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Quick Reference
  • Normal Range: 0-35 IU/L
  • Alternative Name: SGOT (Serum Glutamic-Oxaloacetic Transaminase)
  • Critical Value: >1000 IU/L (suggests massive hepatic injury)
  • AST:ALT Ratio: Normal <1; >2 suggests alcoholic liver disease
  • Sample Type: Serum or plasma (avoid hemolysis)
  • Key Point: Less liver-specific than ALT; also found in heart, muscle, and RBCs

Test Description

What is AST?

Aspartate aminotransferase (AST), also known as serum glutamic-oxaloacetic transaminase (SGOT), is an enzyme that catalyzes the transfer of amino groups from aspartate to alpha-ketoglutarate, playing a vital role in amino acid metabolism and the citric acid cycle.

Where is AST Found?

AST is found in multiple tissues throughout the body:

  • Liver (high concentration)
  • Heart (cardiac muscle)
  • Skeletal muscle
  • Kidneys
  • Brain
  • Pancreas
  • Red blood cells

When cells containing AST are damaged or destroyed, the enzyme is released into the bloodstream, causing elevated serum levels. This makes AST a useful but non-specific marker of tissue injury.

Clinical Use

AST is primarily used as a marker of hepatocellular injury, though it is less liver-specific than ALT (alanine aminotransferase). The test is typically ordered as part of:

  • Comprehensive metabolic panel (CMP)
  • Liver panel (hepatic function tests)
  • Evaluation alongside ALT and alkaline phosphatase (ALP)

Key Characteristics

  • Distribution: AST has both cytoplasmic and mitochondrial isoforms, with the mitochondrial form released during more severe cellular injury
  • Specificity: Less liver-specific than ALT due to presence in cardiac muscle, skeletal muscle, kidneys, brain, and RBCs
  • Half-life: Approximately 17 hours in serum (slightly shorter than ALT's 47 hours), causing AST to rise and fall more rapidly than ALT
  • Sample type: Serum or plasma (avoid hemolysis as RBCs contain AST)
Normal Ranges

AST reference ranges may vary slightly between laboratories depending on the assay method used. The values below represent typical ranges found in most clinical laboratories.

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Population Normal Range Notes
Adult Males 0-40 IU/L Some labs use 0-35 IU/L
Adult Females 0-35 IU/L Typically slightly lower than males
Pediatric Varies by age Higher in neonates, decreases with age
Elderly 0-35 IU/L Similar to adult ranges

Important Considerations

Reference ranges for AST vary significantly between laboratories based on:

  • Assay methodology: Different analyzer platforms may yield different normal ranges
  • Temperature: Measurements standardized to 37°C; older methods used 30°C
  • Laboratory-specific cutoffs: Always compare results to the specific laboratory's reference range
  • Physiological variation: AST may be mildly elevated in individuals with higher muscle mass or after strenuous exercise
  • Hemolysis artifact: RBCs contain AST; hemolyzed samples will show falsely elevated values
Clinical Significance

Elevated AST

Elevated AST indicates cellular damage or death in tissues containing the enzyme. The degree of elevation and the pattern when compared with other liver tests help identify the underlying cause.

Hepatocellular Injury (Most Common)

  • Viral hepatitis (A, B, C, E): Moderate to massive elevations (often >1000 IU/L in acute phase); AST typically less elevated than ALT
  • Alcoholic hepatitis: AST typically elevated more than ALT with AST:ALT ratio >2:1; usually <300 IU/L
  • Drug-induced liver injury (DILI): Acetaminophen toxicity causes massive elevations; other drugs cause variable patterns
  • Ischemic hepatitis ("shock liver"): Massive elevations (>1000-3000 IU/L) in setting of hypotension or hypoxia
  • Autoimmune hepatitis: Moderate to severe elevations with predominant AST and ALT elevation
  • Non-alcoholic fatty liver disease (NAFLD): Mild to moderate elevations; ALT typically higher than AST
  • Non-alcoholic steatohepatitis (NASH): Mild to moderate elevations; AST:ALT ratio may increase with fibrosis
  • Cirrhosis: Often normal or mildly elevated; AST:ALT ratio typically >1 in advanced disease
  • Hemochromatosis: Mild to moderate elevations with iron overload
  • Wilson's disease: Variable elevations with copper accumulation; very high in fulminant presentations

Cardiac Injury

  • Myocardial infarction: Rises 6-8 hours post-infarction, peaks at 24-48 hours, normalizes in 3-4 days; less sensitive than troponin
  • Myocarditis: Variable elevations depending on severity
  • Heart failure: Mild elevations possible with hepatic congestion
  • Cardiac surgery: Transient elevations post-operatively

Skeletal Muscle Injury

  • Rhabdomyolysis: Marked elevations; CK elevation more prominent; check creatinine and myoglobin
  • Polymyositis/dermatomyositis: Moderate elevations with muscle inflammation; CK and aldolase also elevated
  • Muscular dystrophy: Mild to moderate chronic elevations
  • Strenuous exercise: Mild transient elevations; more common after unaccustomed exercise
  • Intramuscular injections: Mild transient elevations from local muscle damage
  • Trauma: Variable elevations depending on extent of muscle injury

Other Causes

  • Hemolysis: RBC lysis releases AST (artifact if hemolyzed sample; clinical if in vivo hemolysis)
  • Acute pancreatitis: Mild to moderate elevations
  • Renal infarction: AST release from damaged kidney tissue
  • Sepsis/systemic infection: Variable elevations from multiple organ involvement
  • Malignancy: Hepatic metastases, hepatocellular carcinoma, or other tumors
  • Celiac disease: Mild elevations may occur
  • Macro-AST: Rare benign condition with immunoglobulin-bound AST causing persistent elevation

Decreased AST

Low AST levels are rarely clinically significant and typically not pursued. Possible causes include:

Causes of Low AST

  • Pyridoxine (Vitamin B6) deficiency: AST requires B6 as cofactor; rare cause of low levels
  • Chronic kidney disease: Uremia may reduce AST activity
  • Normal variant: Some healthy individuals have AST at lower end of normal range
Interpretation Guidelines

Severity Classification

The degree of AST elevation helps narrow the differential diagnosis and assess severity of injury:

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Severity AST Level Common Causes
Mild Elevation 1-5× ULN
(36-175 IU/L)		 Chronic hepatitis, NAFLD, medications, cirrhosis, hepatic congestion
Moderate Elevation 5-10× ULN
(175-350 IU/L)		 Chronic viral hepatitis, alcoholic hepatitis, autoimmune hepatitis, acute obstruction
Severe Elevation 10-50× ULN
(350-1750 IU/L)		 Acute viral hepatitis, drug-induced hepatitis, autoimmune hepatitis
Massive Elevation >50× ULN
(>1750 IU/L)		 Acetaminophen toxicity, ischemic hepatitis, acute viral hepatitis, autoimmune hepatitis, acute bile duct obstruction

De Ritis Ratio (AST:ALT Ratio)

The ratio of AST to ALT provides important diagnostic clues about the underlying liver pathology:

De Ritis Ratio
AST:ALT Ratio = AST (IU/L) ÷ ALT (IU/L)

Named after Fernando De Ritis who first described the clinical significance of this ratio in 1957

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AST:ALT Ratio Interpretation Common Conditions
<1.0 Normal or early liver disease Acute viral hepatitis, NAFLD, chronic hepatitis B or C (early)
1.0-2.0 Chronic liver disease or mild alcohol use Chronic hepatitis, moderate NAFLD, mild alcoholic liver disease
>2.0 Alcoholic liver disease or cirrhosis Alcoholic hepatitis (classic finding), advanced cirrhosis, Wilson's disease (fulminant)
>3.0 Strongly suggests alcoholic hepatitis Severe alcoholic hepatitis, decompensated alcoholic cirrhosis

Why Does Alcohol Cause High AST:ALT Ratio?

Several mechanisms explain why AST is disproportionately elevated in alcoholic liver disease:

  • Pyridoxine depletion: Chronic alcohol use depletes vitamin B6, a cofactor for ALT synthesis more than AST
  • Mitochondrial AST release: Alcohol causes mitochondrial damage, releasing mitochondrial AST isoform
  • ALT activity reduction: Alcohol and pyridoxine deficiency reduce ALT activity in hepatocytes
  • Fibrosis/cirrhosis: Advanced liver disease reduces hepatocyte mass, affecting ALT production more than AST

Pattern Recognition: Hepatocellular vs. Cholestatic

Comparing AST/ALT elevations with alkaline phosphatase (ALP) helps distinguish between hepatocellular injury and cholestatic disorders:

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Pattern AST/ALT ALP Common Causes
Hepatocellular Markedly elevated
(>5× ULN)		 Normal or mildly elevated
(<3× ULN)		 Viral hepatitis, drug-induced hepatitis, ischemic hepatitis, autoimmune hepatitis
Cholestatic Normal or mildly elevated
(<3× ULN)		 Markedly elevated
(>4× ULN)		 Bile duct obstruction, primary biliary cholangitis, drug-induced cholestasis
Mixed Moderately elevated
(3-10× ULN)		 Moderately elevated
(3-10× ULN)		 Infiltrative disease, sepsis, some medications, partial obstruction

Critical AST Elevations (>1000 IU/L)

Massive AST elevation requires urgent evaluation for potentially life-threatening conditions:

  1. Acetaminophen toxicity: Check acetaminophen level, obtain history of ingestion time, consider N-acetylcysteine therapy
  2. Ischemic hepatitis ("shock liver"): History of hypotension, hypoxia, or cardiac arrest; AST/ALT often >3000 IU/L and rapidly rising; check lactate, consider imaging
  3. Acute viral hepatitis: Obtain viral hepatitis serologies (HAV IgM, HBsAg, HCV Ab, HEV if indicated)
  4. Autoimmune hepatitis: Check autoantibodies (ANA, ASMA, LKM), immunoglobulins
  5. Acute bile duct obstruction: RUQ ultrasound or MRCP; check bilirubin and ALP
  6. Acute Budd-Chiari syndrome: Consider in appropriate clinical context; imaging with Doppler ultrasound or CT/MRI

Note: The magnitude of AST elevation does NOT correlate with prognosis in acute hepatitis. Rapidly declining aminotransferases with rising bilirubin and INR suggests acute liver failure.

Interfering Factors

Factors That Increase AST

Medications (Hepatotoxic):

  • Acetaminophen (dose-dependent hepatotoxicity)
  • NSAIDs (ibuprofen, naproxen, diclofenac)
  • Statins (HMG-CoA reductase inhibitors)
  • Antibiotics: amoxicillin-clavulanate, isoniazid, rifampin, sulfonamides, tetracyclines, macrolides
  • Anticonvulsants: phenytoin, valproic acid, carbamazepine
  • Antifungals: ketoconazole, fluconazole, terbinafine
  • Cardiovascular drugs: amiodarone, methyldopa, quinidine
  • Methotrexate (dose-dependent)
  • Anabolic steroids and oral contraceptives
  • Antiretrovirals (various agents)
  • Herbal supplements: green tea extract, kava, certain traditional Chinese medicines

Pre-analytical Factors:

  • Hemolysis: RBCs contain AST; hemolyzed samples show falsely elevated AST (most common pre-analytical error)
  • Strenuous exercise: Can elevate AST for 24-48 hours, especially in unconditioned individuals
  • Intramuscular injections: Can cause mild transient elevation from muscle trauma
  • Sample storage: AST is relatively stable at room temperature but decreases with prolonged storage

Physiological Factors:

  • Obesity (associated with NAFLD)
  • Metabolic syndrome and insulin resistance
  • Pregnancy (usually normal, but check for HELLP syndrome or acute fatty liver if elevated)
  • Higher muscle mass (mild elevations possible)

Factors That Decrease AST

  • Pyridoxine (Vitamin B6) deficiency: AST requires B6 as cofactor; deficiency reduces enzyme activity
  • Chronic kidney disease (uremia): May reduce AST activity in advanced disease
  • Sample storage: Prolonged storage can decrease AST levels

Pseudoabnormal Results

Conditions causing falsely elevated or persistent AST elevations without true hepatocellular injury:

  • Macro-AST: Rare benign condition where AST binds to immunoglobulins or other large molecules, creating high-molecular-weight complex with prolonged half-life; causes persistent elevation without clinical significance; diagnosed by polyethylene glycol precipitation or gel filtration
  • In vitro hemolysis: Most common cause of falsely elevated AST; always check for hemolysis flag on lab report
  • Rhabdomyolysis without liver disease: Elevated AST from muscle source; CK massively elevated, ALT normal or minimally elevated

Clinical Pearl: Evaluating Hemolyzed Samples

When AST is elevated and the sample is hemolyzed, clinical correlation is essential:

  • If ALT is normal or minimally elevated, AST elevation likely artifactual from hemolysis
  • If ALT is proportionally elevated, liver disease is likely despite hemolysis
  • If uncertain, repeat sample with careful collection technique (avoid small gauge needles, excessive vacuum, vigorous mixing)
Clinical Pearls
  • "AST/ALT ratio greater than 2:1 - think alcohol": Classic mnemonic for alcoholic hepatitis. The ratio is typically >2.0 in alcoholic liver disease (especially >3.0 in severe cases) due to pyridoxine depletion affecting ALT more than AST, plus release of mitochondrial AST.
  • "AST lives everywhere, ALT loves the liver": AST is found in heart, muscle, kidneys, brain, and RBCs, making it less specific for liver disease than ALT. Always consider non-hepatic sources when AST is disproportionately elevated compared to ALT.
  • "The higher the better" (for acute viral hepatitis): Counterintuitively, very high aminotransferases (>1000-3000 IU/L) in acute viral hepatitis suggest robust immune response and typically predict good recovery. Rapidly falling aminotransferases with rising bilirubin and INR is the ominous pattern suggesting acute liver failure.
  • AST rises and falls faster than ALT: AST has a shorter half-life (~17 hours vs. ALT's 47 hours), so it rises more quickly after acute injury and falls more rapidly during recovery. This can help establish timing of hepatic injury.
  • Never interpret AST in isolation: Always correlate with ALT, alkaline phosphatase, bilirubin, and clinical context. The pattern of abnormalities is more informative than any single value.
  • "Shock liver" pattern - massive AST with hypotension history: Ischemic hepatitis typically causes AST and ALT >1000-3000 IU/L (often >3000 IU/L) within 24-72 hours of hypotensive episode, with rapid improvement once perfusion restored. LDH also markedly elevated. History of cardiac arrest, severe hypotension, or respiratory failure is key.
  • Don't forget non-hepatic sources: If AST elevated out of proportion to ALT, always consider: myocardial injury (check troponin), muscle injury (check CK), or hemolysis (check for hemolyzed sample, LDH, haptoglobin).
  • AST:ALT ratio increases with fibrosis: As liver disease progresses to cirrhosis, the AST:ALT ratio typically increases and may exceed 1.0 even in non-alcoholic liver disease. This reflects reduced hepatocyte mass and synthetic function.
  • Aminotransferase magnitude doesn't predict prognosis in chronic disease: A patient with cirrhosis and near-normal AST/ALT can be far sicker than someone with acute hepatitis and AST/ALT >1000. Look at synthetic function (albumin, INR) and clinical status.
  • "AST <300 in alcoholic hepatitis": Alcoholic hepatitis rarely causes AST >300 IU/L despite active inflammation. If AST >300-400, consider superimposed acetaminophen toxicity, ischemic injury, or alternative diagnosis.
  • Serial measurements more useful than single values: Trending AST over hours to days helps distinguish acute injury patterns (acetaminophen, ischemic) from chronic elevations (chronic hepatitis, NAFLD) and assess response to treatment.
  • R-ratio for distinguishing injury patterns: Calculate R = (ALT ÷ ALT ULN) ÷ (ALP ÷ ALP ULN). R >5 = hepatocellular, R <2 = cholestatic, R 2-5 = mixed. Helps guide diagnostic workup.
  • Check medication list systematically: Drug-induced liver injury is common and often overlooked. Review ALL medications including over-the-counter drugs, supplements, and herbals. Onset can be weeks to months after starting medication.
  • When AST is normal but patient has liver disease: Normal or minimally elevated AST doesn't exclude significant liver disease, especially in cirrhosis where hepatocyte mass is reduced. Synthetic function tests (albumin, PT/INR) and imaging are critical.
References
  1. Kratz, A., Ferraro, M., Sluss, P. M., & Lewandrowski, K. B. (2004). Laboratory reference values. New England Journal of Medicine, 351, 1548-1564.
  2. Lee, M. (Ed.). (2009). Basic skills in interpreting laboratory data. Ashp.
  3. Farinde, A. (2021). Lab values, normal adult: Laboratory reference ranges in healthy adults. Medscape. https://emedicine.medscape.com/article/2172316-overview?form=fpf
  4. Nickson, C. (n.d.). Critical Care Compendium. Life in the Fast Lane • LITFL. https://litfl.com/ccc-critical-care-compendium/
  5. Farkas, Josh MD. (2015). Table of Contents - EMCrit Project. EMCrit Project. https://emcrit.org/ibcc/toc/
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