ALLERGY
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ALLERGY
 Common
 ≈ 20%
 Atopy is the tendency to produce an exaggerated IgE immune response to
otherwise harmless environmental substances
 Allergic disease is the clinical manifestation of this inappropriate IgE immune
response.
Factors influencing susceptibility to allergic diseases
1. unexplained
2. Environmental factors such as pollutants, cigarette smoke, and the incidence
of bacterial and viral infection Infections in early life bias the immune
system against the development of allergies.
3. A family history (the strongest factor).
PRESENTING PROBLEMS IN ALLERGY
A GENERAL APPROACH TO THE ALLERGIC PATIENT
Clinical assessment
 usually occurs within minutes of exposure to allergen
 Symptoms (angioedema, urticaria, wheezing etc).
 Ask about: Other allergic symptoms, Past and present, and about family
history of allergic disease. Identify potential allergens in the home and
workplace, and always take a detailed drug history, including compliance,
side-effects and the use of complementary therapies
Investigations
1.
Skin prick tests:

is the 'gold standard' of allergy testing

A droplet of diluted standardized allergen solution is placed on the
forearm, and the skin is superficially punctured through the droplet
with a sterile lancet.
 After 10 minutes, a positive response is indicated by a local weal
and flare response ≥ 2 mm larger than the negative control.

A major advantage of skin prick testing is that patients can clearly
see the results, which may be useful in gaining compliance with
avoidance measures.
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

Disadvantages include the remote risk of a severe allergic reaction, so
resuscitation facilities should be available.
Antihistamines inhibit the magnitude of the response and should be
discontinued for at least 2 days before testing; corticosteroids do not
influence test results
2. Specific IgE tests

An alternative to skin prick testing
 sensitivity and specificity of specific IgE tests is lower than skin prick
tests, but they may be very useful if skin testing is inappropriate
3. Supervised exposure to allergen (challenge test)
 Placebo-controlled allergen challenges
 usually performed in specialist centers
 Include bronchial provocation testing, nasal challenge and food
challenge
 May be useful in the investigation of occupational asthma or food
allergy.
4. Mast cell tryptase

Serum levels peak at 1-2 hours, remaining elevated for 24 hours.

useful in investigating a possible anaphylactic event
 Acute samples should be accompanied by a convalescent sample to
assist interpretation.
5. Non-specific markers of atopic disease: total serum IgE and
eosinophilia
 Peripheral blood eosinophilia is common in atopic individuals
 eosinophilia greater than 20% or an absolute eosinophil count
greater than 1.5 × 109/l should initiate a search for a non-atopic
cause
 ↑total IgE:
 Atopy is the most common cause
 parasite and helminth infections
 lymphomas
 Churg-Strauss vasculitis
 Significant allergic disease can occur despite a normal total IgE
level. Thus total IgE quantitation is not indicated in the routine
investigation of allergic disease.
ALLERGY
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Management
1. Avoidance of the allergen, and the advice of specialist dietitians and
occupational physicians may be required
2. Antihistamines
3. Corticosteroids
4. Sodium cromoglicate: inhaled prophylactically, it is partially effective
in preventing acute asthma and allergic rhinitis but has no effect if given
after allergen exposure. It is poorly absorbed and therefore ineffective in
the management of food allergies
5. Antigen-specific immunotherapy: sequential administration of
escalating amounts of dilute allergen over a prolonged period of time
carries a risk of iatrogenic anaphylaxis and should only be performed in
specialized centres.
6. Omalizumab, a monoclonal antibody against IgE, inhibits the binding of
IgE to mast cells and basophils. It is effective in moderate and severe
allergic asthma and rhinitis, and may also have a role in the management
of severe peanut allergy.
7. Preloaded self-injectable adrenaline (epinephrine) may be life-saving
in the acute management of anaphylaxis.
ANAPHYLAXIS
 Is an acute medical emergency.
 A potentially life-threatening, systemic allergic reaction.
 Caused by the release of histamine and other vasoactive mediators.
Clinical assessment
 Assess: severity, the time between allergen exposure and onset of
symptoms, potential triggers, if not immediately obvious, a detailed history
of the previous 24 hours may be helpful.
 The most common allergens are foods, latex, insect venom and drugs
 A history of previous local allergic responses to the offending agent is
common
 if an allergen is inhaled, the major symptom is frequently wheezing.
Features of anaphylaxis may overlap with the direct toxic effects of drugs
and venoms
ALLERGY
 C/F:
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ALLERGY
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Investigations
1. Measurement of acute and convalescent serum mast cell tryptase
concentrations may be useful to confirm the diagnosis
2. Specific IgE tests may be preferable to skin prick tests when
investigating patients with a history of anaphylaxis.
Management
The immediate management includes: ABCDT
1. A:Airways: ensuring airway patency
2. B:Breathing: administration of oxygen
3. C:Circulation: restoration of blood pressure (laying the patient flat,
intravenous fluids)
4. D: Diagnosis: anaphylaxis & risk factors
5. T: Treatment:
 Adrenaline (epinephrine) reverses the action of histamine within
minutes. It should be given intramuscularly (adult dose, 0.3-1.0 ml
1:1000 solution) and repeated at 5-10 minute intervals if the initial
response is inadequate.
 This should be followed by intravenous antihistamines
(chlorphenamine 10-20 mg i.m. or slow i.v. injection), which
limit ongoing inflammation.
 Corticosteroids (hydrocortisone 100-300 mg) prevent late-phase
symptoms in severely affected patients.
 Supportive treatments including nebulised β2-agonists may also
be indicated.
 Identify the trigger factor, educate the patient regarding
avoidance and management of subsequent episodes, identify
whether specific treatment such as immunotherapy is indicated.
 If the trigger factor cannot be identified or cannot be avoided,
recurrence is common.
 Patients who have previously experienced an anaphylactic event
should be prescribed self-injectable adrenaline and they and their
families or carers should be instructed on its use.
 The use of a MedicAlert (or similar) bracelet will increase the
likelihood that adrenaline will be administered in an emergency.
 Referral to specialist assessment
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ANGIOEDEMA
 Is the episodic, localized, non-pitting swelling of submucous or
subcutaneous tissues
 May occur alone or in conjunction with urticaria
 Is most commonly the result of mast cell degranulation, which may be
spontaneous or triggered by an allergic IgE-mediated response.
 Other important causes include drug reactions (e.g. to ACE inhibitors) and
C1 inhibitor deficiency.
Clinical assessment
 Localized soft tissue edema, most frequently affecting the face, extremities
and genitalia.
 Involvement of the larynx or tongue may cause life-threatening respiratory
tract obstruction,
 Edema of the intestine may cause abdominal pain and distension.
 usually accompanied by urticaria, and patients frequently have a history of
other allergic symptoms
Etiology:
1.
2.
3.
4.
IgE-mediated.
Specific trigger such as food, animal dander or insect venom.
Physical stimuli as: heat, cold or vigorous exercise.
Drug-induced angioedema is common: most frequently associated with ACE
inhibitors, aspirin and non-steroidal anti-inflammatory agents (both topical
and systemic), radiocontrast media, opiates and antibiotics
5. Hereditary angioedema.
Investigations
1. skin prick tests or specific IgE tests may be useful
2. Exclude underlying conditions that may precipitate idiopathic angioedema
in susceptible individuals, such as hypothyroidism and underlying infection:
a full blood count, thyroid function, CRP and liver function tests
3. Angioedema without urticaria may indicate hereditary or acquired C1
inhibitor deficiency, and complement studies including C3, C4 and C1
inhibitor levels should be performed.
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Management
1. Oral antihistamines are the mainstay of treatment of allergic or idiopathic
angioedema, and may be used prophylactically or after the onset of
symptoms. They are ineffective in hereditary angioedema and ACE
inhibitor-associated angioedema.
2. Patients should be advised to seek urgent medical attention if they
experience tongue or throat swelling, as this may cause fatal airway
obstruction
SPECIFIC ALLERGIES
1.INSECT VENOM ALLERGY
 Local reactions to insect stings may cause extensive swelling around the site
lasting as long as 7 days.
 usually do not require specific treatment
 Generalized reactions vary from mild to life-threatening
 Toxic reactions to venom after multiple (50-100) simultaneous stings may
mimic anaphylaxis.
 exposure to large amounts of insect venom frequently stimulates the
production of IgE antibodies, and thus may be followed by allergic
reactions to single stings
 Antigen-specific immunotherapy with bee or wasp venom reduces the
incidence of recurrent anaphylaxis from 50-60% to 10% after 2 years of
treatment
 Immunotherapy is effective for treatment of allergic rhinitis, allergic asthma
and stinging insect hypersensitivity. Clinical studies to date do not support
the use of allergen immunotherapy for food hypersensitivity, chronic
urticaria and/or angioedema.
2.PEANUT ALLERGY

is the most common food-related allergy
 More than 50% of patients present before the age of 3 years, and some
individuals react to their first known exposure to peanuts, possibly because
of sensitization by topical creams

life-long avoidance is recommended
3.BIRCH ORAL ALLERGY SYNDROME
 Characterized by birch pollen hay fever, and local angioedema after contact
with fresh fruit (especially apples), vegetables and nuts.
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 Cooked fruits and vegetables are tolerated without difficulty
 It is due to shared or cross-reactive allergens which are destroyed by
cooking or digestion

Confirmed by skin prick testing using fresh fruit.
 Severe allergic reactions are unusual.
4.HEREDITARY ANGIOEDEMA (inherited C1 inhibitor deficiency)
 Autosomal dominant disorder
 Caused by decreased production of C1 inhibitor protein
 Spontaneous or triggered by local trauma or infection
 Face, extremities, upper airway and gastrointestinal tract edema.
 The most important complication is laryngeal obstruction, often associated
with minor dental procedures, which may be fatal.
 Episodes of angioedema are self-limiting and usually resolve within 48
hours.
 Present in childhood or adolescence, but may go undiagnosed for many
years.
 A family history can be identified in 80% of cases.
 Not associated with allergic diseases, and is specifically not associated with
urticaria.
 Acute episodes are always accompanied by low C4 levels
 Confirmed by C1 inhibitor measurement: the majority of patients have C1
inhibitor levels < 50% of normal. A minority of patients have a
dysfunctional protein, which can be assessed with functional assays.
 Prevention is with attenuated androgens (e.g. danazol) which increase
endogenous production of complement proteins
 Severe acute attacks should be treated with infusion of purified C1 inhibitor
preparations. Alternatively, fresh frozen plasma is a source of C1 inhibitor
and may be life-saving.
ALLERGY
5.Acquired C1 inhibitor deficiency
 Rare
 Presents in late adulthood. clinically indistinguishable from HAE
 Associated with autoimmune and lymphoproliferative diseases
 Treatment of the underlying
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