The document provides an overview of liver function tests (LFTs), including their use, limitations, classification, and interpretation. Some key points:
- LFTs evaluate liver biochemistry and injury but cannot detect overall liver function. Clinical history is most important.
- Tests evaluate transport, injury, cholestasis, synthetic function, and substances cleared by the liver.
- Elevated enzymes like ALT/AST indicate liver cell injury while alkaline phosphatase and GGT indicate cholestasis. Albumin and PT assess synthetic function.
- LFTs can screen for disease, assess severity, and monitor treatment response but lack full sensitivity and specificity. Clinical context is critical for interpretation.
2. Background
Liver - to perform various kinds of biochemical
synthetic, excretory functions
No single test can detect globel liver function
‘Liver injury test’ – more appropriate terminology
Clinical history, physical examination most important in
interpretation of LFT
3. Use
Screening
Pattern of disease: differentiate acute viral hepatitis,
various cholestatic & CLD
Assess severity & to predict outcome
Follow up - to evaluate response to therapy (Eg.
Autoimmune hepatitis)
4. Limitations
Lack sensitivity :
Normal in certain liver disease like congenital hepatic fibrosis,
non cirrhotic portal fibrosis
Lack specificity :
Sr. albumin – decreased in chronic disease,
malabsorption,nephrotic synd. Etc.
Aminotransferase – may be raised in cardiac or muscular
disease
Except bile acid – other LFT changes for pathological process
outside liver
So important to keep clinical profile in mind
5. Classification of liver function test
Test for transport & drug metabolism
Test of biochemical activity
- Test of liver cell injury
- Test of cholestasis
Test of liver synthetic capacity
Test to detect substances cleared from plasma by liver
Specific investigation of liver disease
Other test – imaging studies , histologic studies
6. Test for transport & drug
metabolism
Serum bilirubin
Urine bilirubin
Urobilinogen
7. Serum bilirubin
Endogenous anion derived from hemoglobin degradation from RBC.
Confirms jaundice, indicates its depth , used to assess the progress
8. Types
Total , direct (conjugated & delta), indirect
(unconjugated)
Conjugated hyperbilirubinemia is defined as a serum
direct/conjugated bilirubin concentration greater than
1.0 mg/dL if the total serum bilirubin (TSB) is <5.0
mg/dL or > 20% of TSB if the TSB is >5.0 mg/dL
Unconjugated hyperbilirubinemia : over production or
impaired uptake or conjugation of bilirubin
Conjugated hyperbilirubinemia : decreased excretion or
backward leakage of pigment
9. Total bilirubin:
- not sensitive indicator for
hepatic dysfunction
- may not accurately reflect
degree of liver damage
Unconjugated
hyperbilirubinemia
Hemolytic
Rhesus or ABO incompatibility
Red cell membrane defect
G6PD deficiency
Internal hemorrhage
Sepsis
Polycythemia
Cong. Hypothyroidism
Criggler najjar syndrome
Gilbert syndrome
Galactosemia ( initially f/b conjugated)
11. Urine bilirubin
Conjugated bilirubin – water soluble – may be found in
urine
Early hepatobiliary disease like in acute viral hepatitis –
positive, while patient may or may not be icteric
12. Urobilinogen
Formed in terminal ileum & colon from conjugated
bilirubin by anaerobic microbial flora
20% daily undergo enterohepatic circulation – small
fraction excreted in urine
In hepatocellular dysfunction – UBG escapes hepatic
uptake thus appear in urine
13. Transaminase -Test of liver cell injury
ALT/SGPT (Alanine
aminotransferase)
More sensitive & specific for liver
disease
Shorter half life so for acute liver
disease
Normal range: 10 -50 U/L
AST/SGOT ( Aspartate
aminotransferase)
Rise – early indication for rejection
post transplant
Isolated rise – hemolysis,
rhabdomyolysis, myopathy,
cardiomyopathy
Normal range : 10 – 40 U/L
14. Causes of deranged
aminotransferase
Mild elevation (1-3
times)
Moderate elevation (3-
10 times)
Marked elevation (>10
times)
Neonatal hepatitis Wilson disease (CLD) Acute viral hepatitis
Extra hepatic biliary
atresia
Autoimmune hepatitis
(CLD)
Ischemic hepatitis
NASH Viral / parasitic hepatitis Drugs
Drug toxicity Chronic hepatitis B & C Acute budd chiari
syndrome
Drugs
Cholestatic liver disease
15. Points to remember
Sudden decline in levels is a bad sign – indicates fulminant
hepatitis
Sr. bilirubin level gradual rise than aminotransferase in acute
viral hepatitis. May be declining (steady fall) before sr.
bilirubin in uncomplicated viral hepatitis
Secondary elevation s/o chronic hepatitis
AST:ALT >2 Wilson’s disease (few studies)
17. Alkaline phosphatse
Synthesized by canalicular membrane of hepatocyte –
excreted in bile into intestine
Found in liver, bone, intestine, kidney , placenta
Sensitive but not specific for cholestasis
Raised along with GGT – biliary damage
Raised : biliary epithelial damage
malignant infiltration
cirrhosis
osteopenia due to vit D deficiency
graft rejection
18. Normal range : 45 -115 U/L
High ALP
Cholestatic disorder
Acute viral hepatitis (normal or
mod. increased)
Infiltrative liver disease
Abscess
Drugs : antibiotics, tricyclic
antidepressant, ACE inhibitor
Bone metastasis
Low ALP
Wilson’s disease (ALP: Bili <4)
Cong. hypophosphatemia
Hypothyroidism
Pernicious anemia
19. GGT
Synthesized by epithelium of small bile ductule &
hepatocytes
Sensitive but not specific
Present in biliary epithelium , kidney, pancreas, brain,
spleen, small intestine
In neonates higher value
Normal value : 0 – 30 U/L
21. Test of synthetic function
Serum albumin
Prothrombin time
Lipid profile
22. Serum Albumin
Principal form of protein – only synthesized in liver
Half life 20 days
In absence of other causes – low albumin s/o chronic
liver disease
In decompensated liver disease, an abrupt decrease in
levels following acute illness ( viral infection)
Normal range : 3.5 – 5.5 g/dl
23. Prothrombin time
Time to convert prothrombin to thrombin
Not specific for liver disease but high prognostic value
Abnormal coagulation , (deranged after vit k deficiency is
excluded) indicates significant hepatic dysfunction ( CLD,
ALF, ACLF)
Normal value : PT :10 -14 sec INR: > 3 sec
ALF: Uncorrectable (6-8 hours after administration of one
dose of parenteral vitamin K) coagulopathy with INR >1.5 in
patients with hepatic encephalopathy, or INR > 2.0 in patients
without encephalopathy
24. Lipids & lipoproteins
Synthesized in liver except chylomicrones
Marked increased in chronic cholestasis ( like in PFIC) –
xanthoma >5times level
GSD ( mainly type 1)
25. Test to detect substances cleared
from plasma by liver
Plasma ammonia
Amino acids ( specifically tyrosin, phenylalanine,
methionine)
Raised in acute or chronic liver failure
Non specific indication of liver dysfunction
34. Case 4
3.5 year old MCH
In PICU
H/o fever, respiratory distress – 3
days. Increased irritability from 1
day
Outside treated with antipyretic,
antibiotics from 2 days. i/v/o deranged
LFT shifted to KEM hospital
O/E: HR – 128/min, RR -40/min
S/E: P/A: mild hepatomegaly. L2 below
SCM
CNS :irritable
CBC –WNL
Sr. bilirubin: 8.6 (T), 6.4(D)
SGPT – 846
SGOT – 654
GGT – 84
ALP – 245
PT– 16/11.03 INR – 1.45 (After 1
dose vit K)
Sr. protein -6.2 albumin – 3.5
35. Case 5
In PICU
On mechanical ventilator
H/o Fever, respiratory distress, 1
episode of convulsion
CBC – 11.0, TLC – 23000, platelet
– 4.5 lac
Sr. bilirubin: 8.6 (T), 6.4(D)
SGPT – 846
SGOT – 654
GGT – 64
ALP – 200
PT– 13/11.03 INR – 1.17 (After 1
dose vit K)
Sr. protein -6.2 albumin – 3.5
36. Case 6
9 month old FCH
H/o mild yellowish discoloration
of sclera from 3months of life &
itching over whole body from 4
months of life
Outside taken treatment but
symptoms persist so referred
O/E – icterus present
Scratch marks over whole body +
S/E – mild hepatomegaly
CBC –WNL
Sr. bilirubin: 6.5(T), 3.8(D)
SGPT – 220
SGOT – 236
GGT – 23
ALP – 100
PT– 11.6/11.03 INR – 1.06 (After
1 dose vit K)
Sr. protein -5.0 albumin – 3.6