits (50 to 60 units), or within
normal limits, whereas the bilirubin remains
for some days, and occasionally for a week
or so, at the level of 2 to 3 mg. per 100 ml.
These patients have been observed to be
entirely well clinically, and their ambulation
has been without undue effect. In this regard, it might be stated that at this stage
of convalescence, on 1 occasion, a patient
demonstrated a sharp rise in SGOT, whereas
bilirubin was 2 mg. per 100 ml. Subsequently, the patient developed a clinical
relapse. This finding would suggest that
there is prognostic value in a determination
of transaminase performed at approximately the time the patient is permitted to
ambulate, and possibly even some days
after ambulation has been effected.
Not included in Figure 1 were data from
6 patients with hepatic damage usually
secondary to shock. In 5 cases, damage to
the liver followed myocardial infarction, and,
in the sixth, after massive gastrointestinal
hemorrhage from an ulcer. These values
ranged between 2000 to 10,000 SGOT units.
These heights, it should be noted, in our
experience are never attained by myocardial
necrosis alone, and as a corollary, in patients
with suspected or actual heart necrosis such
high levels should be interpreted as indicating complicating hepatocellular damage.
In these instances, elevated SGPT also
paralleled those obtained for SGOT. Inasmuch as SGOT is always higher than SGPT
at the usual levels (up to 500 units SGOT)
observed in uncomplicated myocardial
necrosis,32 a parallel elevation of SGPT in
such a case also probably indicates complicating hepatocellular damage.
In the duct-obstruction group, 33 of 37
Feb. 1960
TRANSAMINASE IN JAUNDICE
101
obstructive jaundice
(with terminal central
liver necrosis)
\$tfCm
34yr.,FEMALE
CO
Xn 100
<
2<z
w
z<
50
\1
o
oCO
zCO
3
a: •
0
20
15
^i
CD S
o 10
^o
h
o * 5
I—
FIG. 4. Comparison of SGOT in obstruction of the bile duct and in hepatic
central necrosis.
cases had maximal values for SGOT less
than 300 units. The data indicate that the
levels of SGOT during the course of obstruction of the ducts seldom reaches levels of 500
SGOT units. Figure 4 illustrates the contrasting findings for SGOT in duct obstruction and hepatic cell damage in the same
patient. The initial course was that of an
acute obstruction, after which the values for
SGOT and bilirubin decreased sharply, only
to level off for the next 25 days. Clinically,
this course indicated partial relief, followed
by persistence of a low-grade obstruction.
Suddenly, 2 days prior to death, the patient
lapsed into sustained shock. An electrocardiogram at this time was interpreted as
revealing a myocardial infarct. SGOT at
this time had risen sharply to 760 and, by
the next day, to 1800 units. At necropsy, a
large stone was observed in the common
duct, along with extensive central necrosis
in the liver and a myocardial infarction.
m
102
Vol. 88
SACKS AND L A N C H A N T I N
300
-i
1
1
-i
r
1
1
1
1
1
1
r
thorazine jaundice
37 yr. female
• SGOT
O S6PT
_1
2 200 —
•
—
to
1-
z
3
_
NAS
LU
-5
9«
TRAN
1 100 — b>4
SE
E
V)
S3
ca
- g2
ca
!••
2
40
4 6
ITJ77T
8 10 12 14 16 18 20 22 24 26 28
JUNE
6
JULY
-fVO-T-
T
30
_f
E20rO
O 18
o
o
o
*'«
J.4
o
2 12
•
l'° Urn*
=J
CD
8
_.
6
•
/
m °
*
• •
/
/
/
o
o -
/
7
• o
°
o
• BILE DUCT
STASIS
O HEPATITIS
8
is 4
P 2>
.7
0
200
400
600
800
1000 2000
3000
SGOT UNITS/ML
FIG. 5 (upper). Transaminase and bilirubin pattern in thorazine jaundice.
FIG. 6 (lower). Highest SGOT plotted against concomitant serum bilirubin (SGOT:bilirubin ratio).
The maximal levels for SGOT observed in
examples of dnig-induced jaundice seem to
be associated with 2 types of hepatic alterations. In the first group (cholangiolitic
hepatitis), levels less than 500 units were
associated with 3 instances of Thorazine
and 2 of methyltestosterone therapy. A
typical example of a case of Thorazine-
Feb. 1960
TRANSAMINASE
induced jaundice is illustrated in Figure 5.
In contrast to this group, the Marsilidrelated cases all manifested values greater
than 500 units. A biopsy in 1 instance of the
latter was that of toxic hepatitis, virtually
indistinguishable from the lesion of viral
hepatitis. Not seen in this study, but reported by Wroblewski and LaDue29 are
values up to 25,000 units in carbon tetrachloride liver necrosis.
Five patients with cholangiolitic hepatitis
all had values less than 500 units. The significant data relative to these patients are
indicated in Table 1.
In the 17 examples of portal and 1 of
biliary cirrhosis, the values for SGOT were
well below 300 units per ml. Some of these
patients were deeply jaundiced. In portal
cirrhosis, the levels for SGOT usually re-
IN
103
JAUNDICE
turned to normal with remission. Several
of these patients had a clinical relapse after
acute excesses of alcohol and these episodes
were associated with corresponding elevations in the SGOT. When in remission, the
latter patients revealed a normal SGOT.
Six cases of cancer of the liver with
icterus manifested values for SGOT well
below 300 units. Two cases with extensive
involvement of the liver revealed normal
levels of SGOT. Two patients with metastatic carcinoma of the liver and 1 hepatoma
had values of 640, 1060, and 960, respectively. The 2 secondary cases revealed
extensive necrosis of hepatic parenchyma
adjacent to tumor and the hepatoma itself
was massively necrotic. Similar findings
have been reported in other papers. The
findings of elevated values for SGOT in 2
TABLE 1
CHOLANGIOLITIC H E P A T I T I S
Alkaline
Phosphatase
Bilirubin
Case
•
Cephalin
Flocculation
Thymol
Turbidity
SGOT*
<1.0
0-3 U.
<2+
1
68f
3.5
0
2.7
2
3
4
5
9.0
17.4
41.0
13.0
9.5
11
3.8
3.5
±
3
10
10
2.7
<SU.
3+
Method of Study
Etiology
Normal values
<40U.
130)
124/
350
130
145
130
Serum
Open biopsy
Serum
Idiopathic
Serum
Idiopathic
Clinical
Open biopsy
Clinical
Open biopsy
0
* Serum glutamic oxalacetic transaminase.
t Icterus index.
TABLE 2
FINDINGS IN PANCREATITIS
Amylase
Biliary Calculi
SGOT'
1
2
3
4
5
6
7
Serum
Random urine
units per 100 ml.
units per 100 ml.
mg. per 100 ml.
units
40
1200
423
810
2875
603
190
—
8.7
4.0
1.7
4.5
1.8
1.1
0.35
260
1160
102
830
390
140
780
4338
5297
1900
4714
5086
2400
Where found
* Serum glutamic oxalacetic transaminase.
None
Gallbladder
None
In duct
Only in gallbladder
None
None
How diagnosed
Autopsy
X-ray
X-ray
Surgery
Surgery
X-ray
X-ray
104
Vol. 33
SACKS A N D L A N C H A N T I N
nonicteric patients in whom hepatic cancer
was present suggests its use in situations
where jaundice is absent and where metastases are thought to be present in the liver.30
Four of 7 persons with pancreatitis had
values of 105 to 380 units of SGOT in serum
collected at the height of the illness, usually
at the time of admittance. In 3 patients, the
values were greater than 500 units. The
relation of several variables are seen in
Table 2. All but Cases 6 and 7 revealed some
degree of jaundice, but these results do not
demonstrate any relation between the degree of jaundice and the height of SGOT.
These findings are similar to the 26 patients
studied by Chinsky and Sperry,3 except
that none of theirs manifested such high
SGOT as observed in Cases 2, 4, and 7 in
this series.
SGOT-SGPT ratio. Table 3 records com.
parative values for SGOT and SGPT when
performed with the same sample of serum.
TABLE 3
COMPARATIVE V A L U E S F O B SERUM GLUTAMIC OXALACETIC T R A N S A M I N A S E (SGOT) AND
SERUM GLUTAMIC P Y R U V I C TRANSAMINASE (SGPT) I N T H E D I S O R D E R S INDICATED*
Hepatitisf
Duct Obstruction!
SGOT SGPT Ratio
SGOT
SGPT
Ratio
860
910
39
820
1230
27
1.04
0.73
1.44
114
94
96
76
74
40
1.5
1.27
2.4
1810
1150
1.57
2800
275
1200
350
2.33
0.78
1190
690
910
900
910
870
350
590
760
630
1.36
1.97
1.54
1.18
1.44
780
30
1230
90
0.63
0.33
1270
580
1230
320
1.03
1.81
1000 1050
1050 730
600 550
300 670
170 335
50 200
0.95
1.43
1.09
0.44
0.5
0.25
2050
900 2.27
1420
125
2160
250
0.65
0.5
1200
890
990
530
335
350
2.26
2.65
2.82
1220
670
1310
1110
0.93
0.60
1700
181
1100
180
1.54
1.0
850
630
90
130
780
940
660
345
33
68
340
320
1.28
1.82
2.72
1.91
2.29
2.93
SGOT SGPT
Ratio S G O T
1450
1630
1710
760
690
670
455
565
565
550
630
480
3.18
2.88
3.02
1.38
1.09
1.39
1380
1680
980
1300
1.40
1.29
1030
690
440
410
320
280
980
1170
480
290
280
290
1.05
0.58
0.91
1.41
1.14
0.96
167
30
94
Cirrhosis§
SGPT Ratio S G O T SGPT Ratio
Bilirubin
1.85 200
0.6
240
65
44
3.07
5.45
3.8
6.0
85 1.10 161
209
39
71
4.12
2.94
16.0
13.0
158
107
19
20
8.31
5.35
2.8
2.4
204
60 3.4
12.6
61
19 3.21
6.8
90
45
1.68
1.39
150
67
89
48
192
52 3.69
181
35 5.17
75 160 0.46
255
150
45
75
5.66
2.0
390
260
200
140
270
140
2.78
1.52
1.42
2.3
2.9
2.5
231
44 5.25
231
140 1.65
2.2
220 190 1.15 222 460 0.48 11.0
89
35 2.54
100
20 5.0
200
86 2.32
79
21 3.76
88
59 1.49
210
178
75
* Horizontal lines separate the one or more available pairs of results in each case,
t R a t i e , S G O T : S G P T ; average, 1.46; range, 0.33 t o 3.18.
t Ratio, S G O T : S G P T ; average, 2.78; range, 0.46 t o 5.66.
§ R a t i o , S G P T : S G P T ; average, 3.03; range, 0.48 t o 8.31.
100
90
90
2.1
40.0
1.97 39.0
0.83 36.0
Feb. 1960
TRANSAMINASE
There were 54 determinations in 18 patients
with hepatitis, 17 in 14 with duct obstruction, and 16 in the 8 with cirrhosis. Inasmuch as the values for SGOT (mentioned
under "Methods") are spectrophotometric
data and the values for SGPT are from
'Colorimetric procedures, the ratios and
relative values as obtained will not fit any
previous comparative scheme. Those investigators who have used only the colorimetric results, therefore, should divide the
value for SGOT in the table by 1.38 and
the ratios by 1.38 in order to obtain comparative findings; for those desiring to
compare spectrophotometric results, the
SGPT must be multiplied by 2 and the
ratio divided by 2. It is obvious from these
findings that the lowest SGOT:SGPT ratio
is observed in hepatitis, with an average of
1.46, whereas cirrhosis leads to the highest
average, namely, 3.03. Inasmuch as in the
lower range of values there is overlap of the
duct-obstruction and cirrhotic group with
the hepatitis, hepatitis per se can not be
specifically diagnosed on the basis of a low
ratio. On the other hand, inasmuch as the
patients with hepatitis reveal a maximal
ratio of 3.18, it would follow that ratios in
excess of approximately this value would
tend to exclude hepatitis. Again, despite the
difference in the average ratio of ductobstruction and cirrhosis, the individual
cases overlap completely, and this ratio is
not suitable for distinguishing the two.
Whereas 1 patient with cirrhosis had a
ratio of 8.31, the next highest in this group
: was 5.45, a value which was within the
upper ranges of the duct-obstruction group.
Further data are required to ascertain
whether or not, in a large number of comparative determinations, ratios in excess
, of 5.66 are observed only in cirrhosis and
* not in the duct-obstruction group.
DISCUSSION
The findings obtained from this study
. virtually confirm those described originally
by Wroblewski and others. In addition to
these established findings, our study demonstrates that a level of SGOT greater than
500 units per ml. is sufficient for preliminary
diagnosis of hepatocellular damage or
IN
JAUNDICE
105
pancreatitis, and, as a corollary, practically
excludes surgical obstruction. Levels of
enzyme less than the 500 range, however, do
not solve the problem of differential diagnosis, inasmuch as all types of jaundice may
be associated with values of this order.
Values for SGPT paralleled the values for
SGOT in hepatitis and, on the whole, were
disproportionately less in the nonhepatitis
cases, as listed in Table 3. Although the
analysis of SGPT has been reported to be
helpful in making a distinction in the various
states of jaundice, 23 ' 33 as indicated in Table
3, there is a great overlap in the various
types of jaundice, a finding that also has
been reported by others. 4 ' 6 Our findings
have resulted in the conclusion that, when a
value for SGOT in excess of 500 units is
obtained, a value for SGPT is not required
in the evaluation of the jaundice, inasmuch
as it merely parallels the SGOT finding. In
those instances of jaundice in which the
SGOT is nondiagnostic, however, i.e., less
than 500 units, the assay of SGPT may have
value, in that hepatitis would tend to be
excluded if an SGOT:SGPT ratio in excess
of 3.18 was obtained. The ratios themselves
can not be used for positive identification of
hepatitis, or duct-obstruction, or cirrhosis,
owing to the overlap of the ratios in these
groups.
While searching for an additional parameter in the SGOT range less than 500 units,
it was realized that extremely high levels of
serum bilirubin were frequently associated
with unusually low or normal levels of
SGOT in the duct-obstruction group, an
observation also noted by Wroblewski.26
Conversely, persons in the hepatitis group
more often manifested extremely elevated
levels of SGOT in the face of only a moderate
elevation in serum bilirubin. This relation
is demonstrated in Figure 6, in which the
highest values for SGOT obtained in each
instance are plotted against the corresponding level of serum bilirubin. With a few
exceptions, it may be seen that a line of
demarcation can be drawn through the
plotted points that delineate the 2 groups.
This line corresponds to an SGOT: bilirubin
ratio of approximately 40, below which one
notes the majority of the duct-obstruction
106
SACKS AND
TABLE 4
SERUM GLUTAMIC OXALACETIC TRANSAMINASE
( S G O T ) : B I L I R U B I N R A T I O IN JAUNDICE
Illness
Cases
Hepatitis
Duct obstruction
Cirrhosis
Pancreatitis
Methyltestosterone
Thorazine
Cholangiolitic hepatitis
Cancer
Marsilid
30
37
18
7
Total
<40
4
36
10
2
(13)*
(97)
(56)
(28)
>40
26
1
8
5
(87)*
(3)
(44)
(72)
5 (100)
—
4
2 (50)
2 (50)
7
6
6 (86)
1 (14)
6 (100)
3}
114
—
65
49
* The numbers in parentheses refer to the per
cent of the total number of cases for each illness.
patients, and above which the majority of
the hepatitis group are found. This ratio is
tabulated for all groups of this series in
Table 4 (the patients with central necrosis
of the liver are not included).
In the right column of Table 4 (ratio
greater than 40), there is listed 1 person
with obstruction of the bile ducts. On the
other hand, 48 of the 49 persons (97 per
cent) in this group had a medical type of
jaundice. These statistics indicate that a
ratio greater than 40 presumptively excludes
the bile duct-stasis cases from hepatitis, but
this ratio in no way provides a basis for
separating the various medical cases into
each of their specific types.
In the group with ratios less than 40, only
4 of the 65 patients (6 per cent) had hepatitis. Inasmuch as 2 of the 4 had values in
excess of 500 units, it actually left only 2 (or
3 per cent) of the hepatitis cases with values
less than 500 units and a ratio of less than
40. In other words, with this ratio and less
than 500 units of SGOT, there is only a 3
per cent chance that a given patient in this
group would have hepatitis. On the other
hand, because duct-obstruction accounted
for only a little more than half (36:65) of
the examples included in this group, it
obviously could not be distinguished from
the other 29 instances of medical type of
jaundice associated with a ratio of less
than 40.
Vol. 33
LANCHANTIN
It should be mentioned that cases of lowgrade obstruction producing minimal bilirubinemia are not included in this study,
inasmuch as they resulted in extremely
variable SGOT:bilirubin ratios. Presumably
this was caused by the inability to be certain
when the peak bilirubin and SGOT were
present. The same problem was encountered
for values obtained in convalescent hepatitis,
i.e., when the biliribin has begun to drop
sharply.
Similar parameters were investigated
relating the values for SGOT to other hepatic
function tests, but no consistent pattern
was observed. In 1 series of studies by Latner and his associates,14 the SGOT: alkaline
phosphatase ratio resulted in an index for
differential diagnosis. This was not observed
to be the situation in this study; however,
the differences in our respective procedures
for assaying alkaline phosphatase may be
the reason for this lack of agreement.
SUMMARY
The use of the determination of serum
glutamic oxalacetic transaminase (SGOT)
in 120 patients with jaundice of varying
etiology is described. Values for SGOT of
1000 units and more were observed to be
diagnostic of hepatocellular damage. Values
exceeding 500 units of SGOT per ml. seem
to exclude presumptively surgical obstructive jaundice, and such values were observed
in most instances of viral hepatitis, hepatitis
associated with Marsilid, and in massive
hepatic necrosis. The levels in 3 patients
with carcinoma of the liver and 3 with
pancreatitis also exceeded this amount.
Values less than 500 units of SGOT per ml.
were nonspecific for the type of jaundice
present. In this range, SGOT: bilirubin
ratios greater than 40 presumptively exclude
duct-obstruction; ratios less than 40 presumptively exclude hepatitis. In the presence of jaundice and levels for SGOT in
excess of 500 units, data on SGPT do not
provide additional information. With values
for SGOT less than 500 units, serum
glutamic pyruvic transaminase (SGPT)
may be of help in excluding hepatitis from
consideration if the SGOT:SGPT ratio
exceeds 3.18. On the other hand, the ratio
Feb. 1960
107
TRANSAMINASE IN JAUNDICE
is not suitable for distinguishing ductobstruction from cirrhosis.
5. C H I N S K Y , M., W O L F F , R. J., AND SHERRY, S.:
SUMMARIO IN INTERLINGUA
6. D E N N E Y , J. L., M O A U L E Y , C. B . , M A R T I N , H .
E . , W A R E , A. G., AND SEGALOVE, M . : E v a l u -
Es describite le uso de determinationes de
transaminase glutamic oxaloacetic del sero
(TGOS) in 120 patientes con jalnessa de
varie etiologias. Esseva constatate que
valores pro TGOS amontante a plus que 1000
unitates indicava un diagnose de injuria
hepatocellular. Valores de plus que 500
unitates de TGOS per ml pare excluder le
presumption de jalnessa obstructive. Tal
valores esseva observate in le majoritate del
casos de hepatitis virusal, de hepatitis associate con le administration de Marsalid, e de
massive necrose hepatic. Le nivellos notate
in 3 patientes con carcinoma del hepate e in
3 con pancreatitis etiam excedeva le mentionate valor. Nivellos de minus que 500
unitates de TGOS per ml esseva nonspecific
con respecto al typo de jalnessa presente. In
iste region, proportiones de TGOS a bilirubina de plus que 40 pare excluder le presentia de obstruction de ducto; proportiones
de minus que 40 pare excluder hepatitis. In
le presentia de jalnessa e de nivellos de
TGOS amontante a plus que 500 unitates,
datos concernente le concentration de transaminase glutamic pyruvic del sero (TGPS)
non provide informationes additional. In le
presentia de jalnessa e de nivellos de TGOS
amontante a minus que 500 unitates, determinationes de TGPS es possibilemente de
valor in tanto que proportiones de TGOS
a TGPS amontante a plus que 3,18 exclude
le possibilitate de hepatitis. Del altere latere,
le proportion de TGOS a TGPS non permitte le distinction inter obstruction del
ducto e cirrhosis.
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