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١

�The liver is the largest organ in the

body

�It is located below the diaphragm

in the right upper quadrant of the

abdominal cavity and extended

approximately from the right 5th rib

to the lower border of the rib cage.

�The liver is separated into a right

and left lobe, separated by the

falciform ligament. The right is

much larger than the left .

The liver performs

thousands of tasks that

impact all body systems.

Liver have two channels

that can supply and oxygen

nutriment : hepatic artery

and hepatic portal vein .

The corresponding

channels is hepatic vein

and bile ducts.

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٢

The working cells of the liver are

known as hepatocytes, which have a

unique capacity to reproduce in

response to liver injury.

Liver regeneration can occur after

surgical removal of a portion of the

liver or after injuries that destroy

parts of the liver.

Although the liver's ability to react

to damage and repair itself is

remarkable, repetitive insults can

produce liver failure and death.

Functions of liver① Excretory function: bile pigments,

bile salts and cholesterol are excreted in

bile into intestine.

② Metabolic function: liver actively

participates in carbohydrate, lipid,

protein, mineral and vitamin

metabolisms.

③ Hematological function: liver is also

produces clotting factors like factor V,

VII. Fibrinogen involved in blood

coagulation is also synthesized in liver.

It synthesize plasma proteins and

destruction of erythrocytes.

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٣

④ Storage functions:

glycogen, vitamins A, D and

B12,and trace element iron

are stored in liver.

⑤ Protective functions and

detoxification: Ammonia is

detoxified to urea. kupffer

cells of liver perform

phagocytosis to eliminate

foreign compounds.

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٤

What is Purpose of LFTs?

• LFTs alone do not give the

physician full information,

but used in combination

with a careful history,

physical examination

(particularly ultrasound and

CT Scanning), can

contribute to making an

accurate diagnosis of the

specific liver disorder.

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٥

liver function tests1. Detect the presence of liver disease

2. Distinguish different types of liver

disorders

3. Extent of liver damage

4. Follow the response to treatment

A. Can be normal in serious liver

disease

B. Can be abnormal in non hepatic

diseases

C. Rarely suggest a specific diagnosis

D. They suggest a general category of

liver disease, such as hepatocellular

or cholestatic

•LFTs are divided into

� True tests of liver function,

such as serum albumin,

bilirubin, and prothrombine

time,

� Tests that are indicators of

liver injury or biliary tract

disease.

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٦

Classification of liver functions test①Excretion: Measurement of bile

pigments, bile salts.

②Serum enzymes: Transaminase (ALT,

AST), alkaline phosphate(ALP), 5’-

nucleotidase, LDH isoenzyme.

③Synthetic function: Prothrombin time,

serum albumin.

④Metabolic capacity: Galactose

tolerance and antipyrine clearance

⑤Detoxification: Serum ammonia

Excretion : Bilirubin

�Bilirubin is the main bile

pigment that is formed

from the breakdown of

heme in red blood cells.

�The broken down heme

travels to the liver, where it

is secreted into the bile by

the liver.

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٧

via bile duct to intestines

Stercobilin

excreted in feces

Urobilinogen

formed by bacteria KIDNEY

Urobilin

excreted in urine

BLOOD

CELLS

CO

Biliverdin IXα

Heme oxygenase

O2

Bilirubin (water-insoluble)

NADP+

NADPH

Biliverdin

reductase

Heme

Globin

Hemoglobin

reabsorbed

into blood

LIVER

Bilirubin diglucuronide

(water-soluble)

2 UDP-glucuronic acid

Bilirubin

(water-insoluble)via blood

to the

liver

INTESTINE

Metabolism of bilirubin

�A. Indirect bilirubin

(normal value = 0.3 - 1.2 mg/dl)

1. Serum Bilirubin:

�B. Direct bilirubin

(normal value ≤ 0.4 mg/dl)

�C. Total bilirubin Normal value for = 0.3- 1.2 mg/dl.

�Normally, a small amount of bilirubin circulates in the blood.

�Serum bilirubin is considered a true test of liver function, as it reflects

the liver's ability to take up, process, and secrete bilirubin into the bile.

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٨

Indirect bilirubin

Direct bilirubin

Binding with Glucuronic acid

no yes

Reacting with the diazoreagent

Slow and indirect

Rapid and direct

solubility in water small large

Discharged via kidney no yes

Pass through the membrane of cell

yes no

Pass blood brain barrier

yes no

Difference of two bilirubins

� Urobilinogen :Conjugated bilirubin is excreted via

bile salts to intestine.

Bacteria in the intestine break down

bilirubin to urobilinogen for

excretion in the feces (normal value

for fecal urobilinogen = 40 - 280

mg/day)

2. Urine & Stool

Normally there are mere traces of urobilinogen in the urine. average is

0.64mg , maximum normal 4mg/24hours.

� UrobilinUrobilin is the final product of oxidation of urobilinogen by oxygen in

air. The amount change with the amount of urobilinogen excretion .

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٩

� Bilirubin urine:

�Bilirubin is not normally present in

urine and faese since bacteria in intestine

reduce it to urobilinogen.

�The kidneys do not filter unconjugated

bilirubin because of its binding to albumin.

�Conjugated bilirubin can pass through

glomerular filter.

�Bilirubin is found in the urine in

obstructive jaundice due to various causes

and in cholestasis.

� Bilirubin in the urine may be detected

even before clinical jaundice is noted.

Who is a candidate for the test?

�Bilirubin is used to diagnosis of jaundice.

�Abnormal bilirubin levels can be found in

many disorders, including:

Hemolytic Jaundice

Hepatic Jaundice

Obstructive jaundice ( Cholestasis)

Congenital Jaundice

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١٠

Sample Indices Hemolytic

Jaundice

Hepatic

Jaundice

Obstructive

Jaundice

Serum Total Bil ＞1mg/dl ＞1mg/dl ＞1mg/dl

Direct Bil ↑ ↑↑

Indirect Bil ↑↑

Urine Color deeper deep deep

Bilirubin ― ＋＋ ＋＋

Urobilinogen ↑ uncertain ↓

Urobilin ↑ uncertain ↓

Stool Color deeper lighter or normal

Argilous(complete

obstruction)

Aproach to isolated elevation of bilirubin

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١١

Aproach familial elevation of bilirubin

Familial hyperbilirubinaemia , Congenital hyperbilirubinaemia

Degree of elevation of bilirubin

� Not as a prognostic marker

�But is important in :

1. Viral hepatitis: higher bilirubin→greater hepatocellular damage.

2.Alcoholic hepatitis: total serum

bilirubin correlates with poor outcomes

3.Component of the model for end stage

liver disease (MELD)

4.Drug-induced liver disease: elevated

total serum bilirubin indicates more

severe injury.

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١٢

Serum Enzymes�The liver contains thousands of enzymes

�These enzymes have no known function

�probably cleared by reticuloendothelial cells

�liver cells damage → entrance of Enzymes into serum

3 type of Liver enzyme tests

1. Enzymes whose elevation reflects damage to

hepatocytes

2. Enzymes whose elevation reflects cholestasis

3. Enzyme tests that do not fit either pattern.

Enzymes that Reflect Damage to Hepatocytes

Aspartate aminotransferase (AST) = serum

glutamic oxaloacetic transaminase (sGOT)

Alanine aminotransferase (ALT) = Serum glutamic

pyruvic transaminase (sGPT)

�Sensitive indicators of liver cell injury

�Most helpful in recognizing acute hepatocellular

diseases (hepatitis)

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١٣

Alanine transaminase (ALT)

GPTGPT

Aspartate aminotransferase (AST)

GOT

AST ( sGOT) is found in

�Liver

�Cardiac muscle

�Skeletal muscle

� Kidneys

� Brain

� Pancreas

� Lungs

� Leukocytes, and

erythrocytes

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١٤

organ GOT GPT

heart 156000 7100

liver 142000 44000

skeletal 99000 4800

kidney 91000 19000

organ GOT GPT

pancrease

spleen

lung

serum

28000 2000

14000 1200

10000 700

20 16

GPT:

Normal range: 2-59 U/L

GOT:

Normal range: 10-34 U/L

Therefore, when the liver is injured, GPT is

released into the bloodstream.

� sGOT also reflects damage to the hepatic

cells and is less specific for liver disease. It

can also be released with heart, muscle and

brain disorders.

�Therefore, this test may be ordered to help

diagnose various heart, muscle or brain

disorders, such as a myocardial infarct .

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١٥

Alcoholic liver disease

Cancer of the liver

Cholestasis or congestion of the bile ducts

Cirrhosis or scarring of the liver with loss of

function

Death of liver tissue

Hepatitis or inflammation of the liver

Noncancerous tumor of the liver

Use of medicines or drugs toxic to the liver

Acute hemolytic anemia,

Acute pancreatitis or inflammation of the pancreas.

Acute renal failure or loss of kidney function.

Cirrhosis of the liver.

Hepatitis

Heart attack

Primary muscle disease

Recent surgery

Severe burns

Muscle injury

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١٦

Levels of aminotransferases

�<300 U/L are nonspecific and may be found in any

type of liver disorder.

�Minimal ALT elevations

� Asymptomatic blood donors

� Severe liver disease

� Fatty liver is the most cause.

�Extensive hepatocellular injury such:

1) Viral hepatitis

2) Ischemic liver injury (prolonged hypotension or

acute heart failure)

3) Toxin- or drug-induced liver injury.

The pattern of the aminotransferase

�Acute hepatocellular disorders: ALT ≥ AST.

�Chronic viral hepatitis : ALT ≥ AST

�Cirrhosis : AST ≥ ALT

AST/ALT ratio

Normal - 1 or slightly > 1

<1 : NASH or hepatitis

without cirrhosis

2-4:ALD

>4 : Wilsonian hepatitis

Causes of AST /ALT > 2

ALD

Acute wilsonian hepatitis

DDP

Metastasis

cirrhosis

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١٧

Approach to asymptomatic elevation of serum aminotransferase

Alcoholic liver disease

�AST/ALT >2:1 is suggestive

�AST/ALT >3:1 is highly suggestive

�The AST is rarely >300 U/L

�ALT is often normal.

�A low level of ALT in the serum is due to an alcohol-induced

deficiency of pyridoxal phosphate.

Obstructive jaundice�Aminotransferases not greatly elevated

�Exception: passage of a gallstone into the common bile duct →

acute biliary obstruction → aminotransferases 1000–2000 →

decrease quickly → liver-function tests rapidly evolve typical of

cholestasis.

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١٨

Enzymes that Reflect Cholestasis

Are usually elevated in cholestasis

Alkaline phosphatase

5'-nucleotidase

Gama glutamyl transpeptidase (GGT)

Alkaline phosphatase (ALP)

ALP occurs in all tissues,

especially liver and bone.

The alkaline phosphatase

test is often used to help

diagnose certain liver

diseases and bone

disorders .

Normal range: 30 - 95

IU/L (3-13 kings unit)

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١٩

Alkaline phosphatase

�ALP is a hydrolase enzyme responsible for removing phosphate

groups from many types of molecules, including nucleotides and

proteins.

�Most effective in an alkaline environment

�In humans it is present in all tissues throughout the entire body,

but is particularly concentrated in

Liver

Bile duct

Kidney

Bone

The placenta.

Heat-stable :

placenta or a tumor is the source.

Heat –unstable:

intestinal, liver, and bone

Higher levels of ALP than normal

may indicate:

� Liver disease

� Bone disease

� Leukemia

Lower levels of ALP than

normal may indicate:

� Anemia, or a low red blood cell count

� Malnutrition

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٢٠

Mechanism of increase in ALP in liver disease:

�Increase in the activity of ALP in liver disease is not

due to hepatic cell disruption , nor to a failure of

clearance , but rather to increased synthesis of hepatic

ALP .

�The stimulus for this increased synthesis in patients

with liver disease has been attributed to bile duct

obstruction by stone ,tumors , intrahepatically by

infiltrative disorders or space-occupying lesions.

ALP Non Pathologically Elevated

�Age > 60

�Blood types O and B after

fatty meal (influx of

intestinal ALKP into the

blood.)

�Children and adolescents

undergoing rapid bone

growth, (bone)

�Late in normalpregnancies (influx of

placental )

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٢١

Elevation of liver-derived alkaline phosphatase

� Not specific for

cholestasis

�< 3 fold occur in :

Any type of liver disease.

�>4 fold occur in:

Cholestatic liver disorders

Infiltrative liver diseases

such as cancer and

amyloidosis

Level of ALPis not helpful indistinguishing

�Between intrahepatic and

extrahepatic cholestasis

�Obstructive jaundice due to

cancer, common duct stone,

sclerosing cholangitis, or bile

duct stricture.

Aproach to elevation of ALP

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٢٢

5' NTSensitive and specific for

hepatobiliary disorders (HBD)

Normal pregnancy, bone growth and

bone diseases do not affect 5' NT

In pts with HBD, changes in ALP are

usually followed by similar changes

in 5' NT

GGT

�Inducible microsomal enzyme.

�N levels – 5- 40 IU/L.

�Less specific than 5' NT as a marker for

HBD

�Unlike 5' NT, GGT may be released from

many sites beside the hepatobiliary tree.

�Bone – important source of ALP, has little

GGT thus GGT useful for differentiating

hepatic & osseous sources of ALP

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٢٣

� This test measures the total level of the

enzyme lactic dehydrogenase, also called LDH,

in the blood.

� LDH is found in body tissues and organs.

lactate dehydrogenase

Enzymes that do not fit either pattern.

LDH isoenzymes

۩ Tissue or organ injury can release LDH into

the bloodstream, thereby raising the level.

۩ If he or she suspects a heart attack or liver

tissue damage in the body.

۩Normal range: 115-225 IU/L

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٢٤

Tests based on livers function:

� Carbohydrate metabolism

� Lipid metabolism

� Protein metabolism

�Not of much value in liver diseases

� It is often difficult to separate the part

played by the liver from other factors

influencing glucose metabolism.

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٢٥

Basis:�For galactose is a monosaccharide, almost

exclusively metabolized by the liver.

�The normal liver is able to convert galactose

into glucose.

�This function is impaired in intrahepatic disease

and the amount of blood galactose and urine

galactose is excessive.

�The liver can be assessed by measuring the

utilization of galactose.

It is used primarily to detect liver cell injury.

It can be performed in presence of jaundice.

As it measured an intrinsic hepatic function, it may be

used to distinguish obstruction and non obstruction

jaundice.

Method :

�Oral galactose tolerance test

�IV galactose tolerance test(intravenous injection )

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٢٦

Normally or obstructive jaundice:

3gm or less of galactose are excreted in the urinewithin 3 to 5 hours and the blood galactose returns tonormal within one hour.

Result:

Intrahepatic jaundice:

The excretion amounts to 4 to 5gm or more during the first 5 hours.

Normal response:

Shows little or no rise in the blood sugar level.

The highest blood sugar value reached during the test

should not exceed the fasting level by more than 30 mg%.

In infectious hepatitis or

parenchymatous liver

cells damage:

Rise in blood sugar is

greater than above, but the

increases obtained are

never very great.

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٢٧

Tests Based On Lipids Metabolism

Cholesterol-cholesteryl Ester Ratio:

The liver plays an active and important role in

the metabolism of cholesterol including its

synthesis,esterification,oxidation and excretion.

Normal total blood cholesterol ranges from 150 ~

250mg/dl and approx 60 to 70% of this is in erterified

form.

In parenchymatous liver disease:

Their is either no rise or even decrease

in total cholesterol and the ester fraction is

always definitely reduced.

The degree of reduction roughly parallels

the degree of liver damage.

In severe acute hepatic necrosis:

The total serum cholesterol is usually

low and may fall below 100mg/dl, while

there is marked reduction in the % present

as esters.

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٢٨

Tests based on amino acid metabolism

Determination of

blood NH3:

Nitrogen part of aminoacid is converted toNH3 in the liver mainlyby transamination anddeamination and it isconverted to urea inliver only .

Synthetic functions

1. Total plasma proteins/ albumin/ globulin/

A:G ratio

2. Formation of prothrombin by liver

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٢٩

Normal value:

�Total plasma proteins: 80~110mg/dl

�Albumin:40-50mg/dl

�Globulin:25~35mg/dl

�A:G ratio: 1.5~2.5

This yields most useful information in chronic liver

disease.

Liver is the site of albumin synthesis and also

possibly of some of α and β globulins.

In infectious hepatitis:�Quantitative estimations of albumin and

globulin may give normal results in the early

stages.

�Qualititative changes may be present,in

early stage rise in β -globulins and in later

stages γ-globulins shows rise.

In cirrhosis liver or parenchymalliver disease:

The albumin is grossly dicreased and the

globulins are often increased,so that A:G ratio

is reversed, is characteristically seen in

cirrhosis liver.

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٣٠

�Albumin is an important blood protein that is made

only by the liver and excreted by the kidneys.

�Albumin is essential for maintaining

the osmotic pressure in the vascular

system.

�low albumin level produce ascites.

�Albumin is also very important in the

transportation of many substances

such as drugs, lipids, hormones and

toxins that are bound to albumin in the

bloodstream.

Synthesized exclusively by hepatocytes.

Long half-life: 18–20 days

Normal range: 34 - 54 g/L

Not a good indicator of acute or mild hepatic

dysfunction (slow turnover)

This test is normally performed to assist in

diagnosing diseases that affect proteins in the

body, such as cancer, liver disease, renal or

intestinal problems, and immune disorders.

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٣١

Abnormally low contents of albumin may indicate:

�Ascites

� Extensive burns

� Kidney disease

� Liver disease

� Malabsorption syndromes

�Protein-losing enteropathies

�Chronic infections that inhibit albumin synthesis.

Common in chronic liver disorders such as cirrhosis than

in acute liver disease

Reflects severe liver damage and decreased albumin

synthesis.

Immunoglobulins produced by B

lymphocytes

Globulins are increased in chronic

hepatitis and cirrhosis.

In cirrhosis: due to the increased

synthesis of antibodies against

intestinal bacteria.

Cause : cirrhotic liver fails to

clear bacterial antigens that

normally reach through the

hepatic circulation.

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٣٢

Diffuse polyclonal IgG ↑ in autoimmunehepatitis

IgM ↑in primary biliary cirrhosis

IgA ↑ in alcoholic liver disease

�At least 12 different proteins are involved in clotting.

Blood clotting factors are proteins made by the liver and are

associated with the incorporation of vitamin K metabolites

into a protein.

�When the liver is significantly injured, these proteins are

not normally produced.

�PT (Prothrombin time)

�Estimation of plasma fibrinogen

�APTT(activated partial thromboplastin time)

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٣٣

Prothrombin is a plasma protein that is converted

into thrombin during blood clotting.

Prothrombin is formed in the liver from inactive

“preprothrombin” in presence of vitamin K.

thrombin Prothrombin

in presence of vitamin K

Ca2+, PL

٢٥/٠٤/١٤٣٦

٣٤

PT is used to assess the activity of extrinsic blood clotting

pathway .

PT is also a useful test of liver function, since there is a

good correlation between abnormalities in coagulation

measured by PT and the degree of liver dysfunction.

PT is usually expressed in seconds and compared to a

normal control patient’s blood.

Prothrombin time is measured as prothrombin activity.

The term prothrombin time was given to time required for

clotting to take place in plasma to III factor and Ca+ have

been added.

This test may be done:

�When a person has a bleeding problem

�Monitor a person who is taking oral anticoagulants

�Before surgery to make sure a person will not bleed too

much during the operation.

�Prothrombin activity is also sometimes expressed as

“prothrombin index”, which is the ratio of prothrombin

time of the normal control to the patient’s prothrombin time:

Prothrombin index = PT of normal control

PT OF patientx100

٢٥/٠٤/١٤٣٦

٣٥

High PT values may occur when a person:

�Is taking blood-thinning medicines like warfarin

�Is taking other medicines, such as certain

antibiotics, that interfere with the test

�Has severe liver disease

�Has DIC :a complex blood disorder that occurs

when clotting mechanisms are activated

throughout the body

�Has certain rare, inherited bleeding disorders

�Has a vitamin K deficiency

Abnormally low PT values are usually notsignificant.

However, they may occur when a person:

�Has cancer

�Has blood clots

�Is taking certain medicines, such as oral

contraceptive pills

٢٥/٠٤/١٤٣٦

٣٦

Protective functions and detoxification

Blood AmmoniaBlood Ammonia�Produced

�During normal protein metabolism

�Intestinal bacteria in the colon.

�liver plays : detoxification of ammonia by converting it

to urea→ excreted by the kidneys

�Striated muscle → detoxification of ammonia

(combination with glutamic acid )

Elevated ammonia levelsElevated ammonia levelsHas very poor correlation with:

� Presence or severity of acute encephalopathy

�Hepatic function.

٢٥/٠٤/١٤٣٦

٣٧

Elevated ammonia levels Elevated ammonia levels Occasionally useful for occult liver disease in

mental changes.

Correlate with outcome in fulminant hepatic

failure.

In severe portal hypertension and shunting around

the liver even in normal or near-normal hepatic

function.

Some Other Tests For LFTsSome Other Tests For LFTs

�Mitochondrial Antibodies Test

The presence of these antibodies can indicate primary biliary

cirrhosis, chronic active hepatitis, and certain other

autoimmune disorders.

� Platelet count:

In cases of chronic liver disease where cirrhosis exists, the

platelet count can be lowered — although this can occur due

to many conditions other than liver disease.

٢٥/٠٤/١٤٣٦

٣٨

�Fibrinogen

�Synthesized exclusively by hepatocytes

�Plasma fibrinogen – 100-700 mg/dl

�Functions – polymerizes into long fibrin threads by the

action of thrombin � formation of clot

�Haptoglobins

�Forms stable complexes with free Hb � prevents loss of

iron through urinary excretion, protects kidney from damage

�Ceruloplasmin

� Binds with copper and helps in its transport and storage

�Bromosulphathein excretion test

�BSP dye- same mechanism as bilirubin

�Binding

�Conjugation

�Excretion

�BSP – i/v – 45 mins- levels in venous blood

�Normally- <5%.

�Slightly higher in old age

�Sensitive test to detect mild impairement of liver

�Indocyanine green

�This dye is removed by the liver after intravenous injection. A

blood level is obtained 20 min after administration.

� Compared with BSP its hepatic clearance is more efficient, and

it is nontoxic.

٢٥/٠٤/١٤٣٦

٣٩

�Serum bile acids

�Synthesized from cholesterol in the liver, conjugated to

glycine or taurine, and excreted in the bile.

�Bile acids facilitate fat digestion and absorption within the

small intestine. They recycle through the enterohepatic

circulation.

�Detection of an elevated level of serum bile acids is a

sensitive marker of hepatobiliary dysfunction

�A number of different bile acid tests have been described,

including fasting and postprandial levels and determination of

levels after a bile acid load.

�Normal bile acid levels in the presence of

hyperbilirubinemia suggests hemolysis or Gilbert’s syndrome

�ᾳ- feto protein

�Resembles albumin genetically &

functionally

�Formation sites- yolksac,

hepatocytes, enterocytes

�Fetal & neonatal life- major

determinant of plasma oncotic

pressure

� 1 year of age- albumin largely

replaces AFP

٢٥/٠٤/١٤٣٦

٤٠

�There is no ideal study to evaluate the liver’s

diverse functions.

�Abnormal liver biochemistries are often the first

indication of liver disease.

�The widespread inclusion of these tests in routine

blood chemistry panels uncovers many patients with

unsuspected hepatic dysfunction.

�Laboratory testing may provide information about

the severity of liver disease and its prognosis

٢٥/٠٤/١٤٣٦

٤١

٢٥/٠٤/١٤٣٦

٤٢

�USG, CT scan - 1st line

investigation

�ERCP visualization of

biliary tract

�Doppler & MRI hepatic

vasculature & heamody-

namics

�CT & MRI- hepatic masses

& tumours

HepatobiliaryHepatobiliary imagingimaging

٢٥/٠٤/١٤٣٦

٤٣

Despite advances in serological testing

and imaging, liver biopsy remains the

golden standerd to confirm the

diagnosis of specific liver diseases such

as

�Wilson disease

�Nonalcoholic steatohepatitis

�Assess prognosis in many forms of

parenchymal liver disease such as

chronic viral hepatitis

�Evaluate allograft dysfunction in liver

transplant recipients.

Biopsy Biopsy

Indications for liver biopsy

� Evaluation of abnormal liver biochemical tests and hepatomegaly

� Evaluation and staging of chronic hepatitis

� Identification and staging of alcoholic liver disease

� Recognition of systemic inflammatory or granulomatous disorders

� Evaluation of fever of unknown origin

� Evaluation of the type and extent of drug-induced liver injury

� Identification and determination of the nature of intrahepatic masses

� Diagnosis of multisystem infiltrative disorders

� Evaluation and staging of cholestatic liver disease (primary biliary

cirrhosis, primary sclerosing cholangitis)

� Screening of relatives of patients with familial diseases

� Obtaining of tissue to culture infectious agents (e.g., mycobacteria)

� Evaluation of effectiveness of therapies for liver diseases (e.g., Wilson

disease, hemochromatosis, autoimmune hepatitis, chronic viral

hepatitis)

� Evaluation of liver test abnormalities following transplantation

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Contraindications to liver biopsy

Complications�Post-biopsy pain with or without radiation to the right shoulder

occurs in up to one-third of patients.

� Intraperitoneal bleeding is the most serious complication.

Increasing age, presence of hepatic malignancy, and the number

of passes made are predictors of the likelihood of bleeding, as is

the use of a cutting rather than a suction needle

�Pneumothorax may require a chest tube, whereas serious

bleeding may be controlled by selective embolization at

angiography or, if necessary, ligation of the right hepatic artery

or hepatic resection

� Biopsy of a malignant neoplasm carries a 1–3% risk of seeding

of the biopsy track with tumor

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Abnormal in... Liver Test

Cirrhosis, severe hepatocellular injuryAlbumin

Cholestasis, hepatocellular enzyme induction, canalicular injury, children during bone growth, bone disease, pregnancy (placenta origin)

Alkaline phosphatase

Hepatocellular injury (ethanol, drug-induced hepatitis, hepatitis B and C,

ischemic injury, chronic liver disease, NAFLD, chronic viral hepatitis,

alcoholism, nonspecific viral injury, and cholestatic or replacement disease);

acute biliary obstruction; rarely in hyperthyroidism, celiac disease, skeletal muscle disease

Aminotransferases (AST, ALT)

Any acute or chronic liver disease; congenital disorders of bilirubin metabolism.

Bilirubin

Cholestasis5′ nucleotidase

Cholestasis; medications, ethanol; rarely anorexia nervosa, hyperthyroidism, myotonic dystrophy

GGT

Impaired synthesis of vitamin K-dependent coagulation factorsINR

Ischemic injury, Epstein-Barr virus infection, hemolysis, solid tumorLactate dehydrogenase

Alcohol consumption, goutUric acid