At the Molecular Allergology Drinks & Dinner held on 1 September 2026, the evening before ASCIA opened, clinicians, laboratory specialists and researchers examined a familiar problem: a patient has several positive specific IgE results, but the pattern does not match the history. The discussion focused on how allergen arrays, component resolved diagnostics and an understanding of cross reactivity can help make sense of these cases.
What an extract result may conceal
An allergen extract contains a mixture of proteins. Its composition depends on the source material and manufacturing process, so the amount of an individual allergen can vary. This creates two possible difficulties. A clinically important molecule may be poorly represented, or IgE may bind to a shared molecular structure and create several positive results that do not represent separate allergies.
House dust mite Der p 23 provides one example of a relevant molecule that may be underrepresented in conventional extracts. PR 10 proteins, profilins, non specific lipid transfer proteins, tropomyosins and cross reactive carbohydrate determinants can create patterns that span several allergen sources. Component testing helps separate source specific markers from markers of cross reactivity.
CCD can create an impressive laboratory pattern without matching symptoms
Cross reactive carbohydrate determinants, usually abbreviated to CCDs, are carbohydrate structures found on some plant and insect glycoproteins. IgE directed against CCDs can bind to several test reagents and give the appearance of broad sensitisation.
Classical anti CCD IgE usually has limited clinical relevance. Provocation tests are generally negative and skin prick tests are often negative. CCD interference should therefore be considered when in vitro testing shows several unrelated positives that are difficult to reconcile with the patient’s exposures and symptoms.
One dinner case concerned a child with recurrent urticaria and occasional angioedema. In vitro tests reported sensitisation to several foods as well as pollens, while reactions did not consistently follow exposure. Array testing supported strong grass pollen sensitisation and identified CCD reactivity, without supporting the proposed group of IgE mediated food allergies. The combined findings shifted the clinical discussion towards grass pollen allergy, CCD interference and chronic spontaneous or autoimmune urticaria.
Alpha gal requires separate consideration. Although it is also a carbohydrate epitope, it has a distinct clinical association with tick bites and allergy to mammalian meat, offal or other mammalian products.
Which patients may benefit from an allergen array
The discussion supported selective use in clinically complex patients rather than indiscriminate screening. An array may add useful information when:
- the history suggests several possible triggers
- multiple positive results do not match the pattern of symptoms
- a pollen food syndrome or another cross reactive pattern is suspected
- a patient has an unusually restricted diet and existing allergy labels need review
- allergen immunotherapy has produced an incomplete response
- geographic background or migration creates a complex exposure history
- only a small serum volume is available, as may occur in young children
Total IgE alone may not provide a reliable triage rule. In the laboratory experience presented at the dinner, clinically relevant component signals were still found in some patients with total IgE below 20 kU/L.
Results can change the next clinical step
A case involving a young child with severe reactions after eating sandwiches illustrated the practical value of broad profiling. Singleplex tests for several suspected ingredients were negative. Multiplex testing identified sensitisation to seed allergens, including sesame and poppy seed 2S albumins, and a pumpkin seed extract signal that was considered likely to reflect cross sensitisation. The results narrowed the list of possible triggers and reduced the need for unnecessarily broad food avoidance.
Other cases showed how molecular profiles may support confirmation of peanut or tree nut storage protein sensitisation, distinguish storage mite from shellfish sensitisation, or prompt a review of house dust mite immunotherapy when a relevant component such as Der p 23 may not have been covered.
These examples do not make the array a stand alone diagnostic test. The results help determine whether the next step should involve a targeted skin test, a supervised challenge, further functional testing or review of an immunotherapy plan.
Analytical confidence and implementation responsibilities
A small interlaboratory comparison presented at the meeting assessed 1,510 paired allergen level results across five samples. Qualitative agreement was 98.4 percent, and most discordant findings were close to the low positive range. The results supported initial commissioning confidence, but the small number of samples means that ongoing quality assurance remains essential.
Implementation also extends beyond analytical agreement. Laboratories need clear processes for report generation, privacy, cybersecurity and the handling of patient demographic data. Clinicians need reports that explain molecular patterns without encouraging unnecessary avoidance or follow up testing.
Clinical history remains the organising evidence
The dinner discussion ended with a shared principle: the clinical history defines the question, molecular markers help explain the pattern, and clinical assessment determines the diagnosis. As allergen arrays expand, their value will depend on careful patient selection, informed interpretation and close collaboration between clinicians and laboratories.