Download Allergy in Primary Care - Bolton GP Specialty Training

Cow's milk protein allergy
Dr Heidi Northover
2017
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Workshop A - diagnosis and recognition of
CMPA via case studies
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Workshop B - ongoing management of CMPA
- weaning, reintroduction of cm, role of
specialist formulae for the infant > 6
months of age
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Q&A, quiz discussion
Contents
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The basics; allergy vs intolerance
IgE and non IgE mediated reactions
Lactose
The myths and mix ups
Extensively hydrolysed & AA formulae
To test or not to test
Useful resources
Peanut
Tree nuts
Cow’s milk
Egg
Soya
Wheat
Shellfish
Fin fish
Sesame
Life long
Life long
Transient
Transient
Transient
Transient
Life long
Life long
Life long
On average it takes 3.6 months from the first GP
visit to diagnose CMA
 On average, an infant with CMA will visit the GP
18.2 times over the 12 months after their initial visit
 On average, 7.6 GP visits are needed before a
referral to a specialist clinician for CMA
 The average waiting time before seeing a specialist
after referral is 3.7 months.
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Sladkevicius E et al. Resource Implications and Budget Impact of Managing Cows' Milk
Allergy in the UK. J Med Econ. 2010;13(1):119-128
8,350 infants will present to GPs each year with
CMPA in the UK.
Healthcare cost of patient management
 Cost of management over first 12 months following
initial presentation: estimated @ £25.6 million
 ~ £1395 per infant (varies according to clinical
symptoms)
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Direct cost to the NHS of managing all allergic diseases:
estimated at over £1 billion per annum in the UK.
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£900 million per annum spent by primary care on allergy
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Allergy accounts for about 11% of the total community
drugs budget
1000 patients
Eczema & GI
symptoms
GI only
Eczema only
Urticaria & other
symptoms
Number
590
230
100
80
Mean number of GP
visits over 12
months from initial
presentation
19.4
18.1
13.4
15.6
Mean number of GP
visits before starting
clinical nutrition
product
4.5
3.4
1.9
6.1
Mean number of GP
visits before referral
7.6
7.8
6.1
8.2
43%
45%
33%
34%
% referred to a
specialist
ASK ABOUT A PERSONAL & FAMILY HISTORY
OF:
Atopic disease
Food allergy
Feeding history
Breast or bottle (formula) fed
Age at which formula was introduced; were
symptoms associated with change?
Age at weaning to solids; associated symptoms?
Intolerance
Lactose
Symptoms
suggestive of
adverse
reaction to
cow’s milk
Allergy
Reflux
Colic
FPIES
Symptoms
of adverse
reaction to
cow’s milk
Eczema
Proctocolitis
Allergy
involves
Allergy
involves
the the
immune
system’s
immune
system;
reaction
to protein
reaction
to protein
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Intolerance is non
immune mediated
Lactose is a sugar, not a
protein
Therefore lactose does
not cause allergy
Food
hypersensitivity
Immune
mediated
(Allergy)
IgE
mediated
Non IgE
mediated
Non immune
mediated
(Intolerance)
Mixed
reactions
Lactose intolerance
Allergy involves the immune system’s
Lactose is the natural sugar found
in mammalian milk
Disaccharide sugar; glucose +
galactose
Broken down by enzyme, lactase,
in brush border of duodenum
Lactose intolerance is due to
partial or total deficiency
of enzyme lactase
Lactase levels highest at birth,
tend to naturally
reduce thereafter
3 types of lactase deficiency
Congenital; Inherited as autosomal
recessive.
Very rare especially in the UK (Finland & Russia)
Primary; Primary lactase deficiency
Develops during childhood, genetically
determined
Higher rates of lactose intolerance in
Africans, Asians & South Americans
Secondary;
Acquired lactose intolerance; lactase
deficiency after damage to bowel – typically
following acute gastroenteritis in children,
coeliac disease, surgery
Undigested lactose reaches
large bowel
 Creates abnormal osmotic load
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This causes;
 Bacterial fermentation
of lactose to hydrogen gas
 Distension & pain
 Increased faecal water
 Increased gut transit time
 Explosive acid stools &
 Excoriated bottom
reaction to protein
Making the diagnosis
Difficult! History
Elimination and re-challenge
Allergy involves the
immune system’s
Stool pH & reducing substances (hot
fresh sample,
within the
reaction
to protein
hour!)
Normal stool pH ~6
< 5.3 is acidic and diagnostic of carbohydrate(sugar)
malabsorption
Breath hydrogen test rarely used in young children (often
positive < 3 months)
Rarely intestinal biopsy
Who has recommended this?
Allergy involves the
immune system’s
reaction to protein
Colief is lactase drops
Allergy involves the immune
system’s
reaction to protein
Allergy
Food
hypersensitivity
Immune
mediated
(Allergy)
IgE mediated
Non IgE
mediated
Non immune
mediated
(Intolerance)
Mixed
reactions
5-15% of infants show symptoms suggestive
of adverse reaction to cow’s milk protein
2-8% allergic to cow’s milk protein
Easily missed
Wide variety of non specific clinical symptoms
Causes infant & parental distress ++
+/- impaired growth
<50% is type 1, immediate, IgE mediated
>50% is type 4, delayed, non IgE (T cell) mediated
tests not useful
IgE mediated
 Milk protein
Non IgE mediated
 Milk protein (?+ other
 Usually symptoms begin
within minutes of
ingestion
 Usually clear temporal
link to food ingestion
 Often easier to diagnose
 Can be life threatening
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elements
Slower onset
Less easy to link to food
ingestion
Vague & variable symptoms
Not acutely life threatening
Often ‘dose responsive’
Type 4, T cell mediated
ASK ABOUT A PERSONAL & FAMILY HISTORY
OF:
Atopic disease
Food allergy
Feeding history
Breast or bottle (formula) fed
Age at which formula was introduced; were
symptoms associated with change?
Age at weaning to solids; associated symptoms?
Were the symptoms typical of acute (IgE mediated) reaction?
Was the reaction immediate? Within 2 hours?
Were there any symptoms which suggest anaphylaxis?
Has the child previously or subsequently tolerated the
suspected allergen?
What was the response to antihistamines?
No one pathognomonic symptom
Immediate Type 1 (IgE mediated) reactions;
Lip and tongue swelling, difficulty breathing
Many develop symptoms in at least 2 systems;
GI 50-60%
Skin 50-60%
Respiratory tract 20-30%
Typically, but not always, symptoms occur within few days of
introduction of CMP, e.g. after period of breast feeding
Median onset of symptoms from exposure = 24 hours
Mild, moderate or severe
Non IgE (type 4) mediated
reactions
Irritability, distress, colic, arching
Regurgitation, vomiting, difficulty feeding
Loose stools, bloody stools, constipation
Worsening of atopic dermatitis
Iron deficiency anaemia if severe
Failure to thrive
More common in atopic children
Improve on elimination diet
No validated tests
‘CMPA syndromes’
Food protein induced enterocolitis syndrome
CMP induced proctocolitis
CMP induced enteropathy
Allergic dysmotility (GOR, constipation)
CMP ‘sensitive’ eczema
Bolton CCG Primary Care Pathway for the Management of Delayed Onset
(Non IgE) Cows’ Milk Allergy (CMA)
Bolton CCG Primary Care Management Pathway
Acute Onset (suspected IgE) Cow’s Milk Allergy (CMA)
Any extensively hydrolysed protein formula will
be suitable for 90%
Extensively hydrolysed protein
With added MCT (55%)
Similac Alimentum
Aptamil Pepti
Nutramigen LGG
Althera
Aptamil Pepti Junior
Pregestimil
For the other 10%: Single amino acid (“elemental”) formula
SMA Alfamino, Neocate LCP or Puramino
CMPA persists in only a minority; most outgrow by teenage
years (~80%)
Only 1-2% adults have CMPA
Those with positive IgE based tests, co existent asthma &
rhinitis more likely to have persistent allergy
Hypoallergenicity
Standard infant
formula
Intact proteins
‘Comfort’ formula
Extensively
hydrolyzed formula
Partially hydrolyzed
peptide chains
Extensively hydrolyzed
peptide chains
Single amino acid
formula
Single amino acids
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Clinically lactose free
Casein protein based
MAP guideline
Diagnostic elimination diet (DED)
~90% will respond to an EHF (Extensively hydrolysed formula)
Some casein based (Nutramigen, Pregestimil)
Some whey based – taste better! (Aptamil Pepti)
Allow at least 2 weeks, up to 4 weeks for some symptoms to
resolve, but many improve in 48-72 hours
~10 % will not respond and will need single amino acid formula
(Neocate LCP or Puramino)
Continue to breast feed
CMP elimination diet in mum, (may need to exclude
egg too)
Supplement with calcium & vitamin D
MAP guidelines
Formula fed babies with
severe CMPA
Red flag indicators to use an AA formula
Symptomatic on EHF
Severe GI symptoms
Faltering growth
Multiple food allergies
Severe eczema
Symptomatic on breast milk
Anaphylaxis
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Taste
Lactose free
Available over the counter
Acceptable to vegans
Is soya ever ok?
 Child over 6 months of age
 Absolutely refusing to drink EHF or AA formula;
but dietitians can help!
Chief Medical Officer 2004
‘Soya should not be used as first line management of CMPA or
lactose intolerance
Soya milks have high phyto-oestrogen content; long term risk to
reproductive health of infants, male and female (COT 2003)
Soy is a potential allergen, significant risk of cross reactivity of 1015%
Scientific Advisory Committee on Nutrition 'there is no unique
clinical condition which particularly requires the use of a soya
based formula.’
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Rice milk; high levels of arsenic
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2006 DoH advice;
Goat’s milk protein formulae not suitable for
infants under 12 months of age
High chance of cross reaction, ~30%; close
homology
between protein allergens
Low in folate
Similar levels of lactose to cows’ milk
(all animal milks contain lactose)
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GOLD standard is history + improvement on diagnostic
elimination diet
Other tests not usually necessary, unless history of
acute Type 1 reactions or anaphylaxis
Problems with IgE based tests eg Serum specific IgE & Skin
Prick Tests:
Less than 50% of CMPA is IgE mediated
50% of healthy newborns have circulating IgE to cow’s milk
IgE antibodies may appear & be present with no clinical
history of CMPA
Negative tests do NOT exclude allergy
Significant overlap between CMPA and GORD
(~40% of those with GORD have CMPA)
 Associated with other food allergies (eg soya up to
15%)
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Non IgE mediated CMA > IgE mediated CMA
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Associated with atopic dermatitis
Associated with positive family history of food
allergy and atopy
Resourcesrs
Bolton CCG Primary Care Pathway for the Management of Delayed Onset
(Non IgE) Cows’ Milk Allergy (CMA)
NICE February 2011 Food allergy in children and young people
Archives of Disease in Childhood Education and Practice edition October 2010
Volume 95 Issue 5 ‘Identifying and managing cow’s milk protein allergy.’ George du
Toit et al
Diagnosis and management of non-IgE-mediated cow’s milk allergy in infancy a UK primary care practical guide Ventner et al Clin Trans Allergy 2013; 3: 2
BSACI Executive Summary
Workshops
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What was eaten? How much?
How long did it take for the symptoms to
start?
What were the symptoms?
Was there anything to suggest anaphylaxis?
Was an antihistamine given? If so what was
the response?
Has the food been tolerated before or since?
Have reactions occurred more than once?
Personal and family history of atopy?
Bloody stools for 2 months
Began when mum stopped breast feeding & changed to
formula @ 4 weeks of age
No vomiting, irritability or colic
Mother has allergy to cats, dogs, peanuts, and has asthma
Dad’s sister had problems tolerating cow's milk as a baby
Clinical diagnosis of CMPA; start EHF (Aptamil Pepti in this
case)
No tests necessary
Seen in clinic 4 weeks later, 4 months old
Thriving & well
No blood in stools since 36 hours after EHF introduced
Referral to dietitian for weaning advice
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Admitted at 2 months of age with vomiting, loose
stools & colic
Formula fed (“hungry baby” formula as not settling with
feeds)
Taking Colief with little effect
Mum allergic to cow's milk (diagnosed at 3 years of age)
Clinical diagnosis of CMPA; changed to EHF
Seen 3 weeks later: “much better”
Diarrhoea stopped
Less irritable, much happier, sleeping longer
No longer on Colief
Still some vomiting and regurgitation
 Started on anti reflux treatment
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Tom is a 5 month old boy
Mother is a GP
Mother is nut & fish allergic
Baby breast fed for 5 months; well & no problems
First weaning food @ 5 months– Aptamil baby
rice made with formula milk
Within 20 minutes – facial swelling, urticarial rash
& vomiting
Given antihistamines and steroids in ED with
good effect
Follow up with GP; what would you do?
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Diagnose CMPA & prescribe EHF; a clinical
diagnosis & therapeutic trial approach
Diagnose CMPA and recommend soya milk
OTC; soya is cheap and suitable alternative
Refer to secondary care for further
investigation and management; will need
blood or skin prick tests to confirm diagnosis
Advise mum to re-expose in 2 weeks; cannot
diagnose allergy on first exposure
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Diagnose CMPA & prescribe EHF; a clinical
diagnosis & therapeutic trial approach
Diagnose CMPA and recommend soya milk
OTC; soya is cheap and suitable alternative
Refer to secondary care for further
investigation and management; will need
blood or skin prick tests to confirm diagnosis
Advise mum to re-expose in 2 weeks; cannot
diagnose allergy on first exposure
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Diagnose CMPA & prescribe EHF; a clinical
diagnosis & therapeutic trial approach
Diagnose CMPA and recommend soya milk
OTC; soya is cheap and suitable alternative
Refer to secondary care for further
investigation and management; will need
blood or skin prick tests to confirm diagnosis
Advise mum to re-expose in 2 weeks; cannot
diagnose allergy on first exposure
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Sought advice elsewhere
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Oscar is an 11 month old baby boy
Mum is peanut allergic, asthmatic and had
CMPA as a child
Baby exclusively breast fed for 7 months
Always screamed, was irritable, vomited;
mum questioned CMPA; told “not possible”
as baby breast fed.
What would you do?
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At 4 months; Colic and GOR; prescribed
Infacol, Infant Gaviscon & Domperidone; no
change
At 7 months – Aptamil Comfort* introduced;
no better * partially hydrolysed milk
At 8 months – Wysoy; much worse; urticarial
rash, facial swelling, eye swelling, constant
runny nose
At 10 months – Nutramigen LGG; no better
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At 4 months; Colic and GOR; prescribed
Infacol, Infant Gaviscon & Domperidone; no
change
At 7 months – Aptamil Comfort introduced;
no better
At 8 months – Wysoy; much worse; urticarial
rash, facial swelling, eye swelling, constant
runny nose
At 10 months – Nutramigen LGG; no better
So what next?
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Refer for ‘allergy tests’
Review the symptoms & diagnosis
Trial of amino acid formula eg Neocate LCP
Reintroduce trial of cow’s milk
Exclude egg, wheat and rice from diet
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Refer for ‘allergy tests’
Review the symptoms & diagnosis
Trial of amino acid formula eg Neocate LCP
Reintroduce trial of cow’s milk
Exclude egg, wheat and rice from diet
 Cow’s protein milk allergy is common
 Lactose intolerance is uncommon
 Most CMPA is non IgE mediated, vague & variable
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symptoms, poor temporal relationship to food
Parents are invariably exhausted and desperate by
diagnosis
Clinical diagnosis; tests often unhelpful
An allergy focussed history is vital
90% babies with CMPA will respond to an EHF, usually
very quickly (72 hours)
GORD, eczema, soy allergy commonly co-exist
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Risk to all food allergic people:
 Risk is 1.81 micromorts
100+ times more likely to die in RTC than from food
anaphylaxis
Those < 19 years of age; higher risk group
 Risk is 3.25 micromorts
Still more likely to be murdered!
Higher risk individuals; asthma, teenagers, previous history
of anaphylaxis
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Action plan and antihistamine for all
Cetirizine or desloratidine; non sedating, long
acting
Piriton; sedating, short acting
Adrenaline auto injector pens (Epipen ®) JEXT®
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New BSACI guidance October 2016
AAP update on use of adrenaline in anaphylaxis
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As soon as possible after a suspected anaphylactic reaction, an adrenaline
auto injector is prescribed (as recommended by NICE), by A&E or the GP.
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Prescriber to give training on how and when to use an auto-injector; aim
to start treatment early (improves outcome) & before help arrives; delays
may lead to more severe and treatment resistant anaphylaxis.
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BSACI has not made a blanket recommendation on the number of autoinjectors anyone should carry as this should be based on a risk
assessment.
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Refer to an allergy specialist for comprehensive risk assessment &
personal action plan, discussion of practical steps on how to minimise
potential risks as part of everyday life.
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Sample action plans available on BSACI website
Accurate diagnosis of the aetiology & allergen(s)
Assessment of severity and future risk, including
consideration of the amount of allergen involved in
previous reactions (trace amounts?)
 Does the patient still need the AAI?
 How easy is it to avoid the trigger?
 Assess other risk factors:
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 Certain co-factors increase the risk of anaphylaxis, asthma in
the case of food allergy, raised baseline serum tryptase and
the age of the patient (teenagers)
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Every patient should have a personally tailored
management plan, which should determine whether
one, two (or no) auto-injectors should be prescribed.
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Adrenaline/epinephrine is the first-line treatment for anaphylaxis; does not
reduce death but does reduce cardiorespiratory symptoms.
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Use in patients with significant airway involvement or hypotension, occurring
as part of an anaphylactic reaction.
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All other medications, including antihistamines and bronchodilators such as
salbutamol, provide adjunctive treatment but do not replace epinephrine.
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Do not hesitate to use epinephrine for possible anaphylaxis, even in the
absence of proof that patients' symptoms are the result of an allergic reaction.
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No absolute contraindications to use in anaphylaxis. Epinephrine in appropriate
doses is safe.
Those patients who should be considered for adrenaline auto-injectors
include;
 Severe systemic reactions where the allergen cannot be easily avoided
 Allergic to high-risk allergens, for example nuts with other risk factors (such
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as asthma), even if the reaction was relatively mild
Who had a reaction in response to trace amounts of allergen/trigger
Who cannot easily avoid the allergen
With continuing risk of anaphylaxis (e.g. food-dependent exercise-induced)
With idiopathic anaphylaxis
Strongly positive skin prick tests
With significant co-factors e.g. asthma requiring brown inhalers
Teenagers
(Parents insist)
(Peanut allergy)
Some patients have never experienced anaphylaxis but still considered to be
at risk; ask for specialist guidance.
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Train patients, parents or carers in both when and how to
use the auto-injector device at the time of prescribing.
Reinforce training when the device is dispensed by the
pharmacist and during allergy clinic appointments.
Pharmacists should be encouraged to undertake device
training at every opportunity.
Prescribing an adrenaline auto-injector is only one step in
managing anaphylaxis risk.
Regular re-training in the use of the auto-injector.
For children, education of parents/carers and school staff
is required.
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In a healthcare setting; up to 500 ug in a teenager/adult
Adrenaline should be given in the muscle of the mid-outer thigh
because that helps achieve peak efficacy and is safer than
injecting a bolus intravenously.
An action plan should be provided for all regardless of whether
they have an AAI
JEXT/Epipen Junior = 150 ug (15-30 kg)
JEXT/Epipen = 300 ug (>30 kg)
The prescriber must take responsibility for
training
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Do not carry out allergy testing without first taking an
allergy focused clinical history.
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Interpret the results of tests in the context of
information from the allergy-focused clinical history.
ASK ABOUT A PERSONAL & FAMILY HISTORY
OF:
Atopic disease
Food allergy
Feeding history
Breast or bottle (formula) fed
Age at which formula was introduced; were
symptoms associated with change?
Age at weaning to solids; associated symptoms?
Were the symptoms typical of acute (IgE mediated) reaction?
Was the reaction immediate? Within 2 hours?
Were there any symptoms which suggest anaphylaxis?
Has the child previously or subsequently tolerated the
suspected allergen?
What was the response to antihistamines?
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Mother made home made brownies
containing hazelnuts and Nutella
(hazelnut spread)
Eaten Ferrero Rocher chocolates
before without problems
Ate a brownie for breakfast, went to
school
Came home and felt ‘hot’ – mum
took her uniform off – covered in red
itchy blotchy rash
No complaints from school
Gave her Piriton – little effect
Repeated Piriton – little effect
Went to bed- rash improved
overnight
 Ate another brownie the next
morning – rash returned
 Referred ? Hazelnut allergy
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History – what was unusual?
Had eaten hazelnuts before without problems
Rash appeared over hours – not typical of type 1 reactions
Piriton didn’t seem to help
So what next?
 SPT to hazelnut
 Negative control 0 mm, positive control 8 mm
 Hazelnut 0 mm
 Serum specific IgE – total = 780
 Hazelnut, brazil, cashew, walnut, pistachio < 0.4
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Recommendations
 Based on the results of the allergy-focused clinical
history, if IgE mediated allergy is suspected:
 Offer a skin prick test and/or blood tests for specific IgE
antibodies to the suspected foods and likely co-allergens
 Do not use atopy patch testing or oral food challenges to
diagnose IgE-mediated food allergy in primary care or
community settings
Likelihood of clinical allergy from specific IgE
Likelihood of clinical
allergy from history
Low (<0.35 Ku/L)
Intermediate (0.35-15 High (>15 Ku/L)
Ku/L)
High, eg urticaria &
Possible allergy
wheeze on more than one
exposure
Probable allergy
ALLERGY
Intermediate eg urticaria
on one exposure
Possible allergy
Possible allergy
Probable allergy
Low eg non IgE
symptoms
No allergy
Possible allergy
Possible allergy
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Allergy tests provide supportive evidence
Should only be used if there is evidence from the history to
suggest the responsible allergen
They should not be used as a screening test
Used incorrectly there is a significant risk of misinterpretation of
the results/misdiagnosis
SPT and SSIgE give a prediction of likelihood of reaction not
severity
Skin prick tests
Oral food challenge
Hair analysis
Patch testing
VEGA testing
Serum specific IgE
IgG4
York test
Skin prick tests
Oral food challenge
Hair analysis
Patch testing
VEGA testing
Serum specific IgE (RAST)
IgG4
York test
Oral food challenge; gold standard but labour intensive and slow
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Avoid antihistamines for 5 days before
Pin-head size amount
Pea size amount
Double every 15 min until normal portion tolerated
Observe for 2 h after food has been eaten
Skin prick tests; cheap, instant results, almost any food can be
tested (prick- prick) – 8 allergens = £47.27
Serum specific IgE; “RAST” or Immunocap; one blood test, risk free,
more expensive, delayed results 8 allergens = £126.97
Patch testing; only useful for contact dermatitis
Maps the allergen sensitization of a patient at a molecular level;
increased accuracy in allergy diagnosis & prognosis
 Currently more than 130 allergenic molecules commercially available
for in vitro testing.
 Enables three key aspects of allergy diagnosis:

 Resolving genuine versus cross-reactive sensitization in poly-sensitized
patients, thereby improving the understanding of triggering allergens
 Assessing, in selected cases, the risk of severe, systemic versus mild, local
reactions in food allergy, thereby reducing unnecessary anxiety for the
patient and the need for food challenge testing
 Identifying patients and triggering allergens for specific immunotherapy
(SIT).
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All sIgE tests including MA & CRD should be evaluated within the
framework of a patient’s clinical history, since allergen sensitization
does not necessarily imply clinical responsiveness.
RAST – specific peanut IgE or Skin prick test
Positive IgE to team
The team is dangerous
The team is a threat
13 players or components to the threat
Is one more dangerous & significant than the others?
13 players or components to the threat
Is one more dangerous & significant than the others?
Component resolved diagnosis tells us that ….
Only 4 players are a real threat
The others may look like a threat (perhaps one is the twin brother of
a star player in another team?) or be insignificant/harmless
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Component resolved specific IgE testing for
peanut allergy more accurately identifies
patients with peanut allergy than the routine use
of peanut extract–specific IgE serology or skin
prick testing.
Among the peanut component proteins, IgE
antibodies to Ara h2, and to a much lesser extent
Ara h1, Ara h3, Ara h6, and Ara h9, have been
identified as the major driver of clinically
relevant allergy.
Sensitization to Ara h2 is found in 40% to 90% of
patients with clinical peanut allergy.
The peanut seed storage proteins Ara h1, Ara h2, and
Ara h3 are all major allergens and seem to be associated
with primary sensitization to peanut in susceptible
individuals. (ie not cross reactions)
 Among these seed storage proteins, Ara h2 in particular,
is considered a risk marker for severe allergic reactions.
 In individuals sensitized to peanut and with a cut off
point of 0.35 kU/L, Ara h2 correctly classified 97.5% of
the patients.
 Importantly, all children with peanut allergy were given
correct classification, using Ara h2.

On investigation, a child with a suspected peanut allergy gives
a positive skin prick test or in vitro (RAST) allergy test for
peanut extract.
 The prognosis can be very different depending on whether
the sensitization is linked to a Bet v 1-like protein (major
allergen component of white birch pollen), a seed storage
protein (Ara h2), or an lipid-transfer protein (LTP).
 In the first case, there is almost no risk of the child’s
experiencing serious anaphylactic shock (Positive RAST
reflects cross reactivity to Bet v 1 like protein)
 In the second and third cases, true allergy to peanut is likely
and the child is advised to carry injectable adrenaline (e.g.,
Epipen or Jext).

Various IgE anti-Ara h2 cut points have been
proposed to predict clinically relevant peanut
allergy & improve diagnostic characteristics
 Nicolaou and Custovic similarly proposed 0.35
kU/L as a threshold.

 In their study, this threshold exhibited a 100%
diagnostic sensitivity.

? Could these thresholds be used to suggest
home introduction of peanuts to patients (if they
fall below the threshold) or to replace an oral
food challenge (if they rise above the threshold).
False-positive results could lead to food
avoidance, which can increase the risk of
developing an allergy down the road.
 "Many children are sensitized to a food, so they
will have a positive test result, but that does not
mean they have a true food allergy"
 1:10 children are positive for peanut IgE (ie
sensitised)
 1:100 are clinically allergic to peanut
 The presence of sIgE reflects allergic
sensitization and not necessarily clinical allergy.

478 children with confirmed food allergy, and 642
of their siblings.
 Caregivers completed detailed screening histories
for both the allergic child and the siblings.
 Skin prick testing (SPT) and serum specific IgE
(sIgE) was performed on the siblings for cow’s
milk, egg white, soybean, wheat, peanut, walnut,
sesame seed, a fish mix, and a shellfish mix.

Sensitization was defined as a positive skin prick
test or positive sIgE with no clinical symptoms.
 Food allergy was defined as a positive skin prick
test (mean wheal diameter, >3 mm) or positive
sIgE (>0.35 kUA/L) plus clinical symptoms.
 34% of the siblings had no sensitization to foods
and no clinical symptoms
 53% had sensitization to food (potential for false
positive in > 50%)
 13% had an actual food allergy

Introduction of peanut-containing foods into the
diets of high-risk infants aged between 4 and 11
months.
 High risk infants are those with early-onset atopic
disease, such as severe eczema or egg allergy.
 Delaying introduction can be associated with an
increased risk for peanut allergy.



Early, sustained consumption of peanut
products was associated with a substantial &
significant decrease in the development of
peanut allergy in high-risk infants.
Conversely, peanut avoidance was associated
with a greater frequency of clinical peanut
allergy than was peanut consumption.
Skin prick test*
Blood test**
Test cost
£1.70
£96.00
Staff cost
£44.49
£30.97
Consumables
£1.08
Total cost
£47.27
*The average cost of a vial is estimated at £17 with 80 drops per vial. Average of eight allergies tested per
person, this equates to a maximum number of ten people tested without wastage.
Add on 30 minutes of nurses’ time @ £0.483 per minute & 10 minutes of doctors’ time @ £3 per minute;
estimated staff cost of £44.49 per test.
One lancet is required for each test, (packs of 200 costing £12 each)
£12 buys two controls with 80 drops in each vial.
**The cost per allergy tested was estimated to be £12. Average of eight allergies tested per person
Add on 2 minutes of nurses’ time @ £0.483 per minute & 10 minutes of doctors’ time @ £3 per minute;
estimated staff cost of £30.97 per test.
(Personal Social Services Research Unit 2009)



Top 9 allergens seen, also some more unusual
fruit and vegetable allergens.
Tree nut, the most common allergy, was seen in
59% of the children (very common in cooking?)
Other more unusual allergens: Chick pea flour,
capsicum, Indian lentils,bulgur wheat, coconut,
corn, aubergine, food dye, garlic, ginger, green
peas, jalapeno peppers, melon, rice, and
tomato.




Aptamil Pepti 1 : £9.87
Aptamil Pepti 2 : £9.41
Nutramigen LGG 1: £10.99
Nutramigen LGG 2: £10.99




Medscape Medical News
Updated Guidelines for Prevention of
Peanut Allergy
Nicola M. Parry, DVM
January 05, 2017




Aptamil Pepti 1 : £9.87
Aptamil Pepti 2 : £9.41
Nutramigen LGG 1: £10.99
Nutramigen LGG 2: £10.99
Danone/Nutricia
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