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Allergic diseases


Allergic diseases Oral manifestations Hypersensitivity reactions The immune system is an integral part of human protection against ... For a skin patch test, ... – PowerPoint PPT presentation

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Title: 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
  • 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 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
  • 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

  • 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 (Fce CD23) on mast cells and
  • 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 Caalso 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.

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  • 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, phosphol
    ipase-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

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  • 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 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 thrombocytopenia 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.

  • 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
  • The staining pattern is normally smooth and
    linear, such as that seen in Goodpasture's nephrit
    is (renal and lung basement membrane)
    and pemphigus (skin intercellular
    protein, desmosome) . 

  • 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.

  • 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,
  • 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.

  • 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
  • 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

  • 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
  • The lesion is characterized by induration
    and erythema.

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  • 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
  • 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

  • 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,
    interferon-gamma, 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.

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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 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

  • 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

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
  • Exposure assess skin with adequate exposure, but
    avoid excess heat loss.
  • Consider anaphylaxis when there is compatible
    history of rapid-onset severe allergic-type
    reaction with respiratory difficulty and/or
    hypotension, especially if there are skin changes
  • 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).

  • 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 11000) adrenaline (epinephrine).
  • Child IM dose (the equivalent volume of 11000
    adrenaline (epinephrine) is shown in brackets)
  • gt12 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.
  • gt6-12 years 300 micrograms IM (0.3 mL).
  • lt6 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

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
  • 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
  • For children - give 20 mL/kg of warmed

When skills and equipment are available
  • Chlorphenamine (after initial resuscitation).
    Dose depends on age
  • gt12 years and adults 10 mg IM or IV slowly.
  • gt6-12 years 5 mg IM or IV slowly.
  • gt6 months-6 years 2.5 mg IM or IV slowly.
  • lt6 months 250 micrograms/kg IM or IV slowly.
  • Hydrocortisone (after initial resuscitation).
    Dose depends on age
  • gt12 years and adults 200 mg IM or IV slowly.
  • gt6-12 years 100 mg IM or IV slowly.
  • gt6 months-6 years 50 mg IM or IV slowly.
  • lt6 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
  • gt12 years and adults 10 mg IM or IV slowly
  • gt6 12 years 5 mg IM or IV slowly
  • gt6 months 6 years 2.5 mg IM or IV slowly
  • lt6 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
  • gt12 years and adults 200 mg IM or IV slowly
  • gt6 12 years 100 mg IM or IV slowly
  • gt6 months 6 years 50 mg IM or IV slowly
  • lt6 months 25 mg IM or IV slowly

Quincke's edema
  • Angioedema or Quincke's edema is the rapid
    swelling (edema) of the dermis, subcutaneous
    tissue,mucosa and submucosal tissues.

  • 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
  • There may also be slightly decreased sensation in
    the affected areas due to compression of the
  • 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
  • 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.

  • Angioneurotic odema is a medical emergency, it
    always better to seek the medical help
  • 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,
    self-limited, and sometimes recurring skin
    condition that is considered to be a type IV
    hypersensitivity reaction associated with certain
    infections, medications, and other various

  • 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
  • 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
  • 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
  • It usually precedes the erythema multiforme by 3
    to 14 days but it can sometimes be present at the

  • 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
  • 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
  • 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
  • InvestigationsNo specific investigations are
  • Nikolsky's sign is positive
  • A punch biopsy may be required to confirm
  • ManagementIn 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.

StevensJohnson syndrome
  • StevensJohnson 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 c
    omplex 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.

  • 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
  • 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
  • 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
    (false-positive 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