After the ambulance: finding out what actually happened
Emergency treatment solves the immediate problem.
It doesn't necessarily answer the diagnostic one.
Was mustard definitely responsible?
Was another ingredient involved?
Was this truly anaphylaxis?
Is there a pattern of cross-reactivity?
Does the person need adrenaline auto-injectors?
What should they avoid in future?
Those questions belong to the next stage: proper allergy investigation.
The newly updated NICE guideline recommends specialist allergy referral following emergency treatment for suspected anaphylaxis.
And this takes us into a surprisingly interesting area.
Allergy diagnosis is part detective work, part immunology and part controlled experimentation.
A blood test can help.
A skin test can help.
Neither can simply announce the truth in isolation.
And the most definitive test — deliberately feeding somebody the food they may be allergic to — sounds alarming until you understand why, when and how specialists use it.
Diagnosing mustard allergy: why the conversation comes before the test
Modern medicine has access to sophisticated blood tests, purified allergen proteins and increasingly clever laboratory techniques.
Yet when somebody arrives at an allergy clinic after reacting to food, one of the most valuable diagnostic tools remains remarkably low-tech.
The clinician asks what happened.
This is the allergy-focused clinical history, and it is the foundation on which the rest of the investigation is built.
Current European diagnostic guidance places the clinical history first, followed where appropriate by tests for IgE sensitisation such as skin-prick testing and specific-IgE blood testing. The oral food challenge remains the reference standard when the diagnosis is uncertain.
That order matters.
Because an allergy test without a story can produce an answer to the wrong question.
The detective work starts with dinner
Imagine somebody says:
"I think I'm allergic to mustard."
That is useful information, but it isn't yet a diagnosis.
An allergy specialist may want to reconstruct the event almost like a detective reconstructing an accident.
What exactly did you eat?
Was mustard definitely present?
How much did you eat?
How long after eating did the symptoms begin?
What happened first?
Did you develop hives or swelling?
Did your throat or breathing change?
Were there gastrointestinal symptoms?
Did you feel faint?
How long did the reaction last?
What treatment did you receive?
Have you eaten mustard safely before?
Have you eaten it since?
What else was in the meal?
Did anyone else eating the same food become ill?
Had you exercised?
Were you drinking alcohol?
Were you unwell at the time?
Had you taken medicines that might have acted as cofactors?
And perhaps most importantly:
Has anything similar happened more than once?
The timing can be particularly revealing.
A classic IgE-mediated food reaction usually develops relatively quickly after exposure, often within minutes and generally within a relatively short period. A symptom appearing the following day raises a different set of possibilities from hives and wheezing beginning ten minutes after eating mustard sauce.
The story doesn't prove the diagnosis.
It establishes how plausible the diagnosis is and tells the specialist what should be investigated.
Why testing everybody for everything would create an allergy epidemic that doesn't exist
It sounds intuitively sensible to take a blood sample and test it against hundreds of foods.
Surely the more things we test, the more information we obtain?
Unfortunately, allergy testing doesn't work like screening a computer for viruses.
The more foods you test without a good clinical reason, the greater the chance of discovering sensitisation that has no clinical importance.
Remember the distinction from earlier in this guide:
Sensitisation means the immune system has IgE capable of recognising something.
Clinical allergy means exposure actually causes symptoms.
Those are not synonymous.
Suppose somebody eats peanuts every week without a problem but a large indiscriminate allergy panel reports peanut-specific IgE.
If the test result is interpreted as:
"You are allergic to peanuts,"
we have not improved that person's health.
We may instead have persuaded them to stop eating a food they tolerate, frightened them unnecessarily and complicated their diet.
This is why allergy tests are most useful when they answer a specific clinical question generated by the person's history.
The laboratory result and the story have to be interpreted together.
So how certain can somebody become?
After history, appropriate testing and perhaps an oral food challenge, many people can receive a clear clinical diagnosis.
But diagnosis is not the same thing as predicting every future exposure.
A specialist may be able to say with good confidence:
Yes, you have IgE-mediated mustard allergy.
What they generally cannot say is:
Exactly 2.7 milligrams will give you hives, 4.3 milligrams will make you wheeze, and 6.1 milligrams will cause anaphylaxis every time.
Human allergic responses do not behave with that kind of mechanical consistency.
This is why good allergy management combines the best available diagnosis with practical avoidance and an emergency plan appropriate to the individual's risk.
And once somebody has been told to avoid mustard, an entirely new question appears:
What exactly counts as mustard?
The jar is obvious.
Mustard powder is fairly obvious.
Mustard seeds become less obvious.
Mustard flour, mustard leaves, mustard oil and foods from related plants raise more complicated questions.
Then we encounter one of the most confusing areas of food allergy labelling:
highly refined oils.
A food allergy is principally a reaction to proteins.
Oil is principally fat.
So can an oil made from an allergenic seed still cause an allergic reaction?
The answer depends very heavily on how that oil was made.
And mustard oil has an additional complication in the UK that has nothing whatsoever to do with allergy.