Estimation of SGOT SGPT
Reading File
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Reading File
Reading File
Reading File
Finding Sources
Reading File
Finding Sources
I now have comprehensive information from authoritative textbooks. Let me compile a thorough answer.
Estimation of SGOT and SGPT
Nomenclature
| Old Name | New (IUPAC) Name | Abbreviation |
|---|---|---|
| Serum Glutamate Oxaloacetate Transaminase | Aspartate Aminotransferase | AST |
| Serum Glutamate Pyruvate Transaminase | Alanine Aminotransferase | ALT |
SGOT/AST and SGPT/ALT are the two most diagnostically useful liver enzymes for detecting hepatocellular injury.
Biochemical Basis (Principle of Estimation)
Both enzymes catalyze transamination reactions - the reversible transfer of an amino group from an amino acid to an alpha-ketoacid:
SGOT/AST Reaction:
Aspartate + α-Ketoglutarate ⇌ Oxaloacetate + Glutamate
SGPT/ALT Reaction:
Alanine + α-Ketoglutarate ⇌ Pyruvate + Glutamate
Cofactor: Both enzymes require pyridoxal phosphate (Vitamin B6) as a coenzyme. This is clinically important - in pyridoxine (B6) deficiency (e.g., alcoholics), measured enzyme activity can be falsely low.
Methods of Estimation
1. Coupled Enzymatic (Kinetic/Spectrophotometric) Method - Standard/Preferred
This is the basis of all modern automated assays. The products oxaloacetate and pyruvate are measured indirectly by a coupled reaction using NADH:
For AST:
Oxaloacetate + NADH + H⁺ → Malate + NAD⁺ (Malate Dehydrogenase)
For ALT:
Pyruvate + NADH + H⁺ → Lactate + NAD⁺ (Lactate Dehydrogenase)
- The rate of decrease in NADH absorbance at 340 nm is directly proportional to enzyme activity.
- This is a kinetic (rate) method - activity is expressed in IU/L (International Units per liter).
2. Colorimetric Method (Reitman-Frankel / Karmen)
- Older method using 2,4-dinitrophenylhydrazine (DNPH) to form a colored hydrazone with oxaloacetate or pyruvate.
- Color intensity (read at 505 nm) is proportional to enzyme activity.
- Read against substrate blank and compared to standard curves.
- Less accurate than kinetic method; now largely replaced in clinical labs.
Tissue Distribution and Specificity
| Feature | AST (SGOT) | ALT (SGPT) |
|---|---|---|
| Primary location | Liver, heart, skeletal muscle, kidney, RBCs | Primarily liver (more specific) |
| Intracellular location | Cytoplasm + mitochondria | Cytoplasm only |
| Half-life | ~17 hours (cytoplasmic); 87 hours (mitochondrial) | ~47 hours |
| Hepatocyte concentration | ~7000x plasma | ~3000x plasma |
| Organ specificity | Low (many tissues) | High (liver-specific marker) |
- ALT is more specific for liver disease than AST in non-alcoholic patients.
- Because hepatocyte AST concentration is higher than ALT, AST rises first in acute hepatocellular injury, but ALT becomes dominant within 24-48 hours due to its longer half-life.
Normal Reference Values
| Enzyme | Reference Range |
|---|---|
| AST (SGOT) | 10 - 40 U/L |
| ALT (SGPT) | 15 - 40 U/L |
Some experts advocate lowering the upper limit for ALT to:
- 30 IU/L in men
- 19 IU/L in women
(based on healthy individuals with normal BMI, normal lipids/glucose, and no hepatotoxic medications)
Clinical Interpretation of Elevated Levels
Magnitude of Elevation
| Degree | Level | Common Causes |
|---|---|---|
| Mild (< 5x ULN) | < 200 U/L | Chronic viral hepatitis, fatty liver, medications, alcohol |
| Moderate (5-15x ULN) | 200-600 U/L | Alcoholic hepatitis, drug hepatotoxicity |
| Marked (> 15x ULN) | > 600 U/L | Acute viral hepatitis, drug-induced hepatitis, ischemic hepatitis, acute biliary obstruction |
AST/ALT Ratio (De Ritis Ratio)
| Ratio | Interpretation |
|---|---|
| ALT > AST (ratio < 1) | Viral/chronic hepatitis, fatty liver, medications |
| AST > ALT (ratio 2:1) | Alcoholic hepatitis (mitochondrial AST release; ratio 3-4:1) |
| AST elevated, ALT normal | Extrahepatic source - cardiac or skeletal muscle |
| Both elevated equally | Hepatic origin most likely |
- In alcoholic hepatitis: AST typically ~2x ALT, rarely > 300 U/L - the mitochondrial AST isoenzyme is responsible.
- In cirrhosis: as fibrosis progresses, ALT declines and AST rises; in end-stage disease, both may be near normal despite severe disease.
- For drug monitoring: if AST rises > 3x ULN, the suspect drug should be stopped.
Conditions Causing Elevations
- AST-predominant: Alcoholic hepatitis, myocardial infarction, skeletal muscle disease, cirrhosis
- ALT-predominant: Viral hepatitis (A, B, C), non-alcoholic fatty liver disease (NAFLD), autoimmune hepatitis, Wilson's disease, hemochromatosis
- Both equally elevated: Hepatocellular damage of any cause, drug-induced liver injury
Important Notes on Assay Accuracy
- Vitamin B6 (pyridoxal phosphate) deficiency - common in alcoholics - can give falsely low AST and ALT readings. Labs should supplement pyridoxal phosphate in the assay reagent or be aware of this limitation.
- Hemolysis - red blood cells contain significant AST; hemolyzed samples give falsely elevated AST.
- Strenuous exercise can raise AST (from skeletal muscle), not ALT.
- End-stage liver disease - both enzymes can be normal or even low due to loss of functional hepatocyte mass.
Sources:
- Henry's Clinical Diagnosis and Management by Laboratory Methods, Chapter on Aminotransferases
- Basic Medical Biochemistry: A Clinical Approach, 6th Ed.
- Textbook of Family Medicine, 9th Ed., Chapter on Liver Function Tests
This is a shared conversation. Sign in to Orris to start your own chat.