Download Allergic diseases

Allergic diseases
Oral manifestations
Hypersensitivity reactions
• The immune system is an integral part of
human protection against disease, but the
normally protective immune mechanisms
can sometimes cause detrimental
reactions in the host. Such reactions are
known as hypersensitivity reactions, and
the study of these is termed
immunopathology.
An allergen is a substance that triggers an allergic reaction
in people who are sensitive to that substance.
Types of hypersensitivity reactions:
•
•
•
•
•
•
•
•
Hypersensitivity reactions can be divided into four types ( by R. Coombs
and P. Gell) :
type I, type II, type III and type IV, based on the mechanisms involved and
time taken for the reaction.
Type V (Autoimmune disease, receptor mediated)- This is an additional type
that is sometimes (often in Britain) used as a distinction from Type 2.
Instead of binding to cell surface components, the antibodies recognize and
bind to the cell surface receptors, which either prevents the intended ligand
binding with the receptor or mimics the effects of the ligand, thus
impairing cell signaling.
Some clinical examples:
Graves' disease
Myasthenia gravis
The use of Type 5 is rare. These conditions are more frequently classified
as Type 2, though sometimes they are specifically segregated into its own
subcategory of Type 2.
TYPE I HYPERSENSITIVITY
• Type I hypersensitivity is also known as immediate
or anaphylactic hypersensitivity.
• The reaction may involve skin (urticaria and eczema),
eyes (conjunctivitis), nasopharynx (rhinorrhea, rhinitis),
bronchopulmonary tissues (asthma) and gastrointestinal
tract (gastroenteritis).
• The reaction may cause a range of symptoms from
minor inconvenience to death.
• The reaction usually takes 15 - 30 minutes from the time
of exposure to the antigen, although sometimes it may
have a delayed onset (10 - 12 hours).
•
Immediate hypersensitivity is mediated by IgE. The primary cellular component in this
hypersensitivity is the mast cell or basophil. The reaction is amplified and/or modified by
platelets, neutrophils and eosinophils. A biopsy of the reaction site demonstrates mainly mast
cells and eosinophils.
•
The mechanism of reaction involves preferential production of IgE, in response to certain
antigens (often called allergens). The precise mechanism as to why some individuals are
more prone to type-I hypersensitivity is not clear. However, it has been shown that such
individuals preferentially produce more of TH2 cells that secrete IL-4, IL-5 and IL-13 which in
turn favor IgE class switch. IgE has very high affinity for its receptor (Fcε; CD23) on mast cells
and basophils.
•
A subsequent exposure to the same allergen cross links the cell-bound IgE and triggers the
release of various pharmacologically active substances . Cross-linking of IgE Fc-receptor is
important in mast cell triggering. Mast cell degranulation is preceded by increased
Ca++ influx, which is a crucial process; ionophores which increase cytoplasmic Ca++also
promote degranulation, whereas, agents which deplete cytoplasmic
Ca++ suppress degranulation.
•
The agents released from mast cells and their effects are listed in Table 1. Mast cells may be
triggered by other stimuli such as exercise, emotional stress, chemicals (e.g., photographic
developing medium, calcium ionophores, codeine, etc.),anaphylotoxins (e.g., C4a, C3a,
C5a, etc.). These reactions, mediated by agents without IgE-allergen interaction, are not
hypersensitivity reactions, although they produce the same symptoms.
TYPE I HYPERSENSITIVITY
•
•
•
•
•
•
The reaction is amplified by PAF (platelet activation factor) which causes platelet
aggregation and release of histamine, heparin and vasoactive amines.
Eosinophil chemotactic factor of anaphylaxis (ECF-A) and neutrophil chemotactic
factors attract eosinophils and neutrophils, respectively, which release various
hydrolytic enzymes that cause necrosis.
Eosinophils may also control the local reaction by releasing arylsulphatase,
histaminase, phospholipase-D and prostaglandin-E, although this role of eosinophils
is now in question.
Cyclic nucleotides appear to play a significant role in the modulation of immediate
hypersensitivity reaction, although their exact function is ill understood.
Substances which alter cAMP and cGMP levels significantly alter the allergic
symptoms. Thus, substances that increase intracellular cAMP seem to relieve allergic
symptoms, particularly broncho-pulmonary ones, and are used therapeutically (Table
2).
Conversely, agents which decrease cAMP or stimulate cGMP aggravate these
allergic conditions.
TYPE I HYPERSENSITIVITY
•
•
•
Diagnostic tests for immediate
hypersensitivity include skin (prick and
intradermal) tests, measurement of
total IgE and specific IgE antibodies
against the suspected allergens.
Total IgE and specific IgE antibodies
are measured by a modification of
enzyme immunoassay (ELISA).
Increased IgE levels are indicative of
an atopic condition, although IgE may
be elevated in some non-atopic
diseases
(e.g., myelomas, helminthic infection,
etc.).
There appears to be a genetic
predisposition for atopic diseases and
there is evidence for HLA (A2)
association.
TYPE II HYPERSENSITIVITY
•
•
•
•
Type II hypersensitivity is also known
as cytotoxic hypersensitivity and may
affect a variety of organs and tissues.
The antigens are normally
endogenous, although exogenous
chemicals (haptens) which can attach
to cell membranes can also lead to
type II hypersensitivity. Drug-induced
hemolytic
anemia, granulocytopenia and thromb
ocytopenia are such examples.
The reaction time is minutes to hours.
Type II hypersensitivity is primarily
mediated by antibodies of the IgM or
IgG classes and complement.
Phagocytes and K cells may also play
a role.
TYPE II HYPERSENSITIVITY
• The lesion contains antibody, complement and
neutrophils. Diagnostic tests include detection of
circulating antibody against the tissues involved
and the presence of antibody and complement
in the lesion (biopsy) by immunofluorescence.
• The staining pattern is normally smooth and
linear, such as that seen
in Goodpasture's nephritis (renal and lung
basement membrane) and pemphigus (skin
intercellular protein, desmosome) .
TYPE III HYPERSENSITIVITY
• Type III hypersensitivity is also known as
immune complex hypersensitivity.
• The reaction may be general (e.g., serum
sickness) or may involve individual organs
including skin (e.g., systemic lupus
erythematosus, Arthus reaction), kidneys (e.g.,
lupus nephritis), lungs (e.g., aspergillosis), blood
vessels (e.g., polyarteritis), joints (e.g.,
rheumatoid arthritis) or other organs.
• This reaction may be the pathogenic mechanism
of diseases caused by many microorganisms.
TYPE III HYPERSENSITIVITY
• The reaction may take 3 - 10 hours after exposure to the antigen (as
in Arthus reaction). It is mediated by soluble immune complexes.
• They are mostly of the IgG class, although IgM may also be
involved. The antigen may be exogenous (chronic bacterial, viral or
parasitic infections), or endogenous (non-organ specific
autoimmunity: e.g., systemic lupus erythematosus, SLE).
• The antigen is soluble and not attached to the organ involved.
Primary components are soluble immune complexes and
complement (C3a, 4a and 5a).
• The damage is caused by platelets and neutrophils. The lesion
contains primarily neutrophils and deposits of immune complexes
and complement. Macrophages infiltrating in later stages may be
involved in the healing process.
TYPE III HYPERSENSITIVITY
TYPE III HYPERSENSITIVITY
• The affinity of antibody and size of immune complexes
are important in production of disease and determining
the tissue involved.
• Diagnosis involves examination of tissue biopsies for
deposits of immunoglobulin and complement by
immunofluorescence microscopy.
• The immunofluorescent staining in type III
hypersensitivity is granular (as opposed to linear in type
II such as seen in Goodpasture's syndrome).
• The presence of immune complexes in serum and
depletion in the level of complement are also diagnostic.
Polyethylene glycol-mediated turbidity (nephelometry)
binding of C1q and Raji cell test are utilized to detect
immune complexes.
TYPE IV HYPERSENSITIVITY
• Type IV hypersensitivity is also
known as cell mediated or
delayed type hypersensitivity.
• The classical example of this
hypersensitivity
is tuberculin (Montoux)
reaction which peaks 48 hours
after the injection of antigen
(PPD or old tuberculin).
• The lesion is characterized
by induration and erythema.
TYPE IV HYPERSENSITIVITY
• Type IV hypersensitivity is involved in the pathogenesis
of many autoimmune and infectious diseases
(tuberculosis, leprosy, blastomycosis, histoplasmosis,
toxoplasmosis, leishmaniasis, etc.) and granulomas due
to infections and foreign antigens.
• Another form of delayed hypersensitivity is contact
dermatitis (poison ivy, chemicals, heavy metals, etc.) in
which the lesions are more papular.
• Type IV hypersensitivity can be classified into three
categories depending on the time of onset and clinical
and histological presentation
TYPE IV HYPERSENSITIVITY
• Mechanisms of damage in delayed hypersensitivity include T
lymphocytes and monocytes and/or macrophages. Cytotoxic T cells
(Tc) cause direct damage whereas helper T (TH1) cells secrete
cytokines which activate cytotoxic T cells and recruit and activate
monocytes and macrophages, which cause the bulk of the damage.
The delayed hypersensitivity lesions mainly contain monocytes and
a few T cells.
• Major lymphokines involved in delayed hypersensitivity reaction
include monocyte chemotactic factor, interleukin-2, interferongamma, TNF alpha/beta, etc.
• Diagnostic tests in vivo include delayed cutaneous reaction
(e.g. Montoux test ) and patch test (for contact dermatitis). In vitro
tests for delayed hypersensitivity include mitogenic response,
lympho-cytotoxicity and IL-2 production.
Anaphylactic shock
•
•
•
•
•
•
•
•
•
Anaphylaxis is a severe, whole-body allergic reaction to a chemical that has become
an allergen. After being exposed to a substance such as bee sting venom, the
person's immune system becomes sensitized to it. On a later exposure to that
allergen, an allergic reaction may occur. This reaction happens quickly after the
exposure, is severe, and involves the whole body.
Tissues in different parts of the body release histamine and other substances. This
causes the airways to tighten and leads to other symptoms.
Some drugs (morphine, x-ray dye, and others) may cause an anaphylactic-like
reaction (anaphylactoid reaction) when people are first exposed to them. Aspirin may
also cause a reaction. These reactions are not the same as the immune system
response that occurs with "true" anaphylaxis. However, the symptoms, risk for
complications, and treatment are the same for both types of reactions.
Anaphylaxis can occur in response to any allergen. Common causes include:
Drug allergies
Food allergies
Insect bites/stings
Pollens and other inhaled allergens rarely cause anaphylaxis. Some people have an
anaphylactic reaction with no known cause.
Anaphylaxis is life-threatening and can occur at any time. Risks include a history of
any type of allergic reaction.
Symptoms
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Symptoms develop rapidly, often within seconds
or minutes. They may include the following:
Abdominal pain or cramping
Abnormal (high-pitched) breathing sounds
Anxiety
Confusion
Cough
Diarrhea
Difficulty breathing
Difficulty swallowing
Fainting, light-headedness, dizziness
Hives, itchiness
Nasal congestion
Nausea, vomiting
Palpitations
Skin redness
Slurred speech
Wheezing
Presentation
• There is often (but not always) a history of previous sensitivity to an
allergen, or recent history of exposure to a new drug (e.g.
vaccination). Initially, patients usually develop skin symptoms,
including generalised itching, urticaria and erythema, rhinitis,
conjunctivitis and angio-oedema.
Signs that the airway is becoming involved include itching of the
palate or external auditory meatus, dyspnoea, laryngeal
oedema (stridor) and wheezing (bronchospasm). General
symptoms include palpitations and tachycardia (as opposed
to bradycardia in simple vasovagal episode at immunisation time),
nausea, vomiting and abdominal pain, feeling faint - with a sense of
impending doom; and, ultimately, collapse and loss of
consciousness.
Airway swelling, stridor, breathing difficulty, wheeze, cyanosis,
hypotension, tachycardia and reduced capillary filling suggest
impending severe reaction.
Quick reference anaphylaxis algorithm
•
Rapid assessment:
– Airway: look for and relieve airway obstruction; call for help early if there are
signs of obstruction. Remove any traces of allergen remaining (e.g. nut
fragments caught in teeth, with a mouthwash; bee stings without compressing
any attached venom sacs).
– Breathing: look for and treat bronchospasm and signs of respiratory distress.
– Circulation: colour, pulse and BP.
– Disability: assess whether responding or unconscious.
– Exposure: assess skin with adequate exposure, but avoid excess heat loss.
•
Consider anaphylaxis when there is compatible history of rapid-onset severe allergictype reaction with respiratory difficulty and/or hypotension, especially if there are skin
changes present.
•
Give high-flow oxygen - using a mask with an oxygen reservoir (greater than 10
litres min-1 to prevent reservoir collapse).
•
Lie the patient flat:
– Raise the legs (care, as this may worsen any breathing problems).
– In pregnant patients, use a left lateral tilt of at least 15° (to avoid caval
compression).
Emergency
• Adrenaline (epinephrine) intramuscularly (IM) in the anterolateral
aspect of the middle third of the thigh (safe, easy, effective):
• Adult IM dose 0.5 mg IM (= 500 micrograms = 0.5 mL of 1:1000)
adrenaline (epinephrine).
• Child IM dose (the equivalent volume of 1:1000 adrenaline
(epinephrine) is shown in brackets):
– >12 years: 500 micrograms IM (0.5 mL), i.e. the same as the adult
dose.
300 micrograms (0.3 mL) if the child is small or prepubertal.
– >6-12 years: 300 micrograms IM (0.3 mL).
– <6 years: 150 micrograms IM (0.15 mL).
• Note: half doses of adrenaline (epinephrine) may be safer for
patients on amitriptyline, imipramine, monoamine oxidase inhibitor
(MAOI) or beta-blocker.
When skills and equipment are available:
• Establish airway (in anaphylaxis, airway obstruction from tissue
swelling is difficult to overcome and early expert intubation is often
needed).
• IV fluid challenge:
– Insert one or more large-bore IV cannulae (enable the highest flow).
– Use intraosseous access (if trained to do so) in children when IV access
is difficult.
– Give a rapid fluid challenge:
• Adults - 500 mL of warmed crystalloid solution (e.g., Hartmann's or 0.9%
saline) in 5-10 minutes if the patient is normotensive or one litre if the patient
is hypotensive.
• Use smaller volumes (e.g. 250 mL) for adult patients with known cardiac
failure and use closer monitoring (listen to the chest for crepitations after
each bolus).
• The use of invasive monitoring, e.g., central venous pressure (CVP), can
help to assess fluid resuscitation.
• For children - give 20 mL/kg of warmed crystalloid.
When skills and equipment are available:
• Chlorphenamine (after initial resuscitation). Dose depends on age:
–
–
–
–
>12 years and adults: 10 mg IM or IV slowly.
>6-12 years: 5 mg IM or IV slowly.
>6 months-6 years: 2.5 mg IM or IV slowly.
<6 months: 250 micrograms/kg IM or IV slowly.
• Hydrocortisone (after initial resuscitation). Dose depends on age:
–
–
–
–
>12 years and adults: 200 mg IM or IV slowly.
>6-12 years: 100 mg IM or IV slowly.
>6 months-6 years: 50 mg IM or IV slowly.
<6 months: 25 mg IM or IV slowly.
• Monitor:
– Pulse oximetry
– ECG
– BP
Antihistamines (after initial
resuscitation)
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Antihistamines are a second line treatment for an anaphylactic reaction. The
evidence to support their use is weak, but there are logical reasons for them.
55
Antihistamines (H1-antihistamine) may help counter histamine-mediated vasodilation
and bronchoconstriction. They may not help in reactions depending in part on other
mediators but they have the virtue of safety. Used alone, they are unlikely to be
lifesaving in a true anaphylactic reaction. Inject chlorphenamine slowly intravenously
or intramuscularly.
The dose of chlorphenamine depends on age:
>12 years and adults: 10 mg IM or IV slowly
>6 – 12 years: 5 mg IM or IV slowly
>6 months – 6 years: 2.5 mg IM or IV slowly
<6 months: 250 micrograms/kg IM or IV slowly
There is little evidence to support the routine use of an H2-antihistamine (e.g.,
ranitidine, cimetidine) for the initial treatment of an anaphylactic reaction.
Steroids (give after initial
resuscitation)
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Corticosteroids may help prevent or shorten protracted reactions. In asthma, early
corticosteroid treatment is beneficial in adults and children.
57 58
There is little
evidence on which to base the optimum dose of hydrocortisone in anaphylaxis. In
hospital patients with asthma, higher doses of hydrocortisone do not seem to be
better than smaller doses.
59
Inject hydrocortisone slowly intravenously or intramuscularly, taking care to avoid
inducing further hypotension.
The dose of hydrocortisone for adults and children depends on age:
>12 years and adults: 200 mg IM or IV slowly
>6 – 12 years: 100 mg IM or IV slowly
>6 months – 6 years: 50 mg IM or IV slowly
<6 months: 25 mg IM or IV slowly
Quincke's edema
• Angioedema or Quin
cke's edema is the
rapid swelling
(edema) of
the dermis, subcutane
ous tissue,mucosa
and submucosal
tissues.
Symptoms
• The skin of the face, normally around the mouth, and the
mucosa of the mouth and/or throat, as well as
the tongue, swell up over the period of minutes to
several hours.
• The swelling can also occur elsewhere, typically in the
hands. The swelling can be itchy or painful.
• There may also be slightly decreased sensation in the
affected areas due to compression of the nerves.
• Urticaria(hives) may develop simultaneously.
• In severe cases, stridor of the airway occurs, with
gasping or wheezy inspiratory breath sounds and
decreasing oxygen levels.
Causative factors
•
•
•
•
•
•
•
•
Food related products for Quincke's
edema associated with urticaria.
Drugs like penicillin, aspirin, phenytoin
and others,
Infection- bacterial and viral
Venoms, medication and food can
induce anaphylaxis in sensitized
individuals.
Hereditary angio-oedema is an
autosomal-dominant disorder
associated with recurrent episodes of
edema of the subcutaneous tissue
without.
Onset is usually in early childhoodbut
may be delayed even into late adult
life.
Treatment
• Angioneurotic odema is a medical emergency, it
always better to seek the medical help
immediately
• To give airway support in case of medical
support
• Antihistamines
• Corticosteroids
• Adrenaline in acute condition
• C1 esterase inhibitors in case of hereditary
angioneurotic edema
Erythema multiforme
• Erythema multiforme
(EM) is an acute, selflimited, and sometimes
recurring skin condition
that is considered to be a
type IV hypersensitivity
reaction associated with
certain infections,
medications, and other
various triggers.
Symptoms
•
•
•
•
•
Fever
General ill feeling
Itching of the skin
Joint aches
Multiple skin lesions:
–
–
–
–
–
–
–
–
Start quickly and may return
May spread
May appear as a nodule, papule, or macule and may look like hives
Central sore surrounded by pale red rings, also called a "target", "iris",
or "bulls-eye"
May have vesicles and blisters of various sizes (bullae)
Located on the upper body, legs, arms, palms, hands, or feet
May involve the face or lips
Usually even on both sides (symmetrical)
Other symptoms that may occur
with this disease:
• Bloodshot eyes
• Dry eyes
• Eye burning, itching,
and discharge
• Eye pain
• Mouth sores
• Vision problems
Erythema multiforme
History:
• In EM, there may be no prodrome or a mild
upper respiratory tract infection.
• The rash starts abruptly, usually within 3 days. It
starts on the extremities, being symmetrical and
spreading centrally.
• Half of children with the rash have recent herpes
labialis.
• It usually precedes the erythema multiforme by 3
to 14 days but it can sometimes be present at
the onset.
Examination:
•
•
The iris or target lesion is the classical feature of the disease.
Initially there is a dull red flat spot or wheal that enlarges slightly up to 2 cm over 24
to 48 hours.
•
In the middle, a small bump, vesicle, or bulla develops, flattens, and then may clear.
The intermediate ring forms and becomes raised, pale, and swollen. The periphery
slowly becomes purple and forms a concentric lesion, resembling a target. Some
lesions are atypical targets with only 2 concentric rings.
The Koebner phenomenon may occur. This is where a lesion occurs along the line of
trauma and it is typical of psoriasis and lichen planus.
Lesions appear first on the extensor surfaces of the periphery and extend centrally.
The palms, neck and face are often involved but the soles and flexures of the
extremities less often.
There may be mucosal involvement in 70% of patients but it tends to be mild and
limited to just one mucosal surface (for example mouth or vulva).
Oral lesions are most common with lips, palate and gingiva affected. There may be
red conjunctivae and tearing, but eye involvement tends to be mild.
Genital involvement can produce painful hemorrhagic bullae and erosions.
•
•
•
•
•
Erythema multiforme
•
•
•
•
•
•
•
Investigations:
No specific investigations are
indicated.
Nikolsky's sign is positive
A punch biopsy may be required
to confirm diagnosis.
Management:
In recurrent disease due to HSV,
antiviral therapy is helpful.
Symptomatic treatment may
include analgesics, mouth wash
and local skin care.
Steroid creams may be used. If
the mouth is very sore, attention
may have to be given to hydration
and nutrition.
Lubricating drops for eyes may be
required.
Stevens–Johnson syndrome
• Stevens–Johnson syndrome (SJS)
and toxic epidermal
necrolysis (TEN) are two forms of a
life-threatening skin condition, in
which cell death causes
the epidermis to separate from
the dermis
• The syndrome is thought to be
a hypersensitivity complex that
affects the skin and the mucous
membranes. Although the majority of
cases are idiopathic (without a known
cause), the main class of known
causes is medication, followed by
infections and, rarely, cancers.
Symptoms
•
•
•
•
•
SJS usually begins with fever,
sore throat, and fatigue, which is
misdiagnosed and usually treated
with antibiotics.
Ulcers and other lesions begin to
appear in the mucous
membranes, almost always in the
mouth and lips but also in the
genital and anal regions.
Those in the mouth are usually
extremely painful and reduce the
patient's ability to eat or drink.
Conjunctivitis of the eyes occurs
in about 30% of children who
develop SJS.
A rash of round lesions about an
inch across arises on the face,
trunk, arms and legs, and soles of
the feet, but usually not the scalp.
Stevens-Johnson syndrome
Treatment:
•
•
•
•
•
•
SJS constitutes a dermatological emergency. All medications should be discontinued,
particularly those known to cause SJS reactions. Patients with
documented mycoplasma infections can be treated with oral macrolide or
oral doxycycline.
Initially, treatment is similar to that for patients with thermal burns, and continued care
can only be supportive (e.g. intravenous fluids and nasogastric or parenteral feeding)
and symptomatic (e.g.,analgesic mouth rinse for mouth ulcer).
Dermatologists and surgeons tend to disagree about whether the skin should
be debrided.
Beyond this kind of supportive care, there is no accepted treatment for SJS.
Treatment with corticosteroids is controversial.
Early retrospective studies suggested that corticosteroids increased hospital stays
and complication rates. There are no randomized trials of corticosteroids for SJS, and
it can be managed successfully without them.
Intravenous immunoglobulin (IVIG) treatment has shown some promise in reducing
the length of the reaction and improving symptoms. Other common supportive
measures include the use of topical pain anesthetics and antiseptics, maintaining a
warm environment, and intravenous analgesics. An ophthalmologist should be
consulted immediately, as SJS frequently causes the formation of scar tissue inside
the eyelids, leading to corneal vascularization, impaired vision and a host of other
ocular problems.
Skin Tests
• Scratch test (also known as
a puncture or prick
test). This test is done by
placing a drop of a solution
containing a possible allergen
on the skin, and a series of
scratches or needle pricks
allows the solution to enter the
skin. If the skin develops a red,
raised itchy area (called a
wheal), it usually means that
the person is allergic to that
allergen. This is called a
positive reaction.
Intradermal test.
•
•
•
•
Intradermal test. After examining
and cleaning the skin, a small
amount of the allergen is injected
just under the skin, similar to
a tuberculosis test.
During this test, a small amount
of the allergen solution is injected
into the skin.
An intradermal allergy test may be
done when a substance does not
cause a reaction in the skin prick
test but is still suspected as an
allergen for that person.
The intradermal test is more
sensitive than the skin prick test
but is more often positive in
people who do not have
symptoms to that allergen (falsepositive test results).
Patch test.
• Patch test.
• For a skin patch test,
the allergen solution
is placed on a pad
that is taped to the
skin for 24 to 72
hours.
• This test is used to
detect a skin allergy
called contact
dermatitis.
Allergy blood tests
• Allergy blood tests look for substances in the blood
called antibodies. Blood tests are not as sensitive as skin
tests but are often used for people who are not able to
have skin tests.
• The most common type of blood test used is the
enzyme-linked immunosorbent assay (ELISA, EIA). It
measures the blood level of a type of antibody (called
immunoglobulin E, or IgE) that the body may make in
response to certain allergens. IgE levels are often higher
in people who have allergies or asthma.
• Other lab testing methods, such as radioallergosorbent
testing (RAST) or an immunoassay capture test
(ImmunoCAP, UniCAP, or Pharmacia CAP), may be
used to provide more information.