Liver Function Test(LFT)

Liver Function Tests (LFTs) – Complete Interpretation Guide 


Most “LFTs” do not directly measure liver function — only albumin and PT/INR truly reflect liver synthetic function.


COMPONENTS OF LFT PANEL

Test

Normal Range (approx)

What it Reflects

Key Pitfalls 

AST (SGOT)

5–40 IU/L

Hepatocyte injury (also muscle, heart)
  • Not liver-specific (muscle, heart, hemolysis) 
  • Level does NOT correlate with severity 
  • May normalize in end-stage cirrhosis

ALT (SGPT)

5–40 IU/L

Hepatocyte injury (more liver-specific)
  • Normal ALT does NOT exclude liver disease 
  • Not a marker of liver function 
  • May be normal in alcoholic liver disease (B6 deficiency)

ALP

40–120 IU/L

Cholestasis, biliary obstruction
  • Not liver-specific (bone, placenta) 
  • Physiological rise in pregnancy, adolescence 
  • ALP alone cannot diagnose cholestasis

GGT

10–60 IU/L

Confirms hepatic origin of ALP
  • Sensitive but NOT specific 
  • Elevated in alcohol use, enzyme-inducing drugs 
  • Normal GGT does NOT rule out liver disease

Total Bilirubin

0.2–1.2 mg/dL

Excretory function
  • Degree of jaundice ≠ severity of liver failure 
  • May be normal in early liver disease 
  • Influenced by hemolysis

Direct (Conjugated) Bilirubin

<0.3 mg/dL

Hepatic / post-hepatic pathology
  • Not specific for obstruction (also ↑ in hepatocellular injury) 
  • Presence alone does not localize cause

Albumin

3.5–5.0 g/dL

Chronic liver synthetic function
  • NOT useful in acute liver injury (long half-life ~20 days) 
  • Low levels common in sepsis, malnutrition, nephrotic syndrome

PT / INR

INR ~1.0

Acute liver synthetic function
  • Elevated INR not always liver-related (vit K deficiency, warfarin, DIC) 
  • Must assess response to vitamin K


INTERPRETATION — STEP-BY-STEP 

STEP 1: Identify the Dominant Pattern

1️⃣ Hepatocellular Pattern

  • ↑↑ ALT, AST
  • ALP normal or mild ↑
  • Bilirubin may be ↑

Common causes

  • Acute viral hepatitis
  • Drug-induced liver injury (DILI)
  • Ischemic hepatitis (shock liver)
  • Autoimmune hepatitis

 AST vs ALT clue

  • ALT > AST → Viral, NAFLD
  • AST > ALT (≥2:1) → Alcoholic liver disease


2️⃣ Cholestatic Pattern

  • ↑↑ ALP
  • ↑ GGT
  • Mild ↑ AST/ALT
  • ↑ Conjugated bilirubin

Common causes

  • Gallstones
  • Malignancy (pancreatic, cholangiocarcinoma)
  • Primary biliary cholangitis
  • Drug-induced cholestasis

#ALP ↑ + GGT ↑ = Hepatic source
#ALP ↑ + GGT normal = Bone disease


3️⃣ Mixed Pattern

  • Both AST/ALT and ALP significantly ↑

Seen in

  • Sepsis-associated liver injury
  • Drug-induced liver injury
  • Acute biliary obstruction


STEP 2: Interpret Bilirubin Type

Unconjugated (Indirect) Hyperbilirubinemia

  • Hemolysis
  • Gilbert syndrome
  • Ineffective erythropoiesis

🟡 Urine bilirubin: negative


Conjugated (Direct) Hyperbilirubinemia

  • Hepatocellular dysfunction
  • Cholestasis / obstruction

🟡 Urine bilirubin: positive


STEP 3: Assess Liver Synthetic Function 

Albumin

  • ↓ in chronic liver disease
  • Normal in acute hepatitis (long half-life ~20 days)

PT / INR

  • Earliest and most sensitive marker of liver failure
  • Reflects ↓ clotting factor synthesis (II, VII, IX, X)

—> Rising INR = worsening hepatic function 


SPECIAL INTERPRETATION CLUES 

#AST / ALT >1000 IU/L — DDx

  • Ischemic hepatitis (most common in ICU)
  • Acute viral hepatitis
  • Acetaminophen toxicity


#Isolated ALP Elevation

  • Confirm hepatic origin with GGT
  • If GGT normal → think bone pathology


#Alcoholic Liver Disease Pattern

  • AST <300 IU/L
  • AST:ALT ≥2:1
  • ↑ GGT
  • Normal or mildly ↑ ALT


NAFLD / NASH

  • Mild ↑ ALT > AST
  • Normal bilirubin initially
  • Normal INR early


Cirrhosis (Decompensated)

  • Mild AST/ALT elevation
  • ↑ Bilirubin
  • ↓ Albumin
  • ↑ INR
  • Thrombocytopenia (portal HTN marker)


LFT PATTERN SUMMARY TABLE 

Condition

AST/ALT

ALP

Bilirubin

Albumin

INR

Acute hepatitis

↑↑↑

N/↑

↑

N

↑

Cholestasis

↑

↑↑↑

↑↑

N

N

Alcoholic liver disease

AST>ALT

↑

↑

↓

↑

Cirrhosis

Mild ↑

↑

↑

↓↓

↑↑

Ischemic hepatitis

↑↑↑↑

N

Mild ↑

N

↑


COMMON PITFALLS 

1. Normal LFTs ≠ normal liver function

2. ALT/AST ≠ severity of liver failure

3. ALT / AST ≠ Severity of Liver Failure

Why?

AST and ALT reflect hepatocyte injury, not remaining functional liver mass.

Key concept

  • More injury ≠ less function
  • Less injury ≠ better prognosis

Classic examples

Scenario

AST/ALT

Reality

Acute viral hepatitis

2000–3000

Usually recovers

Ischemic hepatitis

5000

High mortality

End-stage cirrhosis

Mild ↑ or normal

Severe liver failure

Dangerous misconception

# Falling AST/ALT = recovery
# Falling AST/ALT + rising INR = worsening liver failure

4.Albumin not useful in acute liver injury

Why?

Albumin has a long half-life (~20 days).

So:

  • Acute hepatitis (days–weeks) → albumin remains normal
  • Hypoalbuminemia reflects chronicity, not acuity

Causes of low albumin NOT due to liver

  • Sepsis
  • Nephrotic syndrome
  • Malnutrition
  • Protein-losing enteropathy

When albumin IS useful

  • Chronic liver disease
  • Cirrhosis prognosis (Child–Pugh score)


5. ALP alone does not confirm liver disease

Why?

Alkaline phosphatase comes from multiple tissues:

  • Liver (bile canaliculi)
  • Bone (osteoblasts)
  • Placenta
  • Intestine

Hence

↑ ALP ≠ cholestasis by default

Correct approach

 Check GGT

  • ALP ↑ + GGT ↑ → Hepatic origin
  • ALP ↑ + GGT normal → Bone disease

Exam favorites

  • Paget disease → ↑ ALP, normal GGT
  • Pregnancy → ↑ ALP (placental)
  • Healing fracture → ↑ ALP

One-liner

GGT confirms hepatic source of ALP