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Hematology Profile

The Heme Profile or CBC (Complete Blood Count) is a long-standing platform test of the
clinical laboratory. The test consists of two parts:
The Machine Panel: A battery of physical/chemical measurements conducted by a single
instrument that measures the size and important characteristics of each circulating blood cell.
Modern instruments are able to provide estimations of: WBC, RBC, Hemoglobin, Hematocrit,
MCV, MCH, MCHC, Polys & Stabs, Lymphocytes, Monocytes, Basophils, Morphology,
The Blood Smear: A thin smear of blood is applied on a glass slide, stained, and examined
under a microscope to record the appearance and nature of the cellular components. This part is
not required in all cases. Usually, the numerical parameters from the Machine panel can be used
to determine whether a smear should be done.
This is the basic test for all hematology investigations. It is also used for monitoring
hematological abnormalities or hematological responses to disease.
A brief description of each of the measured parameters:
WBC White Blood Count: A total count of the number of white cells per liter of blood.
Increased in inflammation and infection and in dyscrasias (such as leukemia).
Decreased: In various infections, bone marrow defects, drugs, etc. An examination of the
features described below will indicate which of the white cell types is causing the general
RBC Red Cell Count: A total count of the number of red cells per liter of blood. Increased in
overproduction states of the marrow (polycythemia, chronic oxygen deprivation). Decreased in
anemia. An examination of the red cell indices usually reveals the nature of the abnormality.
Hemoglobin: The total amount of hemoglobin in the blood (irrespective of the number of cells
containing the hemoglobin).
Hematocrit: The total volume of the red cells in the blood.
MCV Mean Corpuscular Volume is an indication of the size of the red cells.
MCH Mean Corpuscular Hemoglobin is a measure of the amount of hemoglobin per red blood
MCHC Mean Corpuscular Hemoglobin Concentration is the amount of hemoglobin per liter of
fluid in each cell.

Polys & Stabs The polymorphonuclear leukocyte white cell line. Usually responds quickly to
stress and infection.
Lymphocytes The lymphocytes are the circulating immune response cells
Monocytes Phagocytic (engulfing) white cells
Basophils Phagocytic white cells
Platelets The small cells which are intimately involved in coagulation and clot formation.
Morphology This is performed using a microscope. The various types of cells are examined and
the nature of any abnormality is described. If significant, it will be reviewed by a hematologist
who will add possible causes of the abnormalities.
The lipid or fat content of the blood is known to be correlated with the risk of developing
cardiovascular disease. The main lipid of concern is cholesterol, which can be found in the
blood in several different forms. This is because cholesterol does not dissolve in the water of
which blood is composed. In order for it to be transported through the blood stream the body
attaches cholesterol molecules to protein and constructs a tiny particle. The combination of
cholesterol and protein is called a lipoprotein (literally a lipid protein). These tiny particles come
in various densities: some are very dense and will eventually sink to the bottom of a tube of
blood, others are lighter and will float to the top of a tube of blood (very much like cream floats
to the surface of milk). Thus, we have high, low, and very-low density lipoproteins and each of
these has a different influence on the body. When we measure the Total Cholesterol in the
blood we are actually measuring the combination of high, low, and very-low density lipoprotein.
Because each of these fractions means something different, it is important to know what the
amount of each.
The LDL-Cholesterol (Low Density Lipoprotein Cholesterol) (LDL-C) constitutes the largest
fraction of cholesterol in the blood. This is the bad cholesterol and the higher its value, the
greater is the risk of developing heart disease. This is the cholesterol that travels from the liver
(where the lipoprotein is assembled) to the tissues where it has an important metabolic role.
However, along the way, it can become trapped in the walls of blood vessels where it causes a

tiny lesion (called a plaque) and contributes to the process of narrowing the blood vessels, like
rust in a water pipe.
The HDL-Cholesterol (High Density Lipoprotein Cholesterol) (HDL-C) is a smaller fraction and
represents the good cholesterol. This is the cholesterol that travels out of tissues. Opposite to
LDL-C, the higher the value of HDL-C the lower the risk of cardiovascular disease.
The VLDL-Cholesterol (Very Low Density Lipoprotein Cholesterol) (VLDL-C) is cholesterol
that is wrapped up with the triglyceride fats in the blood stream. Triglycerides (TG) are oils
consisting of three fatty acid chains attached to a glycerol molecule. Triglycerides are greatly
elevated in diabetes when out of control, in liver disease, and in certain inherited disorders.
Triglycerides rise after meals, which is why a fasting period is required before measuring lipids.
Cholesterol found in VLDL is neutral in terms of atherosclerosis and is another reason why the
measurement of Total Cholesterol may be misleading.
How do you interpret the results?
There are various ways to interpret the results of these tests. You may read about cholesterol in
magazine or newspaper articles and be confused by the fact that the values are so much different
from what you have obtained in the lab. This is because much of the material you read is from
the USA and is expressed in conventional units rather than the SI units that most of the world
employs. To convert American units (mg/dL) into Canadian units (mmol/L) you must multiply
the American value by 0.026 .
The following links describe the interpretation of lipid results based on the most recent (2006)
Canadian clinical guidelines.
Over 2 million Canadians have diabetes. There are three main forms of this condition.
Type I: This occurs when the body fails to produce insulin. As insulin is required to control
(lower) the blood glucose by making it available for metabolism, a lack of insulin allows the
glucose to rise to uncontrolled levels. Ironically, though the blood has too much glucose, the

tissues do not have enough and they begin to metabolize fat in order to get energy. This results
in the production of ketones that may cause metabolic crises and even death. Insulin injections
are required for treatment.
Type II: Most people with diabetes have this form. This is the variety developed later in life that
was formerly called adult onset diabetes. In Type II the body can still produce insulin but it
either does not produce enough or the insulin it does produce is not used effectively. The result
is ineffective utilization of glucose that rises to elevated levels in the blood stream. It can often
be treated by diet and weight loss to reduce the demand for insulin, but treatment with insulin
may be required.
The third type of diabetes is a temporary situation that occurs in pregnancy known as gestational
diabetes. It is found in 2-4% of all pregnancies and poses a risk to the well being of the fetus. It
is standard practice to screen for the presence of this condition in all pregnancies during the first
or second trimesters.
The symptoms of diabetes vary. Some persons with Type II or gestational diabetes have no
symptoms at all but are still at risk from the long-term complications of the disorder. When the
symptoms become overt, the patient feels unwell, is very thirsty, excretes abnormally large
volumes of urine, experiences unexplained weight loss, and may suffer serious metabolic
The diagnosis of diabetes is confirmed with laboratory tests. Screening for diabetes is
recommended (at a minimum) every three years in individuals 40 years of age.
A patient with metabolic decompensation and unequivocal hyperglycemia may be diagnosed as
diabetic with a single glucose measurement. All other patients must have two venous plasma
glucose measurements. The diagnosis of diabetes can be made if one of the following sets of
criteria are met:

Symptoms of diabetes plus a random plasma glucose 11.1 mmol/L


Fasting plasma glucose 7.0 mmol/L


Plasma glucose 11.1 mmol/L in the 2-hour sample of the 75g oral glucose tolerance test

Refer to page S15 of the 2008 Canadian Diabetes Guidelines for more information on the
diagnosis of diabetes as well as the related conditions impaired fasting glucose and impaired
To diagnose gestational diabetes, all pregnant women should undergo a Gestational Diabetes
Screening Test between 24 and 28 weeks gestation unless they have multiple risk factors, in
which case the Screening Test should be performed during the first trimester. In the Screening
Test, the pregnant woman consumes a 50-gram glucose drink and the blood glucose level is
measured after one hour. The test may be performed at any time of the day and fasting is not
required. If the glucose level exceeds 7.7 mmol/L, then a Glucose Tolerance Test should be
carried out: however, a level greater than 10.3 mmol/L is diagnostic of gestational diabetes and
further testing is not required. Unless specified otherwise by the physician, this Tolerance Test
requires the patient to be fasting and consists of measurements of blood glucose before and then
1h, 2h and 3h following a 100-gram glucose drink. If two or more levels exceed their designated
targets, a diagnosis of Gestational Diabetes is made. A physician may elect to treat a patient as a
diabetic if the values get close to these limits.
Refer to page S168 of the 2008 Canadian Diabetes Guidelines for more information on the
diagnosis of gestational diabetes. Note that since the Glucose Tolerance Test is a 100-gram / 3h
procedure as per consensus of BC laboratory physicians (rather than 75-gram / 2h, as suggested
by the Canadian Diabetes Association), different target values apply: these may be found here.
Monitoring Diabetes
Once diabetes is diagnosed, therapy may be instituted. Most monitoring of insulin therapy is
carried out by the patient with a glucose meter. There are two additional tests that are
recommended for all Type I and Type II diabetics on a regular basis: glycated hemoglobin (in
blood) and microalbumin (in urine). Monitoring information specific to British Columbia may
be found at the BC Ministry of Health Services site.

Glycated Hemoglobin
The Glycated Hemoglobin test (also known as Hemoglobin A1c or Hb A1c) should be carried
out every three months. In this test, blood is drawn and analyzed for the amount of glucose that
has become attached to the hemoglobin molecule. Normally, not more than 6% of hemoglobin
molecules have glucose attached; diabetics will have higher percentages. The percentage is
related to the average blood glucose level and is therefore an indication of overall glucose
control. It should be noted that the percentage is reported not as a percentage but as a decimal
(e.g. 6% will be reported as 0.06). If the Glycated Hemoglobin result is too high, more stringent
insulin therapy is required. The Glycated Hemoglobin test should not be used for the diagnosis of
diabetes as there are no recognized standards for using it in this context.
The other monitoring test for diabetes complications is urinary microalbumin. Despite its name,
microalbumin is identical to the protein albumin present in blood: the micro prefix refers to
the fact that its levels in urine are about 1000-fold lower than those in blood. The lab measures
the amount of albumin in the urine sample and reports the result as a ratio to creatinine (a
substance excreted at a constant amount) to correct for the variable dilution of urine. If the
albumin-creatinine ratio exceeds 2.8 (females) or 2.0 (males), further testing may be carried out.
The presence of abnormally high levels of urinary microalbumin indicates that diabetes is
beginning to affect the kidney and therapy to prevent the rapid development of kidney problems
should be initiated.
Useful information about diabetes can also be obtained from the Canadian Diabetes
Association and the American Diabetes Association.
Hepatitis is a condition wherein the liver develops widespread inflammation. There are many
causes of the inflammation and so we have diseases such as:

alcoholic hepatitis (caused by alcohol abuse),

toxic hepatitis (caused by certain noxious materials such as carbon tetrachloride),

viral hepatitis (caused by one of several viruses that attack the liver), and

autoimmune hepatitis (of unknown cause, but due to the bodys own immune system
attacking the liver).

The characteristic laboratory finding in Hepatitis is an increase in the AST (Aspartate

Aminotransferase) and ALT (Alanine Aminotransferase) enzyme tests. If either of these tests is
increased significantly, some form of hepatitis is likely.
The various forms of viral hepatitis can be identified with specific tests. It sounds like alphabet
soup as there are Hepatitis A, B, C, D, and E.
Hepatitis A: Hepatitis A virus spreads via sewage contamination. It causes mild to moderately
severe liver infections but rarely results in permanent damage. Serious infections with Hepatitis
A are caused in persons already suffering from Hepatitis C, intravenous drug users, and male
homosexuals. There is now a vaccination for Hepatitis A. There are two tests for Hepatitis A.
The Hepatitis A IgM antibody test indicates whether the patient has had Hepatitis A in the past
few weeks to 6 months. The hepatitis A total antibody test tells whether someone has had
Hepatitis A at some time in the past. When positive, these tests indicate that the patient is
immune to further infection from Hepatitis A.
Hepatitis B: Hepatitis B virus is transmitted by direct contact with the blood or saliva of
someone infected with Hepatitis B. In the past, this condition was called serum hepatitis.
Hepatitis B is usually self-limiting (cures on its own), but is a moderately severe disorder causing
fever and exhaustion. It generally takes several weeks to months to recover. Up to 10% of cases
are more complicated and experience a very severe acute event, develop a chronic hepatitis, or
become disease carriers without actually being sick (although carriers are prone to developing
late complications such as cirrhosis or liver cancer). There is an effective vaccine for Hepatitis
B. There are a variety of tests for Hepatitis B that can determine infection, infectivity, and
immune response.
Hepatitis C: Hepatitis C has gained wide notoriety because of its transmission in tainted
blood. It is a chronic and often very serious disorder. The test for Hepatitis C does not turn
positive immediately and may take 6 to 8 weeks to do so.

Classification of RBC Morphologic Abnormalities

Roger S. Riley, M.D., Ph.D.
Department of Pathology
Medical College of Virginia
RBC Abnormality

Description of Cells

Associated Conditions

Normal erythrocytes

Round to slightly ovoid

Normal individuals.
biconcave disks,
approximately 7 m in
diameter. Less hemoglobin
in center of cell (zone of
pallor). Regular in size and

("Spur cells")

Spheroid RBCs with few

large spiny projections. 5-10
spicules, irregular spacing
and thickness (must be
differentiated from


Irregular RBC
Anti-RBC antibody, paraprotein.
Cold agglutinin disease,
resembling Chinese letters. autoimmune hemolytic anemia,

Basophilic stippling

Fine, medium, or coarse

blue granules uniformly
distributed throughout RBC.
Fine stippling polychromatophilia. Coarse
stippling - Impaired

Heavy metal poisoning (e.g. lead

and arsenic), hemoglobinopathies,
thalassemias, sideroblastic
anemias, pyrimidine-5nucleotidase deficiency

Bite cells

RBCs with peripheral single

or multiple arcuate defects.
Usually associated with
spherocytes and blister

Oxidant stress. Normal individuals

receiving large quantities of
aromatic drugs (or their
metabolites) containing amino,
nitro, or hydroxy groups. Individuals
with red-cell enzymopathies
involving the pentose phosphate

postsplenectomy, alcoholic
cirrhosis and hemolytic anemia,
microangiopathic hemolytic
anemia, autoimmune hemolytic
anemia, sideroblastic anemia,
thalassemia, severe burns, renal
disease, pyruvate kinase
deficiency, McLeod phenotype,
infantile pyknocytosis, postsplenectomy.

shunt (most notably G6PD

Blister cells

RBCs with vacuoles or

markedly thin areas at
periphery of membrane.

dehydrogenase (G-6-PD)
deficiency. Other oxidant stress.

("Target cells")

Thin, hyopochromatic cell.

Round area of central

Splenectomy, thalassemia,
hemoglobinopathies (hemoglobin
SS, SC, CC, EE, AE, sickle cellthalassemia), iron deficiency
anemia, liver disease,
postsplectomy, familial lecithincholesterol acyltransferase (LCAT)

("Tear drops")

Cell in shape of tear drop.

Usually accompanied by
microcytosis and

Myelophthisic anemia (particularly

myelofibrosis with myeloid
metaplasia), magaloblastic anemia,
b-thalassemia, anemia of renal
failure, tuberculosis, Heinz body
disease, hemolytic anemias,

("Sickle cells")

Irregular, curved cells with

pointed ends

Hb S hemoglobinopathies (sickle
cell anemia, hemoglobin SC
disease, hemoglobin S-betathalassemia, hemoglobin SD
disease, hemoglobin Memphis/S
disease), other
hemoglobinopathies (especially Hb
I, Hb CHarlem, HbCCapetown).

("Sea urchin cells,
crenated cells, burr

RBC with many tiny

spicules (10-30) evenly
distributed over cell

Post-splenectomy, uremia, hepatitis

of the newborn, malabsorption
states, after administration of
heparin, pyruvate kinase
deficiency, phosphoglycerare
kinase deficiency, uremia, HUS.


RBCs with elliptical or oval


Hereditary elliptocytosis,
thalassemia, sickle cell trait, Hb C
trait, cirrhosis, decreased
erythrocyte glutathione, glucose-6phosphate deficiency, iron
deficiency anemia, megaloblastic
anemia, myelophthisic anemia,
hereditary hemorrhagic

telangiectasia, mechanical trauma.

Howell-Jolly bodies

Small (1 mm), round,

Splenectomized patients,
dense, basophilic bodies in megaloblastic anema, severe
hemolytic processes,
hyposplenism, myelophthistic


Increased RBC hemoglobin Hereditary spherocytosis, immune

concentration (MCHC > 36 hemolytic anemias.
g/dL). Usually associated
with spherocytosis


Decreased RBC amount

Iron deficiency, other hypochromic
(MCH) and concentration
(MCHC). Expanded central
zone of pallor

("Horn cells")

Helmet forms


Large RBCs (> 8.5 mm,

Accelerated erythrocytosis.
MCV > 95 fL). Normal MCH Macrocytic anemia (B12 or folate
deficiency)(oval macrocytes)
Increased diameter, normal
MCV. Usually hypochromic Liver disease, postsplenectomy

"Thin" macrocyte

Mechanical damage to red blood

cells from fibrin deposits (DIC,
microangiopathic hemolytic
anemia, thrombotic
thrombocytopenic purpura),
prosthetic heart valves, severe
valvular stenosis, malignant
hypertension, or march
hemoglobinuria, normal newborns,
bleeding peptic ulcer, aplastic
anemia, pyruvate kinase deficiency,
vasculitis, glomerulonephritis, renal
graft rejection, severe burns, iron
deficiency, thalassemias,
myelofibrosis with myeloid
metaplasia, hypersplenism


Small RBCs (< 7.0 mm, < Iron deficiency, thalassemias,

80 fL). Normal or decreased anemia of chronic disease, lead
poisoning, sideroblastic anemia

Nucleated red blood

cells ("NRBCs")

Immature RBCs, basophilic Acute bleeding, severe hemolysis,

myelofibrosis, leukemia,
myelophthisis, asplenia.


Variation in RBC shape.

Many disorders.

Blue-gray coloration of
("Polychromatophilia") RBCS. Due to mixture of
RNA and hemoglobin.

Increased - Increased
erythropoietic activity. Decreased Hypoproliferative states.


Linear arrangement of
Increased fibrinogen,
globulins, or paraproteins
(compare with
autoagglutination, above).

Acute and chronic inflammatory

disorders, Waldenstroms
macroglobulinemia, multiple

("Fragmented cells")

Fragmented RBCs
Mechanical damage to red blood
(compare with keratocytes, cells from fibrin deposits (DIC,
microangiopathic hemolytic
anemia, thrombotic
thrombocytopenic purpura),
prosthetic heart valves, severe
valvular stenosis, malignant
hypertension, or march
hemoglobinuria, normal newborns,
bleeding peptic ulcer, aplastic
anemia, pyruvate kinase deficiency,
vasculitis, glomerulonephritis, renal
graft rejection, severe burns, iron
deficiency, thalassemias,
myelofibrosis with myeloid
metaplasia, hypersplenism


RBCs with spheroidal

shape. Usually dense, small
(< 6.5 mm) RBCS with
normal or decreased MCV,
and absent central pallor

Hereditary spherocytosis and

hemolytic anemias (isoimmune or
autoimmune), microangiopathic
hemolytic anemia, hypersplenism
and post-splenectomy,
myelofibrosis with myeloid
metaplasia, hemoglobinopathies,
malaria, liver disease, older
population of transfused cells,
artifact. Microspherocytes in severe
burns and hereditary

(Fish mouth cell")

Uniconcave RBC, slitlike

area of central pallor

Hereditary or acquired hemolysis.

Hereditary stomatocytosis,
alcoholic cirrhosis, acute
alcoholism, obstructive liver
disease, malignancy, severe
infection, treated acute leukemia,