Liver Function Tests

LIVER FUNCTION TESTS

Liver function tests are helpful screening tool,

which are an effective modality to detect
hepatic dysfunction .
Since the liver performs a variety of functions
so no single test is sufficient to provide
complete estimate of function of liver.
 The Liver disease causing damage to the
hepatocytes, release the enzymes from the
cytosol..
Alkaline Phosphatase (ALT), Aspartate Amino
Transferase (AST), Lactate Dehydrogenase
(LDH) into the blood.
Disease causing biliary obstruction stimulates
the production and release into the blood, of
the enzymes ALP and Gamma Glutamyl
Transfarase (GGT) in the cells lining the biliary
canaliculi and small bile ducts.
In chronic liver disease the hepatic production
of albumin, urea, urate and cholesterol is
often impaired.
In autoimmune hepatic disease, plasma cells
produce and release increased amount of
immunoglobulins into the blood.
Bilirubin metabolism is affected.
Damage to liver cells is associated with the
liberation of liver enzymes.
 LIVER FUNCTION TESTS

Albumin
Globulin
ALP (Alkaline Phosphatase)
Alanine Amino Transferase (Serum Glutamate
Pyruvate Transaminase, SGPT).
AST (Aspartate Amino Transfarase, SGOT)
GGT (Gamma Glutamyl Transfarase)
LDH (Lactate Dehydrogenase)
Prothrombin time
Bilirubin
 ALBUMIN
Normal Range: (4 to 6 g/dL)
Albumin is synthesized within the liver and is
therefore a measure of hepatic function.
Albumin is the protein of the highest
concentration in plasma.
Albumin transports many small molecules in the
blood (for example, bilirubin, calcium,
progesterone, and drugs).
It is also of prime importance in maintaining the
oncotic pressure of the blood (that is, keeping the
fluid from leaking out into the tissues).
When a disease affects the liver cells, the
hepatocytes lose its ability to synthesize albumin,
and serum albumin level is diminished.
Because the half-life of albumin is 12 – 18 days,
severe impairment of hepatic albumin synthesis may
not be recognized for several weeks or even months.
Increase in albumin level occurs in dehydration as
intravascular volume diminishes albumin
concentration measurements must increase
mathematically.
Decrease in albumin level is seen in hepatitis,
extensive metastatic tumor, cirrhosis, hepatocellular
necrosis, malnutrition.
 GLOBULIN
Normal Range: [20-40 g/dl]
Globulins are larger molecules and are sub classified into
three main groups alpha, beta and gamma.
The globulin fraction makes up one-third of total
protein.
The important proteins located in the α1 zone are α1-
antitrypsin.
Some transporting proteins such as thyroid and cortisol
binding globulin also contribute to this zone.

•
Alpha2 globulins include serum hepatoglobulins,
ceruloplasmin, prothrombin and cholinesterase.
Beta1 globulins include lipoproteins, transferring,
plasminogen and complement proteins.
The γ-globulin portion is composed of antibody
immunoglobulins IgA, IgE, IgG and IgM.
IgA is responsible for surface immunity, IgE binds
to mast cell and is responsible for responsible for
the sustained humoral immunity.
The primary disorder associated with
Hypergammaglobulinemia is multiple myeloma.
Increased alpha1 globulin level is seen in
inflammation, necrosis, malignancy or burns.
Decreased alpha1 globulin level is seen in juvenile
pulmonary emphysema.
Increased alpha2 globulin level occurs in
nephritic syndrome.
Decreased alpha2 globulin level occurs in
hemolysis, hyperthyroidism, Wilson’s disease.
Increased beta globulin levels are seen in
hypercholesterolemia and iron deficiency
anemia
Decreased beta globulin levels occur in
malnutrition.
Increased gamma globulin levels are seen in
multiple myeloma, rheumatoid arthritis, SLE,
Hodgkin’s disease, lymphoma, leukemia.
Decreased gamma globulin levels occurs in
conditions like genetic disorders and secondary
immune deficiency.
 ALKALINE PHOSPHATASE
 Normal Range: (ALP) [30 to 120 IU/L]
ALP is found in many tissues, the highest
concentrations are found in the liver, biliary
tract epithelium and bone.
The intestinal mucosa and placenta also
contain ALP.
Damaged or diseased tissue, releases enzymes
into the blood, so serum ALP measurements
can be abnormal in many conditions, including
bone disease and liver disease.
 SERUM GLUTAMIC- PYRUVIC TRANSAMINASE
(ALT). SGPT
Normal Range:( 0 to 35 IU/L)
 ALT is predominantly found in liver; lesser quantities
are found in kidneys, heart, and skeletal muscle.
 This test is used to determine if a patient has liver
damage. ALT is an enzyme involved in the
metabolism of the amino acid alanine.
 Injury to the liver results in release of the enzyme
into the blood.
 Increased value seen in hepatitis (viral,
autoimmune), Use of hepatotoxic drugs, hepatic
ischemia, cirrhosis and hepatic tumor.
SERUM GLUTAMIC OXALOACETIC TRANSAMINASE (SGOT)

(Aspartate aminotransferase)
Normal Range:0 to 35 IU/L

AST is in high concentration in heart muscle, liver

cells, skeletal muscle cells, and to a lesser degree, in
other tissues.
Although elevated serum AST is not specific for
liver disease, it is used primarily to diagnose and
monitor the course of liver disease (in combination
with other enzymes such as ALT, ALP, and bilirubin).
Increased SGOT seen in acute hemolytic anemia,
acute pancreatitis, acute renal failure, hepatic
cirrhosis, hepatic (liver) necrosis (tissue death),
hepatitis, infection mononucleosis, liver cancer,
multiple trauma, myocardial infarction (
heart attack), primary muscle disease
progressive muscular dystrophy, recent
cardiac catheterization or angioplasty.
Recent convulsion, recent surgery, severe deep
burn, skeletal muscle trauma.
Decreased SGOT seen in acute renal disease,
beriberi, diabetic ketoacidosis, pregnancy,
chronic renal dialysis.
 GAMMA - GLUTAMYL TRANSPEPTIDASE (GGT)
Normal Range: 0 to 51 IU/L
This test is used to detect diseases of the liver, bile
ducts, and kidney; and to differentiate liver or bile
duct disorders from bone disease.
 GGT participates in the transfer of amino acids
across the cellular membrane and in glutathione
metabolism.
High concentrations are found in the liver, bile
ducts, and the kidney. GGT compare with ALP is
increased in hepatobiliary disease and bone disease.
GGT is elevated in hepatobiliary disease, but not in
bone disease.
 Increased level - Anemia, biliary obstruction,

bone disease, healing fracture, hepatitis,

hyperparathyroidism, leukemia, liver diseases,
osteoblastic bone cancers, osteomalacia,
Paget’s disease and Rickets.
 Decreased level – Malnutrition and protein

deficiency.
 SERUM GLUTAMIC- PYRUVIC
TRANSAMINASE
(ALT)SGPT
Normal Range: ( 0 to 35 IU/L)
 ALT is predominantly found in liver; lesser
quantities are found in kidneys, heart, and
skeletal muscle.
 This test is used to determine if a patient has
liver damage.
 ALT is an enzyme involved in the metabolism
of the amino acid alanine.
 Increase means cholestasis (congestion of the
bile ducts), cirrhosis, hepatic ischemia, hepatic
necrosis (tissue death), hepatic tumor, hepatitis
and hepatotoxic drugs.
Interfering factors: Drugs that can increase GGT
levels include alcohol, phenytoin, and
phenobarbital. Drugs that can decrease GGT
levels include clofibrate and oral contraceptives.
 LACTATE DEHYDROGENASE (LDH)
Normal range 100 to 190 IU/L
Lactate dehydrogenase (LDH or LD) is an
enzyme present in a wide variety of organisms,
including plants and animals.
 Lactate dehydrogenase catalyzes the
interconversion of pyruvate and lactate with
concomitant interconversion of NADH and
NAD+.
 LDH is in high concentraton in cardiac and
skeletal muscle, liver, kidney, lung parenchyma
and erythrocytes.
 Functional lactate dehydrogenase are homo
or hetero tetramers composed of M and H
protein subunits encoded by the LDHA and
LDHB genes respectively:
 LDH-1 (4H) - in the heart
 LDH-2 (3H1M) - in the reticuloendothelial
system
 LDH-3 (2H2M) - in the lungs
 LDH-4 (1H3M) - in the kidneys
 LDH-5 (4M) - in the liver and striated muscle
Serum LDH almost always is elevated after acute
myocardial infarction (MI).
The serum LDH begins to rise 10 to 12 hours
after the acute event, reaching a peak in 48 to 72
hours, with prolonged elevation for up to 14
days.
Increased serum LDH level, with LDH1 greater
than LDH2 (Flipped enzymes), occurs in MI in
approximately 80% of patients, but also occurs in
acute renal infraction, pernicious anemia, and
hemolysis.
LDH5 may be markedly elevated in hepatitis and
may also be elevated in other hepatic disorders.
 LDH elevated 60% of patient with lymphomas
and 90% of patients with leukemias.
Marked elevations of LDH5 level are seen in
patient with skeletal muscle damage, extensive
burns and trauma.
Pulmonary embolus and infarction may cause
elevations in LDH2 and LDH3.
In nephrotic syndrome, LDH4 and LDH5 rise, but in
nephritis and renal infarction LDH1 and LDH2
raised.
 PROTHROMBIN TIME (PT)
Normal range 11 to 16 sec
Prothrombin time (PT) is a blood test that measures
the time it takes for the liquid portion (plasma) of your
blood to clot.
It measures:
 Factor I (fibrinogen)
 Factor II (prothrombin)
 Factor V
 Factor VII
 Factor X
Increased PT times may indicate
bile duct obstruction, cirrhosis,
disseminated intravascular coagulation, hepatitis,
malabsorption, vitamin k deficiency, coumarin
(warfarin) therapy, factor VII deficiency, factor X
deficiency, factor II (prothrombin) deficiency,
factor V deficiency and factor I (fibrinogen)
deficiency.
The risks are excessive bleeding, fainting or
feeling light-headed, hematoma, infection and
multiple punctures to locate veins.
 Special considerations
Coagulation results from a sequence of reactions
involving several proteins known as coagulation
factors.
The liver produces these proteins and secretes
them into the blood.
In addition, vitamin K is important to blood
clotting because it helps in conversion of
prothrombin to thrombin.
Some people take warfarin to keep their blood
from clotting.
Warfarin inhibits prothrombin conversion.
Because of the link between vitamin K and
prothrombin, people who take warfarin need
to have consistent levels of vitamin K in their
diet, as instructed by their doctor.
Coagulation begins when some of the
coagulation factors contact damaged tissue.
Each factor reaction triggers the next reaction,
in a cascade.
The final product of the coagulation cascade is
the blood clot.
Factor X can be activated by two different
chemical-reaction sequences.
The factors involved in the two sequences are
referred to as the intrinsic system and the
extrinsic system.
 In the extrinsic system, a substance called
thromboplastin or tissue factor (a protein
released by damaged tissues) activates factor
VII.
The PT test is used to evaluate the adequacy
of the extrinsic system.
It measures the clotting ability of factors I
(fibrinogen), II (prothrombin), V, VII, and X.
 When any of these factors is deficient, the PT
is prolonged.
 SERUM BILIRUBIN
Alternative names: Total bilirubin,
unconjugated bilirubin, indirect bilirubin,
conjugated bilirubin and direct bilirubin.
 Bilirubin metabolism begins with the
breakdown of red blood cells in many parts of
the body.
Red blood cells contain hemoglobin, which is
broken down to heme and globin.
Heme is converted to bilirubin, which is then
carried by albumin in the blood to the liver.
 In the liver, most of the bilirubin is
chemically attached to another molecule
before it is released in the bile.
This "conjugated" (attached) bilirubin is called
direct bilirubin; unconjugated bilirubin is
called indirect bilirubin.
Total serum bilirubin equals direct bilirubin
plus indirect bilirubin.
Conjugated bilirubin is released into the bile
by the liver and stored in the gallbladder, or
transferred directly to the small intestines.
 Bilirubin is further broken down by bacteria in
the intestines, and those breakdown products
contribute to the color of the feces.
A small percentage of these breakdown
compounds are taken in again by the body,
and eventually appear in the urine, where
they are referred to as urobilinogen.
Abnormal results mean Jaundice is the
discoloration of skin and sclera of the eye,
which occurs when bilirubin accumulates in
the blood at a level greater than
approximately 2.5 mg/dl.
Jaundice occurs because red blood cells are
being broken down too fast for the liver to
process, because of disease in the liver or
because of bile duct blockage.
If the bile ducts are obstructed, direct bilirubin
will build up, escape from the liver, and end up
in the blood.
If the levels are high enough, some of it will
appear in the urine.
Only direct bilirubin appears in the urine.
Increased direct bilirubin usually means that
the biliary ducts obstructed.
Increased urinary bilirubin may indicate Biliary
trictures, cirrhosis, gallstones in the biliary tract
, hepatitis with associated biliary obstruction,
surgical trauma affecting the biliary tract and
tumors of the liver or gall bladder.