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Editor,—We are concerned that the general readership of Archives of Disease in Childhood may be misled by a paper based on results of non-standardised or obsolete tests used in the diagnosis of children with potentially severe allergies to peanut and tree nuts.1 The implicit confidence of the paper's title is not supported by the experimental approaches.
We would like to express our serious concern about the following specific points.
It cannot be assumed a nut is “the only possible allergen” in a composite food. Any allergenic food can cross contaminate a “safe food.”
Intradermal testing is not considered standard practice and has no place in the modern diagnosis or management of food allergy.2 Rubbing the forearm until erythema is induced makes distinction from dermographism impossible. Skin contacts that cause allergic reactions are usually minimal and non-traumatising. Percutaneous skin prick testing (SPT) with negative and positive controls—neither of which was performed in this study—is easy to perform, causes minimal discomfort compared to blood sampling, and is considered safe. It also provides an immediately available and graphic result for parents. A history of significant reaction to an allergen is not generally considered an absolute contraindication to skin prick testing.3
Interpretation of SPT and serum allergen specific IgE depends entirely on the quality of the allergen extracts employed. Genuine allergy may be missed if concentrations of particular allergenic proteins are low. Negative skin tests with standardised solutions of food allergens usually (> 95% negative predictive value) predict absence of disease and are therefore usually easy to interpret.3 Positive skin tests need to be interpreted with more caution. For instance a peanut SPT of < 6 mm may not be associated with clinical reactivity, irrespective of history.4 5 It appears from the data presented that the authors found this to be true, with a positive IgE against nuts being associated with a positive challenge. A χ2 test of categories of negative and positive IgE in 62 challenged subjects shows a significant association (χ2 = 5.81, 3 df, p = 0.001).
The gold standard for diagnosis of food allergy is an adequately performed double blind, placebo controlled food challenge, but an open challenge is acceptable in most children. A challenge cannot be considered negative until a dose has been consumed that would cause a reaction in most affected individuals. A figure of 8 g has been widely adopted.3 6 The maximum dose in this study (about 2 g) is far too low and might have led to (potentially serious) false negative results. The negative responders may have had genuine severe allergy to a higher dose of the nut tested, to another nut, or to another food not tested. The challenge dose interval can only be dictated by clinical history and 10 minutes may be too short an interval for some subjects.
Good clinical practice requires the application of state of the art techniques. We agree with the authors when they state that to do otherwise is a disservice to families. We suggest that non-standardised practice in the field of investigating anaphylaxis is playing with fire and does nothing to reassure patients.
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