ORGAN FUNCTION TESTS ●​ Serum aspartate transaminase (AST)

●​ Serum alkaline phosphatase (ALP)

INTRODUCTION
Liver Function Tests Based on Excretory Function
A large number of biochemical tests are carried out in
the investigation of diseases. Many of them are well An important physiologic role of the liver is the
associated with the impairment of the function of a removal of toxic endogenous and exogenous
particular organ and are called organ function tests. substances from the blood. The tests based on
Thus, organ function tests are the tests carried out to excretory function of liver are related to bilirubin
assess whether a particular organ is functioning metabolism.
normally or not. The following organ function tests are
most common: Tests Based on Bilirubin Metabolism

●​ Liver function tests Bilirubin is the excretory end product of heme. It is

●​ Renal function tests conjugated in the liver to form bilirubin diglucuronide.
●​ Thyroid function tests Bilirubin is insoluble in water but bilirubin
●​ Lipid profile tests diglucuronide is soluble in water. The bilirubin
glucuronide is excreted in the bile and through the bile
LIVER FUNCTION TESTS goes to the intestine. There, it is reduced by bacterial
enzymes to urobilinogen.
Classification of Liver Function Tests
●​ Bilirubin exists in the serum in two forms:
The liver performs four major functions: -​ Conjugated or direct bilirubin which
is water soluble.
1.​ Excretion/Secretion -​ Unconjugated or indirect bilirubin
2.​ Metabolism which is water insoluble.
3.​ Detoxification
4.​ Storage ●​ The normal concentration of total serum
bilirubin is 0.1 to 1 mg/dL of which direct
As liver performs a multiple of functions, a number of serum bilirubin ranges from 0.1 to 0.4 mg/dL
tests are required to assess hepatic functions. All the and indirect serum bilirubin is 0.2 to 0.7
tests need not be performed in every case. The tests mg/dL.
should be selected according to the clinical symptoms
and signs. Several tests used earlier, e.g. Icterus Clinical Significance of D-BIL
index, thymol turbidity, serum cholesterol:
cholesteryl ester ratio, etc., have now become ●​ Bilirubin is a breakdown product of
outdated due to lack of specificity and or sensitivity. hemoglobin.
The following are the commonly used liver function
tests. Liver function tests can be classified into five ●​ Bilirubin formed in the RES is transported
classes according to the function of the liver as given bound by albumin to the liver.
below: Tests based on excretory function (related
to excretion of toxic endogenous bilirubin and ●​ Bilirubin is water insoluble and is known as
exogenous substances). indirect or unconjugated bilirubin.

It includes measurement of: ●​ In the liver, bilirubin is conjugated to

glucuronic acid to form direct bilirubin.
●​ Serum bilirubin
●​ Urine bilirubin ●​ Conjugated bilirubin is excreted via the
●​ Urine bile salts biliary system into the intestine Here it is
●​ Bromosulfophthalein (BSP) dye tests metabolized by bacteria to urobilinogen and
stercobilinogen.
Tests related to enzymes in diagnosis of liver disease:
Multiple bilirubin-reducing bacteria have been
●​ Serum alanine transaminase (ALT) Identified, including strains of:
 ●​ In hepatic jaundice both conjugated and
●​ Clostridioides difficile (New name: unconjugated bilirubin are increased hence a
clostridia-like) biphasic reaction is observed.
●​ Clostridium ramosum
●​ Clostridium perfringens ●​ Laboratory results in normal persons and
●​ Bacteroides fragilis patients with three different types of jaundice
are shown in Table 25.1.
Clinical Significance of D-BIL
Tests Based on Synthetic Function
●​ TOTAL BILIRUBIN = INDIRECT BILIRUBIN
+ DIRECT BILIRUBIN Liver is the main source of synthesis of plasma
proteins, e.g. albumin, globulin (except y-globulins
●​ Total bilirubin is elevated in obstructive which are synthesized in the reticuloendothelial
conditions of the bile duct, hepatitis, system), blood clotting factors, e.g. fibrinogen,
cirrhosis, in hemolytic disorders and several prothrombin and factors V, VII, IX, X. Impaired
Inherited enzyme deficiencies. function of liver results in decreased protein
synthesis.
●​ Indirect Bilirubin is elevated in pre-hepatic
causes le, hemolytic disorders or liver Determination of Prothrombin Time
diseases resulting in impaired entry transport
or conjugation within the liver, Hepatic synthetic function of several clotting factors
can be assessed by a simple coagulation test, e.g.
●​ Monitoring of indirect bilirubin in neonates is prothrombin time.
of special Importance as it is the indirect or
free bilirubin bound to albumin that is able to Various proteins that participate in blood coagulation
cross the blood brain barrier more easily are synthesized in the liver, e.g. fibrinogen,
increasing the danger of cerebral damage. prothrombin (factor II) and factors V, VII, IX and X. If
any one of these factors is deficient, the deficiency
KERNICTERUS causes prolonged prothrombin time.

-​ Brain damage in newborns with severe Clinical interpretation

jaundice
-​ Can recover, if have received treatment on ●​ An increased prothrombin time indicates the
time failure of hepatic synthesis of one or more of
the above mentioned clotting factors.
Clinical interpretation
●​ As vitamin K is required for the synthesis of
Estimation of direct and indirect bilirubin is useful blood clotting factors, deficiency of vitamin K
for the differential diagnosis of jaundice. Bilirubin can also cause prolonged prothrombin time,
metabolism is deranged in three important diseases. which must be ruled out by estimating the
They are: prothrombin time, before and after
administration of vitamin K. In case of liver
-​ Hemolytic jaundice disease, the prothrombin remains prolonged
-​ Hepatic jaundice even after administration of vitamin K.
-​ Obstructive jaundice
Tests Related to Protein Metabolism
●​ In hemolytic jaundice, unconjugated bilirubin
is increased. Hence, Van den Bergh test is Serum estimation of proteins
indirect positive.
The liver is the principal site of metabolism and
●​ In obstructive jaundice, conjugated bilirubin synthesis of plasma proteins and amino acids. Amino
is elevated and Van den Bergh test is direct acids are metabolized in the liver to ammonia and
positive. urea. Based on these metabolic functions of the liver,
serum estimation of proteins, and ammonia
(discussed earlier) are employed to assess the liver ●​ The normal range for these enzymes is as
cell damage. follows:

Liver cells contain several enzymes. In liver damage, -​ AST or SGOT = 4-17 IU/L
these enzymes are released into blood and levels of -​ ALT or SGPT = 3-15 IU/L
these enzymes increase in blood.
●​ Although, both AST and ALT are commonly
●​ A large number of different enzymes have thought of as liver enzymes because of their
been used in the diagnosis of liver disease. high concentrations in liver, only ALT is
But most commonly and routinely employed markedly specific for liver since AST is
in laboratory are (Table 25.2): widely present in myocardium, skeletal
muscle, brain and kidney and may rise in
-​ Serum aspartate transaminase deute necrosis of these organs besides
(AST) liver cell injury.
-​ Serum alanine transaminase (ALT)
-​ Serum alkaline phosphatase (ALP). RENAL FUNCTION TESTS

●​ Other enzymes which have been found to be Kidney performs following important functions. The
useful but not routinely done in the functional unit in the kidney is the nephron. The
laboratory are: component parts of the nephron are given in Figure
25.1.
-​ Serum 5.-nucleotidase
-​ Lactate dehydrogenase ●​ The chief function of kidney is excretion of
-​ Isocitrate dehydrogenase water and metabolic wastes in urine.
-​ y-Glutamyl transferase.
●​ The glomerular filtration and renal tubular
reabsorption are the two major functions of
kidney that are involved in the formation of
Table 25.2: Enzyme assays in differential diagnosis
of jaundice urine.

Enzyme Hemolytic Hepatic Obstructiv ●​ In order to assess kidney function several

assays or jaundice e or kidney. function tests (renal function tests)
prehepatic Posthepati are performed.
jaundice c jaundice

ALT or Usually Marked Increased

AST normal increase

ALP Normal Increased Marked

slightly increase

Serum Transaminases

●​ Liver is the richest source of:

-​ Aspartate transaminase (AST)

which is previously called serum
glutamate oxaloacetate
transaminase (SGOT)
Urine Analysis
-​ Alanine transaminase (ALT) which
is previously called serum
Routine urine examination is usually the first test
glutamate pyruvate transaminase
undertaken to assess the renal function and very
(SGPT)
often it gives some important information like
proteinuria, hematuria to do further renal -​ Hemoglobin and myoglobin in urine
investigation. Its analysis, therefore, is important in produce a brownish coloration.
evaluating kidney function. The standard urine
analysis includes: -​ Turbidity in a fresh sample may
indicate infection but also may be
1.​ Physical examination due to fat particles in an individual
2.​ Chemical examination with nephrotic syndrome.
3.​ Microscopic examination of urine
●​ Reddish coloration in hematuria is due to
Physical Examination renal stones, cancer, some injury or disease
of kidneys or urinary tract.
A. Physical examination includes:
Specific gravity and osmolality
a.​ The 24 hours urinary output (volume)
b.​ Appearance (color) ●​ The specific gravity indicates the
c.​ Specific gravity and osmolality concentrating ability of the kidney. It normally
d.​ pH varies from 1.016 to 1.025 with an average
e.​ Odor 1.020. It can vary widely depending on diet,
fluid intake and renal function. If renal
Volume function is impaired, the quantity of
eliminated urine will be very less. In this
The daily output of urine in adults is 800 to 2,500 mL condition increased specific gravity may be
with an average of 1,500 mL/day. The quantity seen...
normally depends on the water intake, the external
temperature, the diet and the mental and physical ●​ The urine osmolality of normal individuals
state, cardiovascular and renal function. varies widely depending on the state of
hydration, After excessive intake of fluids,
Polyuria: Volume more than 2,500 mL/day occur in: the osmotic concentration may fall as low as
50 mOsm/kg, whereas with restricted fluid
●​ Diabetes mellitus, up to 5-6 L/day intake it is up to 1,200 mOsm/kg have been
observed. On average, fluid intakes 300 to
●​ Diabetes insipidus, 10-20 L/day 900 mOsm/kg are found.

●​ Later stages of chronic glomerulonephritis, pH

2-3 L/day. Oliguria: Volume 500 mL/day due
to: Fever, diarrhea, acute nephritis, early The urine is normally acidic in reaction with a pH of
stages of glomerulonephritis, cardiac failure. about 6.0 (range 5.5 to 7.5). Alkaline urine is found in
urinary tract infection.
●​ Anuria: Complete cessation of urine occurs
in: Acute tubular necrosis, bilateral renal Odor
stones, surgical shock.
Fresh urine is normally aromatic. Foul smell indicates
Appearance (color) bacterial infection.

Normal urine is transparent pale yellow or amber

color.
Glucose
Variation in color may be physiological or pathological.
Normal urine contains small amounts of glucose
●​ Darkening from the normal pale yellow color which cannot be detected by routine test. Excretion of
indicating more concentrated urine or detectable amounts of reducing sugar in urine is
presence of another pigment. called glycosuria. It may be benign or pathological
(Refer glycosuria).
Protein ●​ Serum urea and creatinine are markers of
renal function. Both these substances are
Increased amount of protein in urine, ie. proteinuria primarily excreted in the urine. Deterioration
can be caused by: of renal function is, therefore, associated
with increases in the serum levels of these
●​ Increased glomerular permeability substances.
●​ Reduced tubular reabsorption
●​ Creatinine is considered a better marker of
Most common type of proteinuria is due to albumin. renal function than urea because urea is
affected by dietary protein intake and liver
Blood function.

Presence of blood in urine is called hematuria and is ●​ An impaired glomerular filtration results in
commonly seen due to some injury or disease of retention of urea and creatinine, which
kidneys or urinary tract. It may be found in renal causes in elevation of blood urea (normal
stones, cancer, tuberculosis, trauma of kidney or range 20-40 mg/dl.) and creatinine (normal
acute glomerulonephritis. range 0.5-1.5 mg/dL). An increase of these
end products in the blood is called azotemia.
Ketone bodies
Microalbuminuria is the earliest sign of renal damage
Detectable levels in urine (ketonuria) are seen in due to diabetes mellitus and hypertension.
condi- tions characterized by increased ketogenesis
e.g. diabetic ketoacidosis and starvation ketoacidosis. Red Blood Cells in Urine (Hematuria)

Bile salts and bile pigments Intact glomerulus does not allow the passage of RBC.
But with severe glomerular damage, RBC leakage
Presence of these in urine is associated with occurs. Thus, detection of microscopic hematuria or
obstruction of the biliary tract Gallstone or carcinoma RBC casts confirms glomerular damage and is an
of the head of pancreas obstructing the common bile earliest sign before the decrease in GFR.
duct.
THYROID FUNCTION TESTS
Microscopic Examination
The thyroid gland secrets the hormones: thyroxine
●​ Microscopic examination of the centrifuged (T4) and triiodothyronine (T3). Clinical conditions
urinary sediment is done to detect: associated with increased or decreased synthesis of
thyroid hormones (hyperthyroidism or
●​ Cells, e.g. RBC, WBC, pus cells hypothyroidism respectively) occur commonly.
Laboratory determinations of thyroid functions are
●​ Crystals, e.g. calcium phosphate, calcium useful in distinguishing patients with euthyroidism
oxalate, amorphous phosphates, etc. (having a normally functioning thyroid gland) from
those with hyperthyroidism or hypothyroidism. The
●​ Casts, e.g. hyaline casts, granular casts, red main thyroid function tests commonly done in clinical
blood casts, etc. practice are shown in Table 25.4. To understand the
thyroid function tests, it is necessary to understand
●​ Presence of crystals in the urine may be a the following basic concepts:
clue to the diagnosis of a specific type of
renal calculus. Various components are ●​ The function of the thyroid gland is to take
observed on microscopic examination of iodine from the circulating blood, combine it
urine in renal disease. with the amino acid tyrosine of thyroglobulin
and convert it to the thyroid hormones
Serum and Urine Markers of Renal Function thyroxine (T4) and triiodothyronine (T3).

Serum Creatinine and urea ●​ Hormone production by the thyroid gland is

tightly regulated through hypothalamic
 pituitary thyroid axis (HPTA) (Fig. 25.2). ●​ The response of the pituitary to TRH and
Thyroid hormones are released in response response of the thyroid to TSH.
to stimulation of the thyroid gland by the
pituitary hormone called thyroid stimulating Major Thyroid Function Tests
hormone (TSH). TSH in turn secreted in
response to stimulation of the pituitary gland Serum Thyroid Stimulating Hormone
by the hypothalamic, thyrotropin releasing
hormone (TRH). The measurement of plasma thyroid stimulating
hormone (TSH) in a basal blood sample provides the
●​ T3 and T4 (70-80%) are transported in single most sensitive, specific and reliable test of
plasma by a thyroid binding globulin thyroid status. Stimulation of the thyroid gland by the
(TBG), a plasma protein The remaining 20 to TSH, which is produced by the anterior pituitary
30% of T3, and T4, is transported by gland, will cause the release of stored thyroid
thyroxine binding prealbumin (TBPA) and hormones.
albumin.
●​ When T4, and T3, are too high, TSH
●​ Only a small amount of the hormone is free secretion decreases.
which is not bound to protein. However, it is
the free portion of the thyroid hormones that ●​ When T4, and T3, are too low, TSH secretion
is the true determinant of the thyroid status increases.
of the patient.
This measurement is used in the diagnosis of
●​ The evaluation of the thyroid status is not a primary hypothyroidism (thyroid gland failure).
simple procedure because it does not
depend solely on the measurement of Normal values of serum TSH:
circulating thyroid hormone. One or more of -​ 2 to 6 μU/mL
the following factors may be abnormal and
these have to be sorted out and evaluated.

●​ The concentration of TBG and its degree of

saturation with T3, and T4.

Table 25.4: Major thyroid function tests.

1.​ Serum thyroid stimulating hormone (TSH)

2.​ Serum free thyroxin (T4) and

triiodothyronine (T3)

3.​ Tests for autoimmune thyroid diseases

include tests for:

-​ Anti-TSH receptor antibodies

-​ Antithyroglobulin antibodies
-​ Antimicrosomal antibodies
Clinical interpretation
-​ Antithyroperoxidase antibodies.

●​ Increased levels are seen in primary

hypothyroidism due to absence of negative
●​ Concentration of free T3 and T4. feedback control on the pituitary (Fig. 25.2).

●​ The status of hypothalamus and anterior ●​ Decreased levels are associated with:
pituitary with their respective outputs of TRH
and TSH. -​ Primary hyperthyroidism
-​ Secondary (anterior pituitary failure)
hypothyroidism
 -​ Tertiary (hypothalamic failure) 3.​ HDL cholesterol
hypothyroidism 4.​ LDL cholesterol

Thyroid Autoantibodies Normal Values and Interpretation

Several types of antibody against thyroid tissue have ●​ The normal range for healthy young adults is
been detected in serum of patients with thyroid less than 200 mg/dL.
disease. Measuring these antibodies helps to
demonstrate the presence of the autoimmune ●​ It may be lower in children.
disorders. For example:
●​ The concentration increases with age.
●​ Graves' disease is commonly associated
with the presence of anti TSH receptor Increased concentration
antibodies.
●​ The total concentration is increased in:
●​ Hashimoto's thyroiditis is associated with the -​ Hypothyroidism
presence of anti-thyroid peroxidase -​ Uncontrolled diabetes mellitus
antibodies (Anti-TPO antibodies, previously -​ Nephrotic syndrome
called antimicrosomal antibodies). -​ Extrahepatic obstruction of the bile
ducts
●​ Thyroglobulin (Tg): It is made uniquely by -​ Various hyperlipidemias
the thyroid. Measurement of Ig is of
particular use in assessing the presence of ●​ Long time elevated cholesterol concentration
any remnant thyroid tissue after thyroid- (more than 240 mg/dl is a serious risk factor
ectomy performed for malignancy. for the develop- ment of coronary artery
Measurement of Tg is an important tool in disease.
assessment of patients with differentiated
thyroid malignancies. After successful thy- ●​ Lowering of plasma cholesterol
roidectomy for thyroid malignancy Tg concentration reduces the incidence of
concentration in blood will fall to coronary heart diseases.
undetectable levels. The reappearance of Tg
in blood is strongly suggestive of tumor ●​ National Cholesterol Education Program
recurrence. (NCEP) defined the levels of serum
cholesterol believed to be desirable,
Clinical Interpretation tolerable or a serious risk factor for
development of coronary artery disease. The
●​ Thyroid peroxidase (microsomal antigen) report classifies total cholesterol
and thyroglobulin antibodies are present in concentration (Table 25.5) which is
the serum of patients with immunological applicable to all individuals over 20 years
mediated thyroid disease, e.g. Hashimoto's age and sex.
thyroiditis and Graves' disease.
Decreased concentration
●​ They may also be found in a small proportion
of healthy individuals, the incidence being Hypocholesterolemia is usually present in:
higher in relations of patients with
hyperthyroidism. ●​ Hyperthyroidism
●​ Hepatocellular disease
LIPID PROFILE TESTS ●​ Certain genetic defects, e.g.
Lipid profile tests are used to estimate increased risk abetalipoproteinemia
of cardiovascular disease which includes
measurement of: Normal Values and Clinical Interpretation

1.​ Total serum cholesterol

2.​ Serum triglycerides
 ●​ The normal range of serum triglycerides is Normal Values and Clinical Significance of HDL
40-145 mg/dL. Mean values rise slowly with Cholesterol
age after the third decade.
●​ Serum level of HDL cholesterol for:
●​ Values below the normal range are of little
clinical significance. -​ Men is 30-60 mg/dL
-​ For women 40-80 mg/dL which is
●​ Elevated concentration is often found in 20 to 30% higher than men.
disturbances of lipid metabolism and in
atherosclerosis and coronary artery ●​ Studies have indicated that when the HDL
disease. The classification of triglyceride cholesterol value is lower than 45 mg/dL in
con- centration according to the NCEP is men and lower than 55 mg/dL in women
listed in Table 25.5. there is an increased risk for heart disease
and the relative risk increases with lower
●​ The serum triglyceride concentration is HDL cholesterol concentrations.
greatly elevated in hyperlipoproteinemia type
I and V and moderately increased in type II b ●​ Higher HDL cholesterol concentrations may
and III. be associated with decreased risk of
coronary disease.
●​ The cause of hyperlipoproteinemia is a
genetic origin but hypertriglyceridemia occur ●​ Thus, HDL cholesterol levels are inversely
commonly secondary to the following related to the risk of cardiovascular disease.
pathologic conditions:
●​ HDL cholesterol level above 60 mg/dl.
-​ Hypothyroidism indicates very low risk for coronary artery
-​ Nephrotic syndrome disease (CAD).
-​ Alcoholism
-​ Obstructive liver diseases. ●​ HDL below 35 mg/dL increases the risk of
-​ Acute pancreatitis CAD.
-​ Uncontrolled diabetes mellitus
-​ Glycogen storage disease (type 1) ●​ Decreased levels are associated with stress,
obesity, androgens, cigarette smoking and
Decreased concentration diseases like diabetes mellitus, augments
the risk of coronary artery disease. HDL
The plasma triglyceride concentration is low in the cholesterol is very low in genetic disorder,
rare disease, abetalipoproteinemia (absence of low Tangier disease.
density lipoproteins).
●​ The ratio of total cholesterol to HDL
HDL Cholesterol cholesterol gives a more accurate and
definite assessment of heart disease risk
Method for HDL-cholesterol estimation (Table 25.6).

Commercial kits are available for the HDL cholesterol LDL Cholesterol
determination.
●​ The value of LDL cholesterol may be
Principle calculated, if the concentrations of total and
HDL cholesterol and triglycerides are
LDL, VLDL and chylomicrons are precipitated by measured.
polyanions in the presence of magnesium ions to
leave HDL in solution. The cholesterol content of the Normal Values and Clinical Interpretation
supernatant fluid is then determined by an enzymatic
method. ●​ The LDL cholesterol in women is somewhat
lower than in men but increases after
menopause.
 ●​ The upper limit for CK-MB activity = 6 U/L.
●​ Low levels of LDL cholesterol lower the risk
Clinical Interpretation
●​ Values above 160 mg/dl. indicate high risk
Increased activity
●​ Values between 130-160 mg/dl, are in
borderline risk ●​ There is a rise in total CK activity following a
myocardial infarction. The degree of
●​ Values below 130 mg/dl, are safer side increase varies with the extent of the tissue
(Table 25.5). damage. CK is the first enzyme to appear in
serum in higher concentration after
●​ Thus, the risk of cardiovascular disease is myocardial infarction and is probably the first
correlated directly with a high concentration to return to normal levels if there is no further
of LDL cholesterol. coronary damage

●​ The highest correlations have been obtained ●​ The serum total CK activity may be
as a risk factor by the ratio of LDL increased in some cases of coronary
cholesterol to HDL cholesterol (Table 25.6). insufficiency without myocardial infarction.
So, the simultaneous determination of
CARDIAC MARKERS CK-MB isoenzyme and LDH1 isoenzyme
help to make the diagnosis.
After myocardial infarction, a number of intracellular
enzymes and proteins are released from the ●​ The CK-MB isoenzyme starts to increase
damaged cells. They have diagnostic importance and within 4 hours after an acute myocardial
are called cardiac markers. Cardiac markers are infarction (AMI) and reaches a maximum
useful in the detection of acute myocardial infarction within 24 hours
(AMI) or minor myocardial injury.
●​ CK-MB is a more sensitive and specific test
●​ The cardiac markers of major diagnostic for AMI than total CK.
interest includes, enzymes such as:
Clinical Interpretation
-​ Creatine kinase (CK)
-​ Lactate dehydrogenase (LD) ●​ For patients having an AMI, serum total LDH
-​ Serum aspartate aminotransferase values become elevated at 12 to 18 hours
(AST) or serum glutamate after onset of symptoms, peak at 48 to 72
transaminase (SGOT). hours and return to normal after 6 to 10 days
(Fig. 25.5).
●​ Non-enzyme proteins such as:
●​ The LDH1 increase over LDH2 in serum
-​ Myoglobin (Mb) after AMI (the so-called flipped pattern, in
-​ Cardiac troponin T and I (cTnT and which the LDH1/LDH2 ratio becomes greater
cTnI). than 1).

Creatine Kinase (CK) ●​ The combination of an elevated CK-MB and

a flipped LDH isoenzyme ratio in a patient
Creatine kinase has three isoenzymes (Refer Chapter suspected of having a myocardial infarct
6) CK-2 or CK-MB isoenzymes are specific for the makes the diagnosis certain. The
heart. combination never occurs in coronary
insufficiency without a myocardial infarction.
Reference Values
Serum Aspartate Aminotransferase (AST)/ Serum
●​ Normal values for total CK ranges from 10 to Glutamate Oxaloacetate Transaminase (SGOT)
100 U/L
AST is found practically in everytissue of the body,
including red blood cells. It is in particularly high ●​ Increase in serum myoglobin occurs after
concentration in cardiac muscle and liver, AMI.
intermediate in skeletal muscle and kidney.
●​ The major advantage offered by myoglobin
Reference Values as a serum marker for myocardial injury is
that it is released early from damaged cells.
The normal concentration of serum AST is 6 to 25 U/L

Clinical interpretation

●​ The serum activity of AST begins to rise

about 6 to 12 hours after myocardial
infarction and usually reaches its maximum
value in about 24 to 48 hours.

Cardiac Troponin

●​ The contractile proteins include the

regulatory protein troponin (See Chapter 33).

●​ Troponin is a complex of three protein

subunits:

●​ It usually returns to normal 4 to 6 days after -​ Troponin C (TnC, the calcium

the infarct. binding component)
-​ Troponin I (TnI, the inhibitory
●​ The increase in activity is not as great as for component)
CK, nor does it rises as early after the -​ Troponin T (TnT, tropomyosin
infarct. binding component).

●​ It is a much less specific indication of ●​ The troponin subunits exist in a number of

myocardial infarction than the rise in CK, isoforms. However, cardiac specific troponin
because so many other conditions, e.g. liver, T (cTnT) and troponin I (cTnI) forms are the
muscle or hemolytic disease, can cause a most useful cardiac markers of acute
rise in serum AST. Prolonged myocardial myocardial infarction.
ischemia, congestive heart failure is also
associated with an increased AST level. Clinical Interpretation

Myoglobin (Mb) The initial rise in cardiac troponins (cTnl and cTnT)
after myocardial infarction occurs at about the same
●​ Myoglobin is an oxygen binding protein of time as CK and CK-MB but this rise continues for
cardiac and skeletal muscle. longer than for most of the enzyme.

●​ Its low molecular weight probably accounts ●​ For patients having AMI serum cTnT and
for its early appearance in the circulation cTnI values become elevated above the
after muscle injury. normal level at 4 to 8 hours after the onset of
the symptoms.
●​ Secondly, cTnT and cTnI also can remain
elevated up to 5 to 10 days respectively,
after an AMI occurs.