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Confirming allergic disease through diagnosis of atopy

Sue Cross
BSc(Hons) PGCE
Respiratory Nurse
Respiratory Education Resource Centre
University Hospital Aintree, Liverpool

Atopy is defined as the production of a specific inappropriate immune response to common ­environmental allergens, such as house dust mite or grass pollen. Many who are atopic go on to develop allergic disease such as asthma, hay fever and eczema. However, not everyone with atopy will develop a ­clinical disease.(1)
The prevalence of diseases associated with atopy has increased in many parts of the world, including the UK, over the past 20-30 years. This has resulted in increased use of health services. In the case of asthma, hospital admissions (particularly among children under the age of five), consultation with GPs and the use of drug ­treatment all rose sharply during the 1980s, and ­consultations for managing hay fever also increased.(2)

Predisposition to allergy
Although genetic susceptibility to allergic disease is important, it is unlikely that the increase in allergic disease over the past few decades can be explained by genetic factors alone.(3) 
If both parents are allergic the risk of allergy in the offspring is 75%; if one parent is allergic the risk is 50%.(4) The incidence of allergy is higher in young people than adults. Longitudinal surveys suggest that children with mild disease are likely to become asymptomatic as teenagers, whereas those with more severe disease will have symptoms that persist throughout life. More boys than girls have asthma and hay fever, although these differences become less apparent later in life.(1) 
The development of sensitisation to an allergen requires exposure to that allergen. Exposure early in life may be associated with a higher risk of sensitisation than exposure later in life, but no evidence exists that reducing allergen load in the home of young children reduces sensitisation or the development of allergic disease.(5)

The most important parts of the diagnosis are the assessment and taking an appropriate history. An immediate relation between exposure to potential ­allergens and the development of symptoms makes both the diagnosis and identification of allergy straight-forward. In 25-50% of cases the predominant symptoms develop 1-10 hours after exposure (late-phase reactions), obscuring the allergic nature of the illness.(6)
Symptoms occur more rapidly after exposure to the causative agent as sensitisation increases. Symptoms of food allergy are usually gastrointestinal (abdominal pain, bloating, vomiting, diarrhoea) or cutaneous (itching, urticaria, angio-oedema). Respiratory symptoms are less common and rarely related to rhinitis. There is usually more than one organ involved.(6) 
Cross-reactions can occur between various food allergens, such as birch tree pollen, and certain foods - apple, carrot, celery, potato, orange, tomato, hazelnut and peanut. Cross-reactivity also exists between latex and some fruits (banana, avocado, kiwi fruit and chestnut).
Itching of the throat and ears is a common manifestation of pollen allergy, and patients allergic to house dust mite experience exacerbations when bed making, vacuum cleaning and sleeping in damp conditions.
The impact of allergic symptoms on an individual's lifestyle should be assessed in terms of impairment of school or work performance and time missed, with ­particular emphasis on the interference in leisure­ ­activities and sleep.

Tests will confirm or refute the diagnosis of atopy, but only a positive test plus a positive history of symptoms will confirm an allergic disease.

Skin prick test
The skin prick test can be performed during the initial consultation with aqueous solutions of a variety of ­allergens. These include:

  • Common inhaled allergens - house dust mite, grass pollen, cat dander or dog hair.
  • Occupational allergens - such as ammonium ­persulphate, platinum salts, antibiotics and latex.
  • Food allergens.

Skin prick testing requires the use of controls - ­diluent as the negative control and a histamine solution as the positive. A drop of allergen solution is placed on the skin of the forearm and a sterile lancet used to press the skin through the solution (use a separate lancet for each allergen). Excess solution is removed with absorbent paper tissue. Reaction is evaluated after 15 minutes.
The test should be performed with standardised allergen solutions. In general practice it may be sufficient to use four allergens (house dust mite, grass pollen, and cat and dog allergen) plus the positive and negative controls to confirm or exclude atopy and recognise the most common allergens encountered. Skin prick tests for foods or occupational triggers are carried out only in specialist centres because of the possibility of a systemic reaction.(7)
The skin prick test result should be interpreted in light of the clinical history. If both the history of allergy and the test result are positive, atopy and the offending allergen are confirmed. If both are negative, allergy is excluded. If there is discordance between the history and the test result, referral to an allergy specialist is recommended.(8)

The advantages of skin prick testing are:

  • It is painless and has a low risk of side-effects.
  • It is informative to the patient.
  • Patient compliance is high.
  • The test for aeroallergens can be performed at health centres.

The disadvantages are:

  • Systemic and topical antihistamines may suppress the weal and flare reaction.
  • The test is less reliable for food allergens (which are less well standardised) than with inhaled allergens.
  • Itching causes a slight discomfort, and ­interpretation is difficult in patients with eczema or dermatographism.(9)

Although skin prick testing is generally safe, ­occasional systemic reactions including anaphylaxis have been reported with food allergens. Testing with food allergens should be performed only in specialist centres.

Serum allergen-specific IgE concentrations
The most common in-vitro test is the radioallergo-sorbent test (RAST). With RAST allergens (antigens) are ­chemically bound to an insoluble matrix. When the patient's serum is added, allergen-specific immuno­globulin E (IgE) binds to immobilised allergen. Radioactively labelled anti-IgE is then added, which attaches to the specific IgE already bound to the allergen. The amount of specific IgE in the patient's blood can be estimated from the amount of bound radio­activity. The advantages of measuring the concentration of allergen-specific IgE are that:

  • It is not influenced by any concurrent drug ­treatment.
  • It can be performed when there is widespread skin disease.
  • It is completely safe.

However, the results are not immediately available and testing is expensive.(10)

Alternative tests
Recently there has been a surge in the number of alternative "allergy tests", such as the antigen leukocyte cellular antibody test, hair analysis, bioresonance diagnostics, autohomologous immune therapy, electroacupuncture and Vega testing. There is no evidence that these tests are useful in diagnosing allergy, and they may disadvantage patients who modify diet and lifestyle to no avail.



  1. Burrows B, Martinez FD, Halonen M, et al. Association of asthma with serum IgE levels and skin-test reactivity to allergens. N Engl J Med 1989;320:271-7.
  2. Sparrow D, O'Connor G, Weiss ST. The relationship of airways responsiveness and atopy to the development of chronic obstructive lung disease. Epidemiol Rev 1988;10:29-47.
  3. Hopkin JM. Wheeze, sneeze and genes. J R Coll Physicians Lond 1994;28:560-3.
  4. Mygind N, Naclerio RM, editors. Allergic and non-allergic rhinitis. Copenhagen: Munksgaard; 1993.
  5. Linsfor A, Wickman M, Hedlin G, et al. Indoor environmental risk factors in young asthmatics: a case-controlled study. Arch Dis Child 1995;73:408-12.
  6. Kay B, ed. Allergy and allergic diseases 2. London: Blackwell Science; 1997. p. 1271-90.
  7. Malling HJ. Methods of skin testing. Allergy 1993;48:55-6.
  8. Muller U, Mosbech H. Immunotherapy with hymenoptera venoms. Allergy 1993;48:57-62.
  9. Pastorello AE. Skin tests for ­diagnosis of IgE mediated allergy. Allergy 1993;48:57-62.
  10. Miadonna A, Leggieri E, Teeschi A, Zanussi C. Clinical significance of specific IgE determination on nasal secretion. Clin Exp Allergy 1983;13:155-64.

British Allergy Foundation
Allergy Diagnostic Centre

Further reading
Mygind N.
Essential allergy.
Oxford: Blackwell Scientific; 1997.
Durham SR.
ABC of allergies.
London:BMJ Books;1998.

Study days/­conferences
14-15 June 2001
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9-11 July 2001
British Society of Allergy and Immunology Conference
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