At least one third of the population suffer with some form of allergy. According to the British Society for Allergy and Clinical Immunology (BSACI) 20% of children reported asthma symptoms in the last year, 18% had allergic rhinitis and 16% had eczema, while 6-8% of children and 4% of adults have one or more food allergies.1 These four conditions make up the bulk of allergic disorders seen in general practice.
In children who present with severe infantile eczema, 50% will have concomitant food allergies to cow’s milk, egg or peanuts when tested. They are then likely to develop wheezing or asthma in mid-childhood with a propensity as teenagers to develop hay fever and associated oral allergies to fruits. The BSACI report that one child in 70 now has a significant peanut allergy.1
Genuinely allergic individuals will usually have a clinical history suggestive of childhood eczema, asthma or rhinitis possibly together with infantile food allergies. More commonly there is an associated family history of parents or siblings having similar allergies – the so-called “atopic” family.
Developing allergies and asthma are closely linked to environmental factors such as childhood obesity, birth by caesarean section, a lack of older siblings, early antibiotic usage and a sterile indoor home environment.
Conditions commonly misattributed to allergy include irritable bowel syndrome, migraine headaches, arthralgia, psoriasis, chronic fatigue and non-specific viral exanthemata.
Presentations such as acute angioedema may not involve an allergic or immune response, but more likely be due to pro-inflammatory mediator release such as leukotrienes in aspirin or salicylate intolerance, bradykinin accumulation associated with ACE inhibitor use, or the depletion of complement C4 levels in hereditary angioedema.
Acute urticaria may be triggered by food or drug allergies, but is also very often related to a viral exanthema or hepatitis. Chronic urticaria is very unlikely to be triggered by an allergy, but rather due to an overproduction or enhanced release of histamine from tissue mast cells and basophils.
Before deciding which allergy test to perform, the GP needs to take a detailed allergy history. Start by asking the patient to record specific symptoms and causality to particular allergen exposure, links to household pets, specific foods, medication, seasonality, diurnal variation in symptoms and positive response to medications such as antihistamines, topical steroids and bronchodilators.
Typical allergic symptoms include localised or generalised itching, urticaria, rhinitis, wheezing, eczema, vomiting, diarrhoea and conjunctivitis.
Measuring specific IgE in the blood to a suspected allergen is very helpful in confirming an allergy, but the GP needs to put in plenty of “spade-work” so as to tease out and narrow down the list of culprit allergens. With over 400 possible specific IgE RAST tests available, and at a cost of £15 per allergen, you need to be selective.
Skin prick allergy testing is much cheaper if used in a larger practice for testing the common aero-allergens such as house dust mite, pet danders, pollens and mould spores. Results will be very useful in directing the management of respiratory allergies – identifying and eradicating the allergen will make medication more effective and reduce incidence of exacerbations.
When skin prick testing for a food allergy, the actual raw food can be pricked and simply transferred by pricking onto the skin (prick-prick test) which is more accurate than many commercial food test allergens.
Remember to always use a standardised lancet to prick through the droplet of allergen placed on the volar aspect of the forearm, and advise avoidance of antihistamine medication for three days before skin prick testing.
Allergy testing using RAST tests or skin prick testing is highly accurate in experienced hands, but interpretation by the unwary or inexperienced may result in confusion and misinterpretation. This is especially the case when a specific IgE blood test is only modestly raised or the skin reactivity minimal. Interpreting the test results must always be done in the clinical context and only after taking a thorough allergy history and examining the relevant organs affected.
|Skin prick test||
|RAST IgE blood tests||
Total IgE is not a good marker for allergy screening, and levels depend on the size of the organ affected. For example total IgE may be non-specifically raised in extensive atopic eczema (without allergy) or it may be artificially low in allergic rhinitis (despite positive allergen-specific IgE levels).
We also see localised IgE production in the nasal mucosa that may not be picked up in the serum, and up to 40% of individuals diagnosed as having non-allergic rhinitis with negative RAST (or skin prick) testing actually do have an allergy.
In this case, a nasal mucous sample will confirm allergy by revealing sheets of eosinophils on light-microscopy when stained with Hansel’s solution.
Allergen patch testing (APT) is very useful for identifying contact dermatitis causative allergens such as nickel, rubber, preservatives, dyes, fragrances and glues, common causes of occupational contact dermatitis. Patch testing may also be used to test for delayed food hypersensitivity reactions (to cow’s milk, wheat and soy) in children.
Testing component allergens
Anaphylaxis should always be fully investigated by a competent allergist. RAST blood testing should be done to measure the level of allergy-specific IgE, and so exclude other causes and over time serial tests can be used to document trends in specific IgE levels. An upward trend in specific IgE, for example peanut or cat dander, would indicate increasing sensitisation and reactivity, while a decreasing specific IgE would indicate resolving allergy and lesser reactivity over time (perhaps retesting every 2-5 years).
Specific component allergens can now be measured in the blood and certain components confer a higher risk for anaphylaxis. For example antibodies to Ara h2 in peanut allergy, Pru p3 in fruit allergy, omega-5 gliadin in wheat allergy and Ovomucoid in egg allergy imply persistent and more severe reactivity. These results would then direct allergen avoidance measures and management strategies, including the appropriate prescribing of adrenalin (Epipen, Anapen or Jext pen), plus antihistamine and oral steroid usage.
|Allergen||Related component test||Risk & prognosis|
|Peanut||Ara h2||Anaphylaxis & persistent peanut allergy|
|Wasp venom||Ves v5||Anaphylaxis & candidate venom desensitisation|
|Wheat||Omega 5 gliadin||Severe wheat allergy and exercise-induced anaphylaxis|
|Peach||Pru p3||Stone-fruit anaphylaxis|
|Egg||Ovomucoid||Persistent & severe egg allergy|
|Cow’s milk||Casein (Bos d 8)||More severe & persistent cow’s milk allergy|
|Hazelnut||Cor a8||Nut anaphylaxis & not oral allergy syndrome|
Finally, the use of indiscriminate allergy testing or ‘screening’, without a thorough allergy history suggestive of clinical reactivity with documented causality, is both expensive and likely to lead to unnecessary dietary restriction and even malnutrition in children (Munchausen by Proxy).
Food intolerance test
Wheat and gluten intolerances have recently become very fashionable. Up to 40% of the general population suspect and report that they have some form of food intolerance at one time or another. This is very difficult to exclude or confirm as the only reliable tests for food intolerance are those for lactose or fructose intolerance and gluten intolerances.
Many commercial tests are aggressively marketed and these include measurement of food specific IgG as opposed to IgE antibodies. It must be stated that these IgG tests do not have any reliable diagnostic value in confirming food intolerance or allergy. IgG antibodies are naturally produced following exposure to foods we commonly eat day-to-day and have no pathologic diagnostic value as shown in numerous clinical trials.2 IgG screening tests are also expensive and result in needless food avoidance.
Oral allergy syndrome
Harmless oral and throat itching with oral allergy syndrome may be associated with allergic rhinitis because of cross-reactivity between pollen and proteins in some foods. It’s most commonly seen in Silver Birch tree pollen allergy. Cooking destroys the allergens and so reduces symptoms.
These patients will have established allergic rhinitis to tree and grass pollens in their teens and then start to notice minor but increasing oral itching to an expanding but finite cross section of fruits, nuts and vegetables. Examples include stone fruits (apple, peach, plum, pear, cherry), hazel walnut, peanut, and raw vegetables (carrot, celery, potato and tomato).
The sensitisation to profiling, a cross-reactive protein found in both pollen and in raw foods, causes minor oral itching that does not progress to any respiratory compromise or anaphylaxis.
Dr Adrian Morris is a GP with special interest in allergy diseases and runs private allergy clinics in London and in Guildford. He is a member of the British Society for Allergy and Clinical Immunology and advisor to the BBC on allergies.
Dr Morris runs an informative website at www.allergy-clinic.co.uk, with detailed guides to numerous allergies and syndromes, and advice on primary care management.
1 British Society for Allergy and Clinical Immunology – most common allergies
Royal College of Pathologists (2002). Allergy and allergy tests: a guide for patients and relatives.