HEMATOLOGY MIDTERM (ANEMIAS)

1. FOLATE AND B12 DEFIENCY

Background
Vitamins
Organic compounds that
act as metabolic catalysts
Two groups fat-soluble
and water-soluble
Folate and vitamin B12
Water-soluble vitamins
important in the
formation of red blood
cells, the nervous
system, and DNA

Vit B12(Cobalamin)
Meat and dairy products
Important coenzyme in 2
biochem reaction
isomerization of
methylmalonyl coenzyme
A (CoA) to succinyl CoA
transfer of a methyl
group from 5-methyl THF
to homocysteine
METABOLISM

vitamin
B12
Required
for DNA
synthesis and red cell
maturation
Two vitamins combine in
methionine synthase reaction
Methyl group is transferred to
homocysteine to make
methionine
Decrease in either leads to
increase in homocysteine level
MEGALOBLASTIC ANEMIA
Deficiency leads to change in
RBC shape
Megaloblastic anemia is a
subgroup of macrocytic anemias
Megaloblastic
erythropoiesis when
defect in DNA synthesis
and the cells are arrested
at the G2 phase
Becomes a buildup of
cells that do not
synthesize DNA so
nucleus develops at a
slower rate than the rest
of the cell
Cytoplasm continues to
grow due to RNA
synthesis
Cells become larger and
megaloblastic

FOLATE(B9)
General term used for any form
of Vit folic acid
Found in leafy green
vegetables, dried beans, liver
and beef

DURONIO, JORICA LYNN D. MLS 3-D

Transfer carbon units in the

form of methyl groups from
donors to receptors
PATHOPHYSIOLOGY
Folic acid and

Page 1

CAUSES OF DEFICIENCY
B12:
Ileal disease (TB,
lymphoma, postradiation, Crohns)
Fish tapeworm
(Diphyllobothrium latum)
infection

HEMATOLOGY MIDTERM (ANEMIAS)

Inadequate
intake(Vegans)
Folate:
Malnutrition: Destroyed
by heat during cooking
Alcoholism (decreased in
2-4 days): impairs
enterohepatic cycle and
inhibits absorption
Increased requirement in
hemolytic anemia,
pregnancy, exfoliative
skin disease
Drugs

demyelination of white
matter of brain
Patient may present with
difficulty walking,
parasthesia, loss of
memory function, and a
positive Romberg test
Lab work
also shows an increase in
size of MCV
Subacute Combined Degeneration
- Degeneration and
demyelination of the dorsal
(posterior) and lateral spinal
columns

Effects on the Body: Folate

Main manifestations
glossitis
symptoms of anemia
(weakness, pallor, shortness of
breath)
GI problems (weight loss and
infertility)
Recommended intake of folate for
adults is 400 micrograms per day,
and for women of childbearing
age is 600 micrograms per day.

HYPERHOMOCYSTEINEMIA
Folate deficiency is number
one cause
Hyperhomocysteinemia is
less than 12 micromoles
per liter
Closely related to CVD
American Heart
Association reported that
47% of all patients with
CVD had
hyperhomocysteinemia

SPECIFIC DIAGNOSTIC TEST

Bone Marrow Exam
Reference confirmatory
test to identify the
megaloblastic
appearance of the
developing RBCs.
Folate,B12,MMA and
Homocysteine assay
Testing serum or plasma
levels using IA
TREATMENT
Distinguishing between the two
vitamin deficiencies

Effects on the Body: Vit. B12

Main manifestations
same as those for folate
but may be a more
serious presentation with
peripheral neuropathy,
degeneration of the
spinal cord, or
DURONIO, JORICA LYNN D. MLS 3-D

SCREENING TEST
Five tests are used to
screen for megaloblastic
anemia:
blood count (CBC)Hb
values <7-8% and
<20%Hct
reticulocyte count
Low retic. count
WBC manual
differential count
hypersegmented
neutrophils
serum bilirubinInc
levels
lactate
dehydrogenaseInc
levels

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HEMATOLOGY MIDTERM (ANEMIAS)

Treatment is to supply the

vitamin
Recommended intake of folate
for adults is 400 mg/day, and
for pregnant women of its 600
mg/day
Recommended intake of vitamin
B12 for adults is 2.4 mg/day,
pregnant women its 2.6 mg/day

2. PERNICIOUS ANEMIA
Background
Originally referred to all
megaloblastic anemias
Pernicious means:
Highly destructive
Injurious
Deadly
First described by Dr.
Thomas Addison

Gastric cells are destroyed

due to autoimmune disorder
No production of Intrinsic
Factors
Vitamin B12 cannot be
absorbed in the Ileum
Results in unbalanced cell
growth and impaired cell
division
SIGNS AND SYMPTOMS
Weight Loss
Tingling or other skin sensations
Tongue Soreness
Fatigue and General weakness
Skin pallor and jaundice (lemon
yellow skin)

CLASSIFICATION
Vitamin B12 deficiency
anemia Intrinsic Factor
deficiency anemia
Macrocytic anemia - due to
megaloblastic dyspoiesis
NEUROLOGIC MANIFESTATION
o Psychotic
o Peripheral neuropathy
o Posterior Spinal Column
Degeneration
o Pyramidal Tract sign

CAUSES
Primarily caused by lack of
intrinsic factors
Leads to Vit. B12 deficiency
Intrinsic factors are needed
for Vit. B12 absorption
Inadequate Diet
Loss of gastric mucosa
Functionally abnormal IF
Insufficient pancreatic
enzymes
Ileal dysfunction
Parasitic Infection
Medication

SCREENING TESTS
CBC
Reticulocyte count
WBC

manual differential count

Serum Bilirubin
Serum LDH

PATHOPHYSIOLOGY
DURONIO, JORICA LYNN D. MLS 3-D

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HEMATOLOGY MIDTERM (ANEMIAS)

OVERVIEW OF ANEMIA

CONFIRMATORY TESTS
Bone Marrow Smear
Reference Confirmatory Test
Serum Cobalamin Assay
Antibodies Assay
Gastric Analysis and Serum
Gastrin
Deoxyuridine Suppresion
Test
Stool Analysis for parasites
*Schilling Test

Antibodies found in serum of

patients with Pernicious Anemia
o Anti-parietal cell antibodies
reacts with gastric cells
o Anti-intrinsic factor
antibodies- can block or bind
with intrinsic factor or its
complex to inhibit absorption
o Thyroid antibodies
Schilling Test
Stage 1 oral plus IM Vitamin
B12
Stage 2 Vitamin B12 plus
Intrinsic Factor
Stage 3 Vitamin B12 and
antibiotics
Stage 4 Vitamin B12 and
pancreatic enzyme
3. NON-MEGALOBLASTIC

SIGNS AND SYMPTOMS

Difficulty concentrating
Dizziness
Fatigue
pale skin or pallor
shortness of breath
Dementia
Depression
loss of balance
numbness or tingling of arms or legs
Other signs and symptoms depending
on the disease ASSOCIATED
SCREENING TEST
RBC Count and MCV
RDW
Reticulocyte count
CONFIRMATORY TEST
Elisa assay vitamin b12 and folate
Examination of peripheral blood smear
and bone marrow smear
Assays for thyroid function
Other test: liver function
4. IRON DEFICIENCY ANEMIA
Most common type of anemia
Decrease in the number of RBCs
in the blood due to lack of iron
Amount of body iron is too low
to support normal red blood cell (RBC)
production.
*Your body needs iron to make a protein
called hemoglobin. This protein is
responsible for carrying oxygen to your
bodys tissues, which is essential for
your tissues and muscles to function
effectively. When there isnt enough iron
in your blood stream, the rest of your
body cant get the amount of oxygen it
needs.
CLASSIFICATION OF ANEMIA

MACROCYTIC ANEMIA
DURONIO, JORICA LYNN D. MLS 3-D

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HEMATOLOGY MIDTERM (ANEMIAS)

Morphological:
- microcytic anemia
- hypochromic anemia
**Hypochromic microcytic
anemias, characterized by the
presence in the circulating blood of
red cells that are smaller than normal
and poorly filled with hemoglobin, fall
into two main categories. The first is a
result of a deficiency of iron, and the
second is a result of impaired
production of hemoglobin; in either
case there is an inadequate amount of
the final product in the red cell.

Etiological:
Inadequate intake of iron
Increase need of body for iron
Impaired absorption
Chronic blood loss

CAUSES of IDA
Inadequate iron intake
Pregnancy
Blood loss due to menstrual
cycles
Internal bleeding
Inability to absorb iron

Whos at risk?
Menstruating Women
Pregnant women
Growing children
Vegetarians
Elderly individuals- who may
not eat a balanced diet, or due
to the loss of gastric acidity with
age
Soldiers -who are exposed to
prolonged maneuvers
Long distance runners - who
are prone in developing exercise
induced anemia called march
hemoglobinuria. It develops
when RBCs are hemolyzed by
foot pounding trauma and iron
is lost as Hb in urine

PATHOGENESIS
DURONIO, JORICA LYNN D. MLS 3-D

Page 5

IDA develops slowly,

progressing through stages that
physiologically blend into one
another but are useful
delineations for understanding
disease progression.
Distribution of Iron:
Storage
compartment
Transport
compartment
Functional
compartment
STAGE 1 IDA
prelatent or subclinical iron
deficiency
progressive loss of storage iron
No evidence of Iron deficiency
in the peripheral blood
No symptoms of anemia
Serum ferritin levels are low
Iron storage is inadequate but
Hb value remains normal
STAGE 2 IDA
Still subclinical (latent)
Exhaustion of the storage pool
of iron
Hb content of reticulocytes
begin to decrease
Serum iron and serum ferritin
levels decrease
TIBC and RDW increases
Transferrin recepetors increases
Hemoglobin levels are still
normal
STAGE 3 IDA
Frank anemia
Hb concentration and Hct are
low relative to reference
intervals
microcytic and hypochromic
RBCs
Serum ferritin levels are
exceedingly low
FEP and transferrin receptor
levels still increases

HEMATOLOGY MIDTERM (ANEMIAS)

Patient experiences symptoms

Signs and symptoms

PALLOR
FATIGUE
GLOSSITIS
Shortness of Breath
Koilonychia
Craving for pica (non food
items)
Angular Cheilosis
Laboratory Diagnosis
Screening tests:
CBC test
peripheral blood smear
- RDW greater than 15%
- Anisocytosis,
microcytosis,
hypochromia,
poiklocytosis (target cells
& elliptocytes)
- No consistent shape
changes to RBCs
decrease in Hb, MCV,
MCH, MCHC
- RBC count & Hct
decreases
Diagnostic test:
Iron studies remain the backbone
for diagnosis of iron deficiency
- Serum ferritin decreases
- Serum iron decreases
- TIBC increases
- transferrin saturation
decreases
( FEP increases)
Specialized tests:
Bone Marrow assessment
EARLY - the iron deficient bone
marrow appears hyperplastic with
a decrease M:E ratio as a result of
increased erythropoiesis
*The late nucleated red blood
cells show the characteristic shaggy
blue cytoplasm due to asynchrony in
maturation

DURONIO, JORICA LYNN D. MLS 3-D

Treatment
First therapy: treat underlying
contributing causes
Oral Supplements of Ferrous
sulfate
- 3 tablets/day containing 60
mg of Fe
should be taken on an
empty stomach to maximize
absorption
Impaired Absorption:
Parenteral administration of iron
dextrans
5. ANEMIA OF CHRONIC DISEASE
Definition
Also known as anemia of
inflammation
Refer to mild to moderately
severe anemias (Hb 7-12 g/dL)
a condition that can be
associated with many different
underlying disorders including
chronic illnesses
Cancer, certain
infections, and
autoimmune and
inflammatory diseases
such as rheumatoid
arthritis or lupus.
Characteristics

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HEMATOLOGY MIDTERM (ANEMIAS)

Inadequate erythrocyte
production
Low serum iron
Low binding capacity (i.e low
transferrin)
Erythrocytes usually are
normocytic and normochromic
Can be also be mildly
hypochromic and
microcytic

Epidemiology
Second most common form of
anemia
Individuals of any age who have
a chronic, inflammatory disease
can potentially develop the
condition
Exact incidence of ADC is
unknown
Its is believe to be
underreported or often goes
unrecognized
The prevalence of all types of
anemia in adults aged 65
years in the US is 10% to 11%.
One third of these cases
are believed to be anemic
due to chronic disorders,
including chronic renal
disease.
Etiology
Autoimmune
Rheumatoid arthritis
Systemic lupus
erythematosus and
connective tissue
diseases
Vasculititis
Sarcoidosis
Inflammatory bowel
disease
Systemic inflammatory
response syndrome
Chronic rejection after solidorgan transplantation
Chronic kidney disease and
inflammation

DURONIO, JORICA LYNN D. MLS 3-D

Acute phase reactants

Infections
Viral infections
Bacterial infections
Parasitic infections
Fungal infections
Cancer
Multiple myeloma and
lymphoma
Solid tumor including
carcinoma
Pathogenesis
Red cell destruction
Inadequate erythropoietin
secretion and resistance to
erythropoietin.
Erythropoiesis as a result of iron
deficiency
IL-6, hepcidin, hypoferremia
Serum iron concentrations are
dependent on iron release from
macrophages and hepatocytes
Inhibition of intestinal
absorption of iron
Signs and symptoms
Varies in severities from
person to person
Usually mild to moderate
anemia
Symptoms include:
fatigue, paleness of
the skin (pallor),
lightheadedness,
shortness of breath, a
fast heartbeat,
irritability, chest pain
In rare cases, it can be
severe and cause more
serious complications

Diagnosis
Based upon:
identification of characteristic
symptoms,
detailed patient history
thorough clinical evaluation and a
variety of specialized tests
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HEMATOLOGY MIDTERM (ANEMIAS)

Clinical tests:

Hemoglobin level

RBC count

Total iron binding

capacity

Serum ferritin level

Serum iron level

Transferrin saturation

Transferrin iron
saturation percentage

Treatment
Therapeutic administration of
erythropoietin
Iron must be administered
concurrently
Best course of treatment is
effective control or alleviation of
the underlying condition

6. Sideroblastic and Refractory

Anemia
- body has iron available but
cannot incorporate
- it into hemoglobin
- two common features:
- ring sideroblasts in the bone
marrow and impaired heme
biosynthesis
- Microcytic, Hypochromic
Congenital Sideroblastic Anemia
X-linked sideroblastic anemia
(XLSA)
caused by mutations of the
delta-aminolevulinic acid
synthase 2 gene (ALAS2)
occurs after the individual
reaches 20
Pyridoxine therapy / Folic acid
therapy

Refractory Anemia
- bone marrow erythrodysplasia,
and ring sideroblasts
- increase in the risk of
progression to overt acute
myeloid leukemia (AML), and
low survival rate
- average age of patients is 65-70
years.
- no sex predilection in RARS.
Exposure to agricultural
chemicals, history of smoking =
increased risk of the
development of RARS
- increased total body iron,
presence of ringed sideroblast
in the bone marrow, and
hypochromic anemia.

ACQUIRED SIDEROBLASTIC
ANEMIA
Due to :
excessive alcohol
pyridoxine deficiency
lead poisoning
copper deficiency
Excess zinc
DURONIO, JORICA LYNN D. MLS 3-D

Antimicrobials that may lead to

sideroblastic anemia
Isoniazid
Chloramphenicol
Cycloserine
linezolid.

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HEMATOLOGY MIDTERM (ANEMIAS)

Signs and Symptoms

skin paleness
fatigue
Dizziness
enlarged spleen and liver
in general, there is growth
retardation in children
hypothermia
there are lead line on teeth
margins
Incoordination
muscular weakness

Screening Test
Peripheral blood exam
- marked unequal cell size and
abnormal cell shape
- Pappenheimer bodies
- Basophilic stippling
- target cells
- Leukocytes and platelets are normal
Decreased MCV
Serum iron, percentage saturation and
ferritin increased
total iron-binding capacity of the cells
is normal to decreased.
Confirmatory Test
BONE MARROW BIOPSY
-presence of ringed sideroblasts
7. PORPHYRIA
O Greek word porphura = purple.
DURONIO, JORICA LYNN D. MLS 3-D

O a group of rare disorders caused

by deficiencies of enzymes of
the heme biosynthetic pathway
O abnormal accumulation of
porphyrins in the blood
also caused by lead poisoning
Excessive alcohol intake
O Cruelly referred to as a
Vampires disease.
O can be inherited or (rarely)
acquired
O With the exception of congenital
erythropoietic porphyria (CEP),
which is autosomal recessive,
all other porphyrias are
inherited as autosomal
dominant disorders
*Porphyrin precursors overproduced in
response to synthetic pathway
blockages, accumulate in the body
and cause diverse pathologic changes
thereby becoming the basis for
diagnostic test.
Other name:
O Hematoporphyria
O porphyrin disorder
Classification of Porphyria:
O By location of the excess
porphyrin production:
1. Erythropoietic
2. Hepatic
By location of the excess
porphyrin production:
1. erythropoietic
a) Congenial erythropoietic
porphyria (CEP)
b) Erythropoietic Protoporphyria
(EPP) or Gunthers disease
c) X-linked sideroblastic Anemia
class of porphyria
By location of the excess
porphyrin production:
2. Hepatic
a.Porphyria cutanea tarda
b. Hepatoerythropoietic
porphyria (HEP)
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HEMATOLOGY MIDTERM (ANEMIAS)

c. Variegate Porphyria (VP)
d. Hereditary Coproporphyria

be suggested in the family of a

person with porphyria.

(HCP)
8. Hemochromatosis &
Hemosiderosis

By clinical manifestations :
1. acute (neurovisceral
manifestations and no
cutaneous photosensitivity ),
2. cutaneous (photosensitivity )
3. mixed (photosensitivity +
neurovisceral manifestations )

Similarities:
Both are involved with abnormal
deposition of iron.
Both affects major organs of the
body

Signs and Symptoms

Seizures
Mental changes, such as
confusion, hallucinations,
disorientation or paranoia
Breathing problems
Muscle pain, tingling,
numbness, weakness or
paralysis
Red or brown urine

Screening and Confirmatory Test

Urine test
If you have a form of acute
porphyria, a urine test may
reveal elevated levels of two
substances: porphobilinogen
and delta-aminolevulinic acids,
as well as other porphyrins.
Stool sample test.
Analysis may reveal elevated
levels of some porphyrins that
may not be detected in urine
samples.
Blood test.
If you have a form of cutaneous
porphyria, a blood test may
show an elevation in the level of
porphyrins in your blood
plasma.
More tests may be needed to
confirm the type of porphyria
you have. Genetic testing may
DURONIO, JORICA LYNN D. MLS 3-D

Hemochromatosis
Background
A hereditary disorder of iron
absorption
HFE- the gene that
causes classic
hemochromatosis.
Discovered in California.
(1996)
These types of HH are called
type 1 (classical HFE gene
mutations.
Resulting in a cysteine-totyrosine substitution at amino
acid 282 (C282Y)
Or a histidine-to-aspartate
substitution at amino acid 63
(H63D)
Secondary hemochromatosis
- is associated with increased
intake and accumulation of
iron of known cause, such as
alcoholic cirrhosis, multiple
blood transfusions,
refractory anemia, and
chronic excess oral iron
ingestion.
Pathogenesis
- Hemochromatosis causes
the body to absorb too much
iron.
Normal:
the body accumulates adequate
iron.
The body reduces absorption to
avoid excessive accumulations

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HEMATOLOGY MIDTERM (ANEMIAS)

Hemochromatosis:
Mechanism for iron absorption
is faulty
Body ends up absorbing too
much iron.

Note: hemochromatosis is
difficult to diagnose because
the symptoms are common to
other diseases
Serum Iron (SI)
Serum Ferritin
Total Iron Binding capacity

30% of Americans have one or

two copies of mutated HFE
gene.
hemochromatosis- mostly seen
in caucasians.
- but can also develop in blacks who
are homozygous for C282Y.
Iron overload builds slowly
- usually taking 25-30 years before the
symptoms appear.
-but organ damage is present before
symptoms.
-more often seen in males in mid/late
fifties.
-Men are affected 10 to 20 times more
often than women.
-can be present in females who dont
menstruate.
Signs and symptoms
Chronic fatigue
Joint pain
- Are first and most common
symptoms of
hemochromatosis.
4 main features:
Cirrhosis of the
liver
b.
Diabetes Mellitus
c.
Skin pigmentation
d.
Heart failure
a.

Later signs and symptoms

include:
o Irregular heart rhythm
o Osteoarthritis and osteoporosis
o Loss of period
o Depression
o Hair loss
o Skin surface changes: blisters
Tests:
DURONIO, JORICA LYNN D. MLS 3-D

*If hemochromatosis is suspected:

Blood test to measure:
transferrin saturation
transferrin saturations of more
than 50% suggest iron overload.
Gene testing is used to confirm
a diagnosis of
hemochromatosis.
2 kinds of gene testing;
Cheek test- mascara like wand
to scrape cheek cells
Whole blood test- collection of
whole blood
Both are about 85% accurate.
Liver biopsy- to confirm
diagnosis
-correlation of serum ferritin
levels to organ disease
Hemosiderosis
- Hemosiderosis (AmE) or
haemosiderosis (BrE)
- is a form of iron overload
disorder
- resulting in the accumulation of
hemosiderin.
- Condition was first described as
Brown lung induration
- By Rudolf Virchow (1864)
- Wilhelm Ceelen
- Correlated his findings to the
clinical symptoms of 2 children
who died of IPH (1931)
- Jan Waldenstrom- diagnosed
first living patient with
hemosiderosis (1944).
- It has been given several names
including:
Haemosiderin accumulation
Pulmonary haemosiderosis

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HEMATOLOGY MIDTERM (ANEMIAS)

Brown induration of lung
Essential brown induration of
lung
Ceelen-Gellerstedt syndrome
Etiology
Literally means an abnormal
accumulation of iron and is
directly related to hemolysis
and hemorrhage
Three kinds of hemosiderosis:
PH associated w/ antibody to
the basement membrane of
lung and kidney.
Ex. Goodpasture syndrome
PH associated with
hypersensitivity to protein in
cows milk. Ex. Heiner syndrome
Idiopathic pulmonary
hemosiderosis

Types include:
Transfusion hemosiderosis
Idiopathic pulmonary
hemosiderosis
Transfusional diabetes
Causes:
The follow list shows some of
the possible medical causes
of Hemosiderosis that are listed
by the Diseases Database:
Iron compounds
GRACILE syndrome
Ineffective erythropoiesis
Blood transfusion and
complications
Porphyria cutanea tarda type 1
(sporadic)
Beta thalassaemia
(heterozygous)
Ceruloplasmin deficiency
Atransferrinaemia, hereditary
Haemochromatosis
Haemoglobin E disease
Porphyria cutanea tarda type 2
(familial)
Beta thalassaemia (severe /
homozygous)

DURONIO, JORICA LYNN D. MLS 3-D

Signs and Symptoms

Long-standing severe
pulmonary hemosiderosis is
associated with the following:
Clubbing
Growth failure

Signs andbsymptoms usually oc

cur after
chronic blood loss or blood in th
e lungs.
Symptoms can include:
coughing, difficulty in
breathing, and wheezing,
resembling pneumonia.
After an acute episode of
pulmonary hemorrhage, the
physical examination may
reveal the following:
Tachypnea
Dyspnea (use of
accessory muscles,
retractions, flaring)
Pallor
Tachycardia
Cyanosis
Crackles
Wheezing
Fever
Pathogenesis
hemosiderosis can result form
hemorrhage within an organ.
Iron liberated from RBC
hemolysis is deposited within
that organ.
Significant hemosiderin deposits
may eventually develop.
hemosiderosis can result form
hemorrhage within an organ.
Iron liberated from RBC
hemolysis is deposited within
that organ.
Significant hemosiderin deposits
may eventually develop.
The lungs are usually affected.
And the cause usually is
recurrent pulmonary

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HEMATOLOGY MIDTERM (ANEMIAS)

hemorrhage, either idiopathic or

due to chronic pulmonary
hypertension.
Kidneys- another common site
of hemosiderin accumulation.
Where hemosiderosis can result
from extensive intravascular
hemolysis
(Intravascular
hemolysis results from the
rupture or lysis of RBC within
the circulation, i.e. the RBC are
lysing in vivo.)
Free Hb is filtered at the
glomerulus, resulting in
deposition of iron in the
kidneys.
The renal parenchyma is not
damaged, but sever
hemosiduria may result in iron
deficiency.

Tests:
CBC count
Stool guaiac test results Frequently positive

DURONIO, JORICA LYNN D. MLS 3-D

Page 13

Analysis of gastric lavages

Immunoglobulin E level - High
levels possible in Heiner
syndrome
Sputum analysis
Urinalysis - Hematuria and/or
proteinuria in pulmonary
hemosiderosis secondary to
immune-mediated
glomerulonephritis,
Goodpasture syndrome, and
SLE
Prothrombin time/activated
partial thromboplastin
von Willebrand factor antigen
and Ristocetin cofactor levels
IgA antiendomysial antibody
level - Facilitates the diagnosis
of celiac disease (However,
histologic examination of a
duodenal biopsy sample
remains the criterion standard.)