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.

1. Interpretation of liver
function test
- Dr. Kinisha Patel
(M.D pediatrics , FISPGHAN)

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)

10.  Conjugated hyperbilirubinemia (hepatocellular,
hepatobiliary)
Neonatal cholestasis
Metabolic liver disease
Inborn error of metabolism
Infections (viral hepatitis – hepatotropic, non hepatotropic, bacterial,
parasitic, fungal)
Drug induced liver injury
Ischemic causes
Autoimmune liver disease

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)

16. Test of cholestasis
 Alkaline phoshphatase
 Gamma glutamyl transferase (GGT)

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

20. High GGT
 Biliary atresia
 Bile ducts paucity
 PFIC 3
 Sclerosing cholangitis
 Acute viral hepatitis
 Acute pancreatitis
 Drugs : phenobarb., phenytoin,
paracetamol, TCA
 GBS
 Obesity
Low GGT
 PFIC 1,2,4
 Bile acid synthetic defect
 ARC syndrome ( arthrogyposis,
renal abnormality, cholestasis
syndrome)
 BRIC

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

26. Globulins
Immunoglobulines :
In autoimmune hepatitis/ chronic active hepatitis - raised
IgG
Primary biliary cirrhosis – raised IgM

27. Bile acids/ bile salts
 Primary bile acids – cholic acid
chenodeoxycholic acid
 Secondary – deoxycholic acid
 Tertiary bile acids – Ursodeoxycholic acid
In cholestasis – increased urine excretion
Low levels – bile acid synthetic defect ( to differentiate
PFIC from BASD)

28. Liver specific other Investigations
(2nd line)
 Septic screen
 Viral markers for hepatitis
 Metabolic screen – TMS, GCMS
 Alfa feto protein
 Sr. ceruloplasmin, urine copper
 Non organ specific antibody – ANA/SMA/LKM
 Thyroid function test
 Urine non glucose reducing substance, GALT
 Urine succinyl acetone
 Sweat chloride test

29.  Radio imaging
 Bone marrow aspiration
 Liver biopsy
 Endoscopy
 Cholangiography

30. Case 1
 2 month 12 days old FCH
 H/O Yellowish discoloration of
skin & sclera from 5th DOL
 Passing pale stool & high color
urine
 O/E: icterus +
 S/E: hepatomegaly 3 cm below
scm
 CBC –WNL
 Sr. bilirubin: 9.4 (T), 6.8(D)
 SGPT – 256
 SGOT – 324
 GGT – 340
 ALP – 620
 PT– 11.6/11.03 INR – 1.06 (After
1 dose vit K)
 Sr. protein -5.0 albumin – 3.6

31. Case 2
 5 year old mch
 H/O fever, vomiting, decreased
oral intake, yellowish discoloration
of sclera, passing high color urine
– 5 days
 h/o travel to village +
 No h/o loose stool, abdominal
distension
 O/E : icterus +
 S/E: mild tenderness in right
hypochodrium. L2 below scm
 Hb – 9.6, TLC – 11200, Platelet – 2
lac
 Sr. bilirubin: 4.4 (T), 2.5(D)
 SGPT – 756
 SGOT – 836
 GGT – 56
 ALP – 124
 PT– 11.03/11.03 INR – 1.0
 Sr. protein -6.8 albumin – 3.9

32. DAY 1 DAY 3 DAY 5
Sr. bilirubin (T/D) 4.4/2.5 12.5/9.6 18.2/16.5
SGPT 756 423 112
SGOT 836 376 104
GGT 56 34 36
Sr. protein /
albumin
6.8/3.9 4.9/3.0 4.9/2.8
INR 1.0 1.40 1.74

33. CASE 3
 8 Year old FCH
 h/o jaundice from 1.5 months,
abdominal distension from 15
days, decreased oral intake +
 Outside admitted , ascitic tapping
done.
 O/E : deep icterus +
 S/E : Hepatosplenomegaly +
(L3,S3 below scm)
 Hb–8.2, TLC–7800, platelet– 2.3 lac
 Outside viral markers – negative
 Sr. bilirubin: 18.8 (T), 14.6(D)
 SGPT – 234
 SGOT – 562
 GGT – 46
 ALP – 76
 PT– 16.4/11.03 INR – 1.48
 Sr. protein -5.0 albumin – 2.6

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

37. Thank you