SGOT (Aspartate aminotransferase, AST, Glutamic oxaloacetic Transaminase)

Sample

1. This is done on the serum of the patient.
2. A random sample can be used.
3. The serum is stable for 24 hours at room temp. and 28 days at 4 °C.

Precaution

1. Avoid hemolysis because RBC contains AST and ALT which will increase the value.
2. Pregnancy may cause a decrease in the AST level.
3. Exercise may increase the AST level.
4. There is a false decreased level in:
   1. Pyridixoin deficiency (Beriberi).
   2. Severe long-standing liver diseases.
   3. Uremia.
   4. Diabetic ketoacidosis.
5. Drugs that may increase the value are:
   1. Antihypertensive.
   2. Digitalis preparation.
   3. Erythromycin.
   4. Anticoagulants like coumarine.
   5. Oral contraceptives.
   6. Isoniazid.
   7. Salicylates.
   8. Opiates.
   9. Hepatotoxic drugs.
   10. Methyldopa.

Purpose of the test (Indications)

1. This is done in suspected liver diseases.
2. This also helps in heart diseases to diagnose acute myocardial infarction.

Pathophysiology

1. This enzyme is distributed in all tissues (primarily all the tissues)  but primarily found in the liver, heart and skeletal muscles in high concentration.
   1. SGOT is found in the plasma, bile, CSF, and saliva.
   2. It is not found in urine unless there is a kidney lesion.
   3. Minimal activity occurs in the skin, kidneys, pancreas, and RBCs.
2. In the liver, it is present in cytosolic and mitochondrial forms.

3. This is also called as GOT (glutamate oxaloacetate transaminase).
4. It is released into circulation:
   1. in liver diseases.
   2. In myocardial infarction, there is a rise after 6 to 8 hours of the damage or chest pain. Abnormal values are seen almost in more than 97% of the cases.
   3. Renal infarction.
   4. Brain infarction.
   5. Skeletal diseases.

5. This test is advised in hepatocellular diseases and coronary occlusive diseases leading to muscle necrosis.
6. The amount of SGOT is directly related to the number of cells affected by the disease or injury.
7. After the cell injury:
   1. It appears in the blood after 6 to 8 hours.
   2. The peak level is in 24 to 36 hours.
   3. It returns to normal in 3 to 7 days.
      1. In acute hepatitis, AST level rises 20 times the normal.
      2. In acute extra-hepatic obstruction, the level rises 10 times the normal and rapidly falls.
      3. In cirrhosis, it depends upon the amount of active inflammation.
8. In chronic injury, the elevated level will persist.
9. In Acute hepatitis, the level may increase 20 times to the normal.
10. SGOT >8 to 10 time more than the normal indicates:
    1. Acute viral hepatitis.
11. SGOT >30 times more than the normal seen in:
    1. Alcoholic patients taking acetaminophen.
12. In acute extrahepatic obstruction like gallstones, the SGOT level rises to 10 times the normal value and it returns normally quickly when the obstruction is relieved.
13. The AST/ALT ratio is usually greater than 1 in:
    1. The patient with alcoholic cirrhosis.
    2. Liver congestion.
    3. Metastatic tumor of the liver.
    4. The AST/ALTThe  ratio of less than 1 is seen in:
       1. Acute hepatitis.
       2. Viral hepatitis.
       3. Infectious mononucleosis.
          1. The ratio will be less accurate if the AST level is more than 10 times normal.
14. The SGOT level as compared to serum is 7800 times in the heart, 7100 times in liver, skeletal muscles 5000 times, kidney 4500 times, pancreas 1400 times, spleen 700 times, lungs 500 times,  and RBCs 15 times.

Normal

Source 1

Age	U/L
Newborn	25 to 75
Infants	15 to 60
Adult	8 to 20
>60 years	Male = 11 to 60
	Female = 10 to 20

Source 2

• Newborn/ infants  = 15 to 60 units/L
• Child = Value like adult
• Adult = 0 to 35 units/L

Elderly = Slightly higher than the adults

Source 4

• Men = 14 to 20 U/L  (0.23 to 0.33 µKat/L).
• Women = 10 to 36 U/L  (0.23 to 0.33 µKat/L).
• Newborn = 47 to 150 U/L  (0.23 to 0.33 µKat/L).
• Children = 9 to 80 U/L  (0.23 to 0.33 µKat/L).

Another source

• Newborn = 25 to 75 U/L
• Infants = 15 to 60 U/L
• Adult
  • Male = 15  to 40 U/L at 37C.
  • Female = 13 to 35 U/L at 37C.
  • Elderly = slightly higher than the adult.
• SGOT > 450 U/L in blunt abdominal injury is an indicator of liver injury.

Source 6

Age	Normal values U/L
0 to 5 days	35 to 140
<3 years	15 to 60
3 to 6 years	15 to 50
6 to 12 years	10 to 50
12 to 18 years	10 to 40
Adult	0 to 35 (female slightly low than males)
Elderly	slightly higher than the adults

Increased SGOT level seen in:

1. Fulminant type of hepatitis especially viral type.
2. In liver cell necrosis or injury like chronic hepatitis,
3. Alcoholic hepatitis.
4. liver metastasis and Hepatoma (increase maybe 5 to 10 folds and is of both enzymes).
5. In necrosis of heart muscle or skeletal muscle e.g acute myocardial infarction.
6. Severe exercise.
7. Severe burn.
8. Hypothyroidism ( in 40 to 90% of cases).
9. In cholestatic and obstructive jaundice.
10. May see a transient increase in acute pancreatitis, acute renal diseases, musculoskeletal diseases, or trauma.
11. Other diseases than liver and heart which can increase the level:
    1. Hypothyroidism.
    2. Dermatomyositis.
    3. polymyositis.
    4. Gangrene.
    5. Toxic shock syndrome.
    6. Shock.
    7. Mushroom poisoning.
    8. Pulmonary embolism and infarction.
    9. Hemolytic anemia.
    10. malignant hyperthermia.

Decreased SGOT level seen in:

1. Chronic renal dialysis.
2. Acute renal diseases leading to Azotemia.
3. Vit.B6 deficiency.
4. Beriberi.
5. Pregnancy.

Myocardial infarction (MI) SGOT pattern:

1. The SGOT level will be raised but this is not a specific test but useful when there is raised the level of Creatine phosphokinase(CPK) and Lactic dehydrogenase(LDH).
2. In Myocardial Infarction:
   1. SGOT appears in 6 to 8 hours. This rise is 3 to 5 times normal.
   2. The peak level is between 18 to 24 hours.
   3. Returns to normal in 4 to 6 days.
      1. The average increase in MI is 4 to 5 times normal.
      2. The increase of 10 to 15 times indicates massive MI.
      3. The abnormal level is seen in >97% of the patient if it is done at the right time.

3. A myocardial injury like Angina, pericarditis and rheumatic carditis does not lead to rising in the level.

Liver diseases SGOT pattern:

1. There is raised the level of SGOT in liver cell necrosis. This may be 10 to 100 times increase.
2. The SGOT level may be compared with SGPT.
3. SGOT/SGPT ratio is usually greater than 1 in a patient with alcoholic cirrhosis, liver congestion, and metastatic tumors of the liver.
   1. The ratio of less than 1 may be seen in acute hepatitis and viral hepatitis.
4. Acute viral hepatitis:
   

1. The rise of SGOT seen before the onset of jaundice.
2. Peak level has seen from 7 to 12 days after the onset of jaundice.
3. The normal level has seen  3 to 4 weeks after the onset of jaundice.
4. Characteristically SGPT is greater than SGOT.

Table showing the increase of SGOT in various conditions:

Clinical condition	The rise in SGOT level with reference to the normal value
Viral hepatitis and liver diseases	may reach 100 times
Infectious hepatitis	ALT > AST
Toxic hepatitis	Extremely high level
Infectious mononucleosis	20 times
Intrahepatic cholestasis	lower values
Extrahepatic cholestasis	Increased value
Cirrhosis	Normal to 4 to 5 times
Metastatic carcinoma	5 to 10 times
Acute myocardial infarction	4 to 5 times
Fatal myocardial infarction	10 to 15 times
Progressive muscular dystrophy	May reach 8 times
Dermatomyositis	May reach 8 times
Pulmonary emboli	2 to 3 times
Acute pancreatitis	2 to 5 times
Crushed muscular injury, Gangrene	2 to 5 times
Hemolytic diseases	2 to 5 times

Critical value: >20,000 U/L seen in alcohol-acetaminophen syndrome.

Comparison of AST (SGOT) / ALT (SGPT)

1. AST (SGOT) is always is raised in acute myocardial infarction, where ALT (SGPT) will be normal unless there is damage to the liver.
2. ALT  (SGPT) is more raised in acute hepatobiliary obstruction than AST (SGOT).
3. ALT (SGPT) is more specific than AST (SGOT) for liver cell injury.
4. The AST/ALT ratio is higher in alcoholic liver diseases.
5. AST (SGOT) is more sensitive to alcoholic liver cell injury.

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