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The SGOT/SGPT Ratio--An Indicator of

Alcoholic Liver Disease
J E R O L D A. C O H E N , MD, and M A R S H A L L M. K A P L A N , MD

The SGOT/SGPT ratio is significantly elevated in patients with alcoholic hepatitis and
cirrhosis (2.85 +- 0.2) compared with patients with postnecrotic cirrhosis (1.74 +_ 0.2),
chronic hepatitis (1.3 +- 0.17), obstructive jaundice (0.81 +-_0.06) and viral hepatitis (0.74
+_0.07). An SGOT/SGPT ratio greater than 2 is highly suggestive of alcoholic hepatitis
and cirrhosis. It occurs in 70% of these patients compared with 26% of patients with
postnecrotic cirrhosis, 8% with chronic hepatitis, 4% with viral hepatitis and none with
obstructive jaundice.

While no single biochemical liver function test is (2) elevation of SGOT and/or SGPT, that is, values great-
sufficiently specific to allow a definite diagnosis in er than 40 Karmen units. All SGOT and SGPT determina-
patients with liver disease, we have been impressed tions were performed on the same blood sample. SGOT
and SGPT were measured in the hospital clinical chemis-
by the consistency with which the serum glutamic try laboratory by the Karmen method. Where serial trans-
oxaloacetic transaminase (SGOT) activity exceeds aminase determinations were available, the set with the
the serum glutamic pyruvic transaminase (SGPT) highest individual transaminase value, be it SGOT or
activity in patients with alcoholic liver disease. SGPT, was used. All liver biopsies were reviewed by one
While this finding has been noted previously (1, 6), of us (MMK) who had no knowledge of the transaminase
values. Patients with the following diagnoses were includ-
it does not appear to be widely recognized or gener- ed in the study: viral hepatitis (52 patients) (9), chronic
ally accepted (7, 8). We therefore reviewed our ex- active hepatitis (48 patients) (10), postnecrotic cirrhosis
perience to determine the diagnostic usefulness of (30 patients) (11), alcoholic hepatitis and/or cirrhosis (104
the SGOT/SGPT ratio. patients) (12), and extrahepatic bile duct obstruction (37
patients). Statistical analysis was by unpaired analysis of
variance.
MATERIALS AND METHODS
Patient Selection. Data from 271 patients with histologi- RESULTS
cally documented liver diseas - and elevated serum trans-
aminases seen between July 1967 and June 1975 form the The mean SGOT/SGPT ratio was significantly
basis of this report. All patients met the following criteria: h i g h e r in p a t i e n t s w i t h a l c o h o l i c l i v e r d i s e a s e
(1) unequivocal liver disease documented by either per- (2.85 --- 0.2) than in each of the following groups:
cutaneous needle biopsy or open biopsy of the liver, and
acute viral hepatitis, 0.74 _ 0.07 (P < 0.001), extra-
hepatic biliary obstruction, 0.81 _+ 0.06 (P < 0.001),
From the Gastroenterology Service, Department of Medicine, chronic active hepatitis, 1.3 --- 0.17 (P < 0.001), and
New England Medical Center Hospital, Boston, Massachusetts
inactive postnecrotic cirrhosis, 1.74 _ 0.20 (P <
02111.
This work was supported by Training Grant AM 07024 and 0.001) (Figure 1). The great majority of patients
Research Grant AM 10571 from the National Institutes of with alcoholic liver disease (92%) and postnecrotic
Health. cirrhosis (70%) had SGOT/SGPT ratios greater than
Address for reprint requests: Dr. Marshall M. Kaplan, Gastro-
enterology Service, New England Medical Center Hospital, 171 1 (Figure 2). Only 12 percent of patients with viral
Harrison Avenue, Boston, Massachusetts 02111. hepatitis and 18 percent of patients with obstructive

Digestive Diseases and Sciences, Vol. 24, No. 11 (November 1979) 835
0163-2116/79/1100-0835503.00/19 1979Digestive Disease Systems, Inc.

tients with obstructive jaundice. 6) and indicates that the SGOT/SGPT 836 Digestive Diseases and Sciences. jaundice had ratios greater than 1. No. compared to only 4% of patients with postnecrotic cirrhosis. while patients aminase values would be expected to be high. The absolute SGPT determination was also of When the SGPT was less than 300 KU. patients with viral hepatitis. SGOT/SGPT ratio of 2 or greater. the ratio was sur. and others (1. Ill i I9 0 Alcoholic Post Chronic Obstructive Viral Liver Necrotic Hepetilis daundice Hepatitis Disease Cirrhosis 104 30 48 37 52 Fig 1. 4% with viral hepatitis. When one looked at patients with an 300 K U in patients with alcoholic liver disease.:.o:ooi oao I #. 8% with clinical presentations consistent with either mild chronic active hepatitis. with chronic active liver disease were in the middle While it is unlikely to find an SGPT level about with 50%. The ratio was calculated from the serum sample that had the highest individual transaminase value.:-. 14 oei 0 o: lm6 eoo 9 leal 9 9::::. any prisingly specific for patients with alcoholic liver type of liver disease may be associated with an disease (Figure 2). in 70% of pa. 11 (November 1979) .'.'_'::: • ::. 91% of pa- some use.. postnecrotic cirrhosis. 9 . 24. be it SGOT or SGPT. Vol.-- :: j'" :i :o . . ol: 9 9 elo e9 : T it. in 90% of SGPT ratio greater than 1. Seventy percent of these pa. and in only 21% of patients with viral hepatitis. ol 9 9.~. in 46% with chron- ic active hepatitis. or obstructive jaundice. SGOT/SGPT ratio in patients with biopsy proven liver disease. SGPT less than 300 KU. That almost 80% of patients with vi- DISCUSSION ral hepatitis had SGPTs greater than 300 reflects the fact that liver biopsy was usually reserved for the This study confirms the finding of Zimmerman sicker patients with viral hepatitis where trans. COHEN AND KAPLAN 10- "i 7- 6- O O o 5- ~ a Q. It was in this group of pa- tients had ratios greater than 2.t. the SGOT/SGPT ratio was most valuable (Figure 3). The SGPT was less than 300 KU in 98% tients with alcoholic liver disease had an SGOT/ of patients with alcoholic liver disease. and viral hepatitis or early alcoholic liver disease where none with obstructive jaundice. compared with only tients with moderately elevated transaminases and 26% of patients with postnecrotic cirrhosis.

heart failure. preliminary results ularly useful in suggesting alcoholic liver disease in from our laboratory show that hepatic GPT activity patients with mild abnormalities of liver function is significantly lower in patients with alcoholic liver Digestive Diseases and Sciences. liver disease is low. A ratio greater than 2 should make hard to obtain. when the trans- Obviously they must be used in conjunction with aminases are less than 300 KU. Other laboratory tests are usually We do not wish to imply that the transaminases abnormal and the likelihood of cirrhosis or alcoholic should be used alone in diagnosis of liver disease. No. although a ratio cellular diseases such as hepatitis. tients with viral hepatitis and common in patients determination of the SGOT/SGPT ratio offers little with postnecrotic cirrhosis as well as in those with additional useful information.SGOT/SGPT RATIO IN ALCOHOLIC LIVER DISEASE . 24. the diagnostic pos- the other commonly employed liver function tests sibilities are broad and the SGOT/SGPT ratio may and considered in the context of the clinical setting. toxic exposures. 7) that in pa- SGOT/SGPT ratios greater than 1 are unusual in pa. In these individuals. tients where the SGOT and SGPT exceed 300 KU. In addition. since both transaminases are often ob. alcoholic liver disease. Vol. be helpful. The p a t h o p h y s i o l o g i c basis o f the elevated tained. 40 20 0 Alcoholic Liver Post Necrotic Chronic _1 L Hepatitis Obstructive Jaundice Viral Hepatitis Disease Cirrhosis 104 50 48 37 52 Fig 2. or greater than 2 makes these diagnoses most unlikely. disease is not known. one is usually dealing with acute hepato- hepatitis or obstructive jaundice. However. A high SGOT/SGPT ratio is partic. 5.ooJ 9 SGOT/SGPT >1 SGOT/SGPT >2 80 I- z 60 tJJ 0 n- ILl Q. However. 11 (November 1979) 837 . Percentage of patients with SGOT/SGPT ratios greater than one and greater than two. the information available should be used to SGOT/SGPT ratio in patients with alcoholic liver its fullest extent. ratio provides useful information in the diagnosis of tests in whom a history of alcohol excess is often liver disease. one suspect alcoholic liver disease. We would agree with others (4. The ratio is not particularly a distinct minority of our own patients with liver helpful in identifying patients with chronic active disease. However.

DeRitis F. FK Mostoff (eds). Vol.t r l l A r l l ~_ 50. Bagenstoss AH: Postnecrotic cirrhosis: Morphology. The Liver. et al: A classification of Relationship between severity of hepatic disease and pres. 1967 pincott. Di. DeGroote J. and pathogenesis. COHEN AND KAPLAN lO0- 0 0 v 75- l- a. pp 1-38 kins. Dis- 1. r l J n rl. EL Coodley (ed). Harinasuta U. to rlJ I l l 10 f l l C f l l / I J o fl. 1973. 1970. Burke MD: Liver function.e r r i . Philadelphia. MatloffDS. Selinger MJ. Schenker S: Laboratory tests. Medicine 46:197-207. Medicine 46:141-162. Percentage of patients with an SGOT/SGPI" ratio greater than one and with the SGPT less than 300 Karmen units. Zimmerman HJ: The differential diagnosis of jaundice. Desmet VJ. Edmondson HA. pp 253-256 2.O l. Med 13.s flJ PTA AIc0holic Post Chronic Obstructive Viral Liver Necrotic Hepatitis Jaundice Hepatitis Disease Cirrhosis 104 3O 48 37 52 Fig 3. 1975. Kaplan MM: Hepatic transaminase Clin North Am 52:1417-1444. Rubin E: The spectrum of alcoholic liver injury. Giusti G: Serum transaminase activi- those with acute viral hepatitis (13). pp 199-217 4. Combes B. Ishak K. Clermont RJ. Thus there may ties in liver disease. 24.9 rl. SeeffLB: Enzymes in hepatic disease. Baltimore. Harinasuta U. Gastroenterology 11. 1972 7. L Schiff (ed). 1967 with alcoholic liver disease. 1975. eases of the Liver. Chalmers TC: The transaminase tests in liver be less GPT available to leak into serum in patients disease. 10. chronic hepatitis. Hum Pathol 6:273-286.e tO f l J I*- 0 r CO i 25- i II. Schiff L: Needle biopsy of the liver. JB Lip- Mallory body type. Zimmerman HJ. agnostic Enzymology. et al: Steatonecrosis-. Lancet 1:685. 1961 3. Progr Liver Dis h 14. 1. Lea EA Gall. disease compared to both normal individuals and 6. 8. JB Lippincott. 1968 activity in alcoholic liver disease. pp REFERENCES 217-221 9. Zimmerman HJ: Alcoholic steatonecrosis. Diseases of the Liver. 12. Williams and Wil- & Febiger. l . Philadelphia.i (. Philadelphia. 1975 1979 (abstract) 838 Digestive Diseases and Sciences. 5. etiol- 60:1036-1046. Gastroenterology 76:1195. Chomet B. Lancet 2:626-628. 11 (November 1979) . 1968 ence of Mallory bodies in the liver. No. Gedigk P. L Schiff (ed). 1971 ogy. Coltorti M.