Allergic Disease: On the Increase

By Adem Lewis / in , , /

Hello, I’m Norman Swan. Welcome to this program,
Allergic Disease: On The Increase, coming to you
on the Rural Health Channel. I’d like to acknowledge
that this program is being broadcast on the land of the Guringai people
of the Garigal clan, part of the Eora nation,
traditional custodians of the land and we acknowledge their Elders
past and present. Tonight, our panel will focus
on allergic disease and the impact on all of us as the incidence and indeed prevalence
increases. Join us in our discussion,
send us your comments and questions via email, text, phone or even Twitter. The details are on your screen now. You can email your questions
to [email protected], you can call us at 1800 646 015, you can text us on 0408 408 932 or you can tweet us on @ruralhealthed Let’s meet our panel. Dr Kim Faulkner-Hogg
is a dietician based at the Allergy Unit at Royal Prince Alfred Hospital
in Sydney and is the coordinator
of the New South Wales branch of the Food Allergy and Intolerance
Interest Group for dieticians. – Welcome, Kim.
– Norman. If only it were tolerance. Alyson Kakakios
is a paediatric allergist and the Head of the Department of
Allergy and Immunology at the Children’s Hospital, Westmead. – Welcome, Alyson.
– Thanks, Norman. Dr Rob Loblay is the Director
of the Allergy Unit at Royal Prince Alfred Hospital
in Sydney and has been extensively involved in
guideline development and legislation and educational program development in the area of allergies
and anaphylaxis. – Welcome, Rob.
– Thanks, Norman. Maria Said is a registered nurse with experience in emergency
and paediatric nursing and is an advocate for individuals
who live with the risk of anaphylaxis. – Welcome, Maria.
– Thank you. Deryn Thompson is a nursing lecturer
at the University of South Australia, especially concerned
with allergies and eczema and is involved with the Professional
Certificate of Allergy Nursing. – Welcome, Deryn.
– Thank you, Norman. NORMAN: What is the Professional
Certificate in Allergy Nursing? It’s a 16-week online postgraduate
professional certificate that we, University of South Australia,
has for nurses. And that is, it’s delivered all online, other than the clinical component
that they do at the end of the course. It composes of 13 topics covering a wide range of manifestations
of allergic disease. So they have a much greater
understanding of the manifestations of allergy, the impact it has on people and of course the evidence-based
education that’s behind it and where the resources are. Does it turn you
into a nurse practitioner? No, it doesn’t turn you
into a nurse practitioner but it does give you a postgraduate
certificate qualification which can direct
some nurses into their jobs within certain allergy departments. It can help their job pathway
that way. But it can also certainly, it’s open
to the rural and community nurses, where they are involved
with seeing many of these people that have got allergic disease. – Advertisement over.
– Thank you. Maria, what’s your story?
Why did you get involved? MARIA: I am a registered nurse and when I had my second child, I realised just how little I knew
about allergy. At age 12 months, I gave my son a peanut
butter sandwich back in the 1990s. NORMAN: A memorable sandwich?
– Yeah. It is quite a memorable sandwich. It took three years for him
to be properly diagnosed. What happened when you gave him
the peanut butter sandwich? The first time, he had erythema. – So redness of the skin.
– Redness of the skin and some hives. I rang my GP and my GP said to give him
some antihistamine. I asked him what else and he said,
‘Just don’t give him peanuts.’ NORMAN: Duh! We kept peanuts in the house and a month later,
he picked up some toast off the table that my husband had left on the table and he put it to his mouth
and with that reaction, he was screaming, he had some swelling. I rang my GP again, and he said, ‘Well, gosh, Maria,
we went through this a month ago. Just give him some antihistamine.’ He had a reaction… NORMAN: Which of course
makes almost no difference? Well, no, but at least I felt
that I was doing something and that I had rung my GP. I felt confident
that I was doing all that I could. At age two, he touched whole peanuts,
shelling them for his grandmother. And with that, he rubbed his eyes
and he started swelling. He didn’t go into anaphylaxis but
he certainly had an allergic reaction. Then at age three,
he had a major reaction to what we think
is contaminated chocolate. And with that, he had some urticaria, he had some difficulty breathing, so he was diagnosed with asthma
by this point. – He’d already developed asthma?
– He’d already developed asthma. He’d been on an antihistamine every day
since he was about two. And he was on his asthma
medication daily. He’d been in and out of hospital
numerous times. They’d served him peanut butter
in the hospital setting. It was pretty scary stuff. So then when he had his anaphylaxis
at age 3.5, I took him to my local hospital. He had just been diagnosed, but even I hadn’t been educated
properly. And I was told about facial swelling,
but nobody mentioned genital swelling. So I took him to my GP and my GP said,
‘No, it’s just a rash after a virus, just keep treating his asthma,’ but then I noticed
the genital angioedema. Took him to the hospital, and I was questioned for three hours
about sexual abuse. NORMAN: You’re kidding?
– No, and it was staff that I knew. They asked me if I wanted to be
transferred to another hospital because I knew so many people there. They drew pictures of him. They questioned myself
and my husband separately. And in the end, I basically said, ‘I want to speak to a paediatrician,
I’m not talking to anybody else’ and my paediatrician then said,
‘This child is having an anaphylaxis. You’ve been treating each
of his symptoms separately.’ And then he was diagnosed and then
he was transferred to Westmead Hospital. NORMAN: What’s he like now? He’s a strapping 22-year-old ratbag kid
who’s a policeman. So… NORMAN: But doesn’t dare eat a peanut. MARIA: No, he doesn’t. Criminals threaten him with a bag
of peanuts rather than a gun. Well, they don’t know.
They don’t know. But I think it’s quite ironic that he has his gun and his handcuffs
and his taser… NORMAN: And his autoinjector. And he has two adrenaline autoinjectors
round his ankle all the time. He had a challenge two years ago, because he hadn’t had a reaction
for 17 years. And I think that was a good experience
for him. He learnt that a tiny amount of peanut
can certainly… – He was just reminded.
– ..trigger a big reaction. And that adrenaline works as well. So I think it was good for two reasons. – Typical story, Deryn?
DERYN: Yes. Quite often in clinical practice, we see that type of story come
with people, with parents, and some of those parents are frustrated because they have said to practitioners
these things are happening, and like Maria even today,
those stories are still coming by, that the doctor has indicated
that it may be something else. You have some stories of people
you come across. We have some pictures of them here.
Typical stories. Tell us about this woman. MARIA: This woman here
went to actually a wedding reception. She’d told them
that she was allergic to walnuts. She disclosed that she was the person
with the allergy at the wedding reception. Yet she was fed a dessert that had walnuts in the crust
of a particular cake. She was five months pregnant and she hesitated in administering
the adrenaline autoinjector. She was rushed to hospital. And even staff at the hospital hesitated
to administer adrenaline. They actually gave her
nebulised adrenaline. She later… We advised her then
to see an allergy specialist. And allergists I have spoken to
since that time have said that you would
administer adrenaline to a pregnant person
intramuscularly, if they were showing signs
of anaphylaxis. And the story of this young man? This young man went to
a charity function. And as he had his meal
put in front of him, he saw that it had grated cheese on it. – And he asked…
NORMAN: He was milk allergic? MARIA: Told them he was milk allergic and he couldn’t have any cheese
on his food and no milk in his meal. The meal was allegedly taken away, turned on to another plate
and brought back to him. After two mouthfuls,
he went into anaphylaxis and needed three doses of adrenaline
to come good. Kim, you must hear stories like that
all the time, people believing they’re pulling your
leg or they’re neurotic or hysterical and they don’t really have an allergy? It’s one of the things that patients
will talk about all of the time and it even goes as far as grandparents
and extended families convincing them that
this is actually real and that a little bit isn’t OK, and a lot of situations
where you are in restaurants that’s the biggest thing
to get across to staff, that it has to be totally avoided. How do you educate families about this so that they actually know
that it’s serious? You can hardly say, ‘Well, just watch.’ No. Certainly if they’ve experienced it
with their child, that’s all the experience
that they need. But it is very difficult
to educate for eating out, because you can never really control
for what is going on in the back room and there is a certain level of trust. Certainly when the children
are very little, we get them to take food with them
to a restaurant, because a lot of restaurants at that age
will accept it. It’s when you get to the adult age, they’re starting to say
that’s not acceptable and these people have done
all of the correct things in identifying themselves,
telling people about it beforehand and therefore thinking
that it is all organised. Now, this program isn’t just about food
allergies but allergy in the broad. Dr Rob Loblay, when somebody says
to you, ‘What is an allergy?’, it sounds like an obvious question – ‘I get a rash, I wheeze,
I get hives,’ – but what is it actually? An allergy is essentially an exaggerated
immune response of the IgE type. NORMAN: So that’s an antibody?
– It’s an antibody. Yes, it’s specialised to provide
protection against parasites but in some people, atopic people, there’s a genetic tendency to produce
exaggerated amounts of IgE antibody against allergens in the environment
which are normally harmless. And so when a person is exposed,
they’ve got high IgE antibody levels and they react, then they’ll exhibit
the immediate signs and symptoms of an allergic reaction by occurring through
the release of histamine and other inflammatory mediators from the mast cells that bind
the IgE antibody. Things that make you sneeze. I used to think of atopy as just asthma, hayfever and eczema. But you’re using it in the context that it’s one of these typical allergic
responses whether it’s from food or pollen
or house dust mite or whatever it is that causes
one of these problems? Atopy itself, by definition, is the genetic tendency to produce
these exaggerated responses. The allergic diseases are the ones
that occur in people who are atopic, depending on what they’re exposed to and depending on a range of
other factors, genetic and otherwise. Alyson, just make sense of this. You hear about contact allergies
from nickel or cosmetics or you hear about atopic asthma,
hayfever and so on, you hear about food allergies, drug allergies like penicillin
and so on. Just make sense of all this for us
before we move on. OK. So atopy, as Rob said, was a term
coined almost a century ago to describe this inherited tendency
on part of particular families to develop these allergic diseases. Like hayfever and asthma. NORMAN: Long before
they knew of antibodies? Long before the IgE was discovered
which was in about 1963. So we then sort of found out
that actually it was the IgE that was associated with what
we mostly think of as allergic reactions which is the immediate sort that come on
and cause your hives and the redness that Maria was describing and when they’re very serious
can cause respiratory difficulties and collapse and death and that’s what’s known as anaphylaxis. That’s the sort of IgE-mediated
type of allergy but you mentioned the contact type, which is actually
a completely different type and is not going to cause you
to have such an acute severe reaction. It’s a delayed type reaction. It’s particularly apparent with things
like nickel and plants and various other contact… Perfume – some people are allergic
to the things in perfumes. That’s a contact dermatitis. It’s not the same as the sort that’s
associated with the allergic diseases. And what about drug reactions? Drug reactions are actually… ..span the whole range
of these allergic diseases, from the sort we all know about,
which is the penicillin reaction, the IgE-mediated penicillin reaction
which can cause anaphylaxis when you inject or take penicillin
by mouth, in someone who’s penicillin allergic, over to very serious drug reactions
which are delayed which often occur or are associated
with like anticonvulsant medications, the barbiturates,
also with sulfonamide medications. They can cause reactions as severe as what’s called
‘toxic epidermal necrolysis’ which is as if the whole body has been
burnt and shreds off the skin. Talk to me about the atopic march. Right, the atopic march
was a term that was coined to describe what we understand about
the progression of allergic diseases. So that in infants and young children… NORMAN: We’ve got a graphic on that
which we might show. ALYSON: In infants and young children, you can see that food allergy
and atopic eczema, which can be associated
with that food allergy, are the most common forms
of allergic diseases, but they tend to go off
as the child ages. However, as those are actually receding, what’s starting to develop in the child is the allergy or atopy
to the inhalant allergens like house dust mites and grass pollens and cat and dog allergens. Then we start to get
the allergic rhinitis or hayfever which is associated with those things
and asthma. They start becoming much more prominent
as the person ages. And as they become young adults it’s actually asthma
and allergic rhinitis that are the most common
atopic diseases. To what extent is that a causative
pathway that you get food allergies and that triggers the rest or it’s just what happens
in the course of things? There is a lot of controversy
about this. I don’t think that the jury is in. NORMAN: You don’t have
to have food allergy? No, you do not. In fact, probably most people
who have inhalant allergen sensitivity and asthma and rhinitis… – And eczema.
– And eczema. ..have not actually had food allergy. We know from studies done
on people with atopic eczema that about 30% of them
have associated food allergies. And that percentage actually diminishes
quite significantly as in the atopic march
as they become older. So that adults with atopic dermatitis
are much more likely to be sensitised to house dust mite
or some of the other inhalant allergens rather than the food allergens. – Yet, the world thinks it’s food?
– That’s right. That’s an incorrect assumption
that it’s all related to food. It’s not. Deryn, what are the common foods
that give trouble with food allergy when you’re going to get it? The common ones for the very young
children are milk, cow’s milk, egg, peanut, and in Australia,
sesame seed is there as well. Kim, which are the hardest ones
to deal with? Are they very different? Peanut is supposed to last a long time and seems to be
the most vicious of them? KIM: It depends I guess on
what we’re looking at within the diet. If we’re looking at just strictly replacing the nutrition
that one particular allergen has, the nut itself, if you just took it out from
the total nutrition part of the diet it doesn’t make a big impact. If you take egg out just from
a nutritional perspective, there’s a lot of other things
that supply protein. However, egg is used in a lot of foods and in a lot of snack foods,
a lot of food preparation. So avoiding it does change the diet
actually quite a lot and can decrease the calories
so you have to be careful. Milk I think probably makes
the biggest impact nutritionally, ’cause milk will provide protein,
as well as calcium, as well as some fat,
vitamin A as well as vitamin D. So if we can’t have milk, we have to be able to replace
all of those food groups, not just simply the calcium side. It requires some planning and we’ll
come back to diagnosis in a minute. Rob, why is it increasing? We hear about the hygiene hypothesis
that we’re living in this clean world and the immune system
is not being trained properly in the first year of life? How true is that? That’s been controversial as well. Well, there’s a lot of supportive
evidence for what’s been called
the hygiene hypothesis. The idea there is that
normally, in early childhood, the immune system learns to react to a whole lot of microorganisms
in the environment and develops immunity. But the theory goes that
in the last 20, 30 years or so, kids are growing up
in a more hygienic environment, not exposed to all the same microbes. And so the immune system,
wanting to be busy all the time, turns its attention to otherwise
harmless antigens. There is quite a lot of evidence
to support it. It’s clearly not the whole story. It certainly doesn’t account for most
of the changes in food allergy that we’ve seen
in the last 15, 20 years, particularly the nut allergies. But they’ve been caused
by paediatricians, haven’t they, by telling parents not to feed
their children these substances and to keep weaning till later. I mean, Israeli kids have less peanut
allergy than the same kids in Britain. ALYSON: Yes. NORMAN: And it’s because
they are exposed to peanuts early. Yes. You’re quite right there, that we’ve actually done a complete 180 in terms of our recommendations
about infant feeding if you like. Over the past couple of decades, as food allergy has doubled
or even tripled in some instances, we’ve been telling parents
of high-risk atopic children that is, people who have a risk
of atopy in their family, to avoid certain highly allergenic foods
such as peanut and the other nuts, cow’s milk and egg
until they’re a certain age. Now that hasn’t worked. Yeah. NORMAN: Yeah. So the interesting study
that you brought up was the study that was done on children
of an ethnically similar background, which was Jewish kids,
half of whom lived in Israel, and half of whom lived in the UK. And in those particular places, the advice given at the time
was to avoid peanut until the age of three years in the UK. This is in the same population
of children. And in Israel, they’re introduced to
peanut from the age of four months in a snack called Bamba
which is highly enriched with allergen. NORMAN: Halva?
– Yeah. The Israeli kids had virtually
no peanut allergy, whereas the rate of peanut allergy
in the UK, as people were religiously
following the guidelines about not introducing peanut
to their children, was doubling over the same time. So have the recommendations changed? ‘Cause the NHMRC has moved
a little bit earlier in terms of solids, but not quite as early
as the allergists would like. No, that’s right. You’re referring
to the Infant Feeding Guidelines recently brought out by the NHMRC which continues to recommend
exclusive breastfeeding until the age of six months, actually. Whereas the ASCIA guidelines
for infant feeding… NORMAN: ASCIA? ASCIA is the Australasian Society
of Clinical Immunology and Allergy and it’s the peak body which oversees
the management of allergic diseases and to which most of us here belong. We’ve brought out infant feeding
guidelines which actually say that parents can now introduce solid foods to their infants
from the age of four months or probably between the ages
of four months and six months, if they’re ready to have them. We’re not saying you’ve got
to force these foods into them. If they’re ready to have them,
in a form that they can have them, and no food is excluded. So Kim, what do you do when… If this is the recommendation
and you’ve got a mother… ‘Cause we’re now getting
into that sort of age where mothers have gone
through this mistaken period where you were exposed
to these foods later, a higher rate of food allergy, they’re coming through to childbirth
with a peanut allergy, and the right thing to do for their kid
is probably to flood them with peanut early on in life,
but the mother’s going to be at risk. What do you do? We often will sit down with the parents, because there are mixed messages
that do come through and some of the parents like to follow
one particular strain of advice and others will go
with another strain of advice. So we do talk about what the risks are. We are still waiting for more research
to come out in this particular area. I don’t think around the world yet
they’ve actually made a 100% decision that this is what we all need to do, but that is the trend at the moment and that’s where the guidelines
have moved forward to it. So we are saying to mums
at this point in time that they shouldn’t be avoiding
any of the allergens in their own diet. They might be avoiding them
to protect themselves? If they’re avoiding it
to protect themselves then it’s going to be
out of their diet… NORMAN: They just have to live with it? If they’re pregnant
and they have to avoid it, then if they eat it, you know,
end case scenario. So in that particular child,
they’re not going to be exposed at least through
what the mother is having. I’m almost frightened
to ask this question, Rob. What about the gluten story? You do get kids and adults
who are wheat allergic and it’s not all coeliac disease? – That’s true.
NORMAN: I just want to touch on this. That’s true. Coeliac disease is a T cell-mediated
immune response against gluten. And the damage occurs
in the small bowel. So there’s an enteropathy. It’s quite different from the Type 1 or immediate IgE-mediated allergies
to wheat that do occur. They can occur in young children. But there’s some interesting syndromes. NORMAN: We haven’t talked
about symptoms here of food allergies. We’re talking about abdominal pain,
vomiting…? No, no, we’re talking about kids
who are allergic to wheat who will develop urticaria, angioedema, anaphylaxis even from exposure to wheat. They could get exercise-induced
anaphylaxis. Yes, there is a syndrome called wheat
dependent exercise-induced anaphylaxis which is a bizarre syndrome where the person can eat wheat safely,
if they don’t exercise. They can exercise safely,
if they haven’t eaten wheat. But if they eat wheat within
about 2 to 6 hours before exercising, then they can have full-blown
anaphylaxis. It’s a very different condition and
not to be confused with coeliac disease. The other thing I wanted to talk about
in terms of prevention was pets. ALYSON: Oh, yes. Because my understanding
of the evidence is the more pets you have
in the first year of life, the better? Yes, there is some
very good evidence actually, some of which has come out
of New Zealand, I might say. NORMAN: They’ve got nothing else
to do there. (Laughter)
ALYSON: I’m not sure it’s that. The evidence is that
if in high-risk atopic families, if they have a pet, particularly a cat
and a dog in the household they’re actually protected from
the development of allergic diseases and from sensitisation
to other sort of allergens. So it’s very difficult
to understand this, but it presumably relates
to the idea of introducing people to large amounts of an allergen
at an early age, thereby inducing tolerance
rather than allergy. Talking about tolerance, you’re testing
tolerance in terms of milk. ‘Cause cooked milk is thought to be able
to treat perhaps milk allergy, not to be tried at home by yourself. No, definitely not. These are aspects of food allergy that are under a lot of study
at present, as we speak, all around the world,
including in Sydney. And what we’re looking at is the fact that we know that certain
people who are allergic to raw milk or I won’t say raw egg but I’ll say
lightly cooked egg who have, you know, can even have full-blown anaphylaxis
to those foods can safely tolerate well-cooked,
baked milk or baked egg. NORMAN: The protein has been denatured? The protein has somehow been altered. And I mean, ‘denatured’
is one of the words to use, but there are many proteins
in both cow’s milk and egg, and some of which are definitely altered
by cooking. So we’re actually actively studying
how long this tolerance or the… We call it desensitisation
at the present ’cause we don’t think
we’ve demonstrated tolerance. NORMAN: Explain this graphic to us, Rob. Because this is not with treatment, but this is the natural course
of egg allergy in most people? ROB: Yeah, well, years ago,
20 years ago, we used to tell people that almost
all kids grow out of their egg allergy by the time they get to school age. This is no longer true,
for reasons that are not entirely clear. NORMAN: But certainly
before they go to university? ROB: Mostly, yes. That’s showing the decline in prevalence
of egg allergy with increasing age. And almost everybody grows out
of their egg allergy by the time they get to adult life. Let’s go to our first case study. Jack is aged 26 months and is brought to Alyson’s practice
by his mother who is anxious about the future. Jack was recently rushed to hospital after eating a small piece
of a muesli bar which contained peanuts
and other tree nuts. He broke out in hives
and had swelling around the eyes. His mother took him
straight to the local hospital, at which point he began wheezing. He was treated with adrenaline and sent
home with an adrenaline autoinjector. Jack also has had eczema, which started
when he was about four months old. What are you going to do
about young Jack? ALYSON: Well, this is such
a common scenario, really. We see this every day. In fact I was on call
at the Children’s Hospital at Westmead Emergency Department
over the weekend and I had two calls about children
coming in with anaphylaxis. So first of all, we’ve got to diagnose –
what caused the anaphylaxis? It’s clearly related in time wise to the
muesli bar which contained peanuts. I’m suspecting peanut or one of the
tree nuts has caused this problem. NORMAN: Remind us
what the tree nuts are? They’re cashew, pistachio,
almond, hazelnut, walnut, pecan, Brazil nut and various other nuts
but those are the main ones, particularly cashew and pistachio
allergy goes along with cashew allergy. We’ve seen a really big rise in
the amount of cashew allergy actually. What’s happened is perfect, is good. Jack has been managed very well
for his episode of anaphylaxis and the reason I’m calling it
anaphylaxis, which is the most severe form
of acute allergic reaction, is that he wheezed,
which indicates a respiratory distress. He was given an adrenaline injection, in this case he was treated
with an EpiPen which is one of the types
of adrenaline autoinjectors which was perfectly correct treatment. He was observed
and then he was allowed to go home. Now, we don’t investigate immediately,
we don’t immediately do skin-prick tests when he is there
in the Emergency Department because we think that it’s best to wait
for two to four weeks after the actual acute episode to be sure of the fact that he hasn’t
sort of released all of his IgE so that we can actually check
that it was actually peanut or one of the tree nuts. So we would bring him back
to our allergy clinic and we would then
do some skin-prick testing. We could do blood testing but it’s best, I think, in this case, ’cause we don’t know exactly
what the nut was, to do the range of skin-prick tests. NORMAN: But some kids will react… Are we talking about patch testing
or prick testing? We’re talking about prick testing, which is we get standardised allergens,
peanut and the other tree nuts, and we put a drop on their skin. Usually the forearm is used but in young children
we can use other areas, and then we touch it into the skin
in a standardised way with a little metal lancet and then we wait for 15 minutes and we see whether a red mark or a lump,
a red itchy lump develops, a bit what would have happened
if he’d gotten hives. And if that does develop, then we know that he’s got specific IgE,
the allergy antibody, to that particular allergen
that we’ve used. Why don’t you just measure the IgE? Well, we could, but it’s not so good when
we’re checking out a range of foods. Because specific IgE… But some of these kids will react
all over the place, won’t they? ALYSON: Not really. You’re right, some do. Especially if they have severe eczema, and that might be one reason
why we don’t do skin-prick testing, we’d probably prefer
to do some blood testing but in his case,
it’s relatively specific, I think. The skin-prick tests are good, they’re well standardised
for the peanut and for the tree nuts. So I think that will be alright, yeah. What if you’re coming at it
the other way, Rob, a kid or adult thinks
they’re food allergic, they’ve got odd symptoms
but they never had anaphylaxis and then you do the tests on them – how do you make your way through that? Just having the test doesn’t necessarily
say you’ve got the allergy? That’s exactly right. It’s the exact flip of what Alyson
is doing with this young child? Both the skin-prick test
and the blood test, the RAST blood tests, need a specific IgE
against particular allergens, either in the tissues or in the blood. But they only detect IgE antibodies. They do not diagnose disease. And so the challenge then is
to try and work out how to interpret each particular test. Size matters. So the bigger the skin test and the higher the titre of the antibody
in the blood… NORMAN: We’ve got this graph here
coming up. ROB: ..the more likely it is to be
related to clinical symptoms. But it’s a probability function. So that graph there shows
on the vertical axis the probability of reacting
in a challenge test against on the horizontal axis
the size of a skin-prick test. The bigger the test, the more likely
they are to react to a challenge. NORMAN: It’s still not one on one.
ROB: Not 100% by any means. NORMAN: We’ve also got the blood test
here which shows the same thing. ROB: Shows the same thing but it’s important to emphasise that these tests only predict
the likelihood of reacting. They cannot tell you
how severe a reaction might be. NORMAN: This is the IgE test
with peanut? ROB: Yeah, that’s the blood test. Or whether the person is going to get
anaphylaxis or not. The severity of the reaction depends
on a whole range of other factors, beyond just the level of the IgE… The danger is somebody could go and see
somebody who’s inexperienced, does all these tests
and said you’re allergic, change their diet
and it’s all unnecessary, particularly with the profound effects
you talked about earlier. So you’ve got to be careful. They do need to be careful. And that’s where the allergists know that some of these things
need to be tested. So they have to eat the food
in order to determine whether or not they have got
an allergy to it. Whether or not that goes ahead
is the judgement of the doctor. Alyson, he’s come up with a peanut
allergy, something like that? Let’s say that he does come up
on skin-prick testing to peanut, and to none of the other tree nuts, to none of the tree nuts. We say, OK,
he’s had a definite anaphylaxis at the age of 26 months to peanut. And that puts him in a higher risk
category for having another reaction. Again, we can’t tell whether
it’s going to be anaphylaxis or not. But it certainly puts him
in a high risk category so we would definitely have
to educate him and his mother… He’s only 26 months
so it will be mostly his family but if he goes to child care,
we’ll have to educate them as well. We’ll have to educate them
about peanut in food and how he must be excluding it. We have to educate his mother,
his family and the child care centre about… Does it mean the child care centre
can’t have peanut at all? No, it does not mean that. I mean, many child care centres
these days elect to be without peanut and tree nuts because they’re relatively
easy to exclude, unlike cow’s milk and egg
which are staple parts of the diet which are virtually impossible
to exclude. We don’t insist that child care centres
are free of peanut. We know that that can actually lead
to other problems, such as blame if another parent
accidentally brings in something with peanut
and a child has a reaction. What we prefer to do is to educate
and to say, ‘Right, Jack is coming
to your child care centre, he has a peanut allergy
which puts him at risk of anaphylaxis. He must have his action plan.’ So we would draw up
this particular action plan and this is specific for the EpiPen. We have another action plan
which is specific for a different type
of adrenaline autoinjector. This is to be filled out by the doctor
who prescribes the EpiPen. And it leaves room here
for a photograph of Jack, so that he’s readily identifiable, his age, what he’s allergic to,
which will be peanut. And the doctor signs it down here. And over on this side,
it runs through step-wise the way of managing
an allergic reaction, from mild symptoms, progressing down
to the much more severe type, which is called anaphylaxis. And the management,
particularly if he starts having any respiratory symptoms
such as wheezing, has to be the injection
of the adrenaline, using the EpiPen in the manner that’s
been described and shown to his family and hopefully the child care centre. The instructions are also
down on the side there and also on the side of the EpiPen. But Rob, GPs can’t prescribe EpiPen? Well, first of all, EpiPen is
an over-the-counter medication. Anybody can buy it,
you don’t need a prescription. But it is available on the PBS, so it can be subsidised. The PBS prescription
can be provided by a specialist in clinical immunology or allergy, paediatric allergists,
emergency physician, and in country areas,
GPs are able to prescribe under the PBS of their own accord. If the child’s admitted to a hospital. If the child presents to the surgery, the GP can still prescribe
under the PBS by consultation with a specialist,
and that can be done over the phone. If you need to ask a question –
[email protected] that’s the email address, you can call us on 1800 646 015, you can text us on 0408 408 932 and you can tweet us on
@ruralhealthed Maria, take us through
how these autoinjectors work. There are actual training devices of both adrenaline autoinjectors,
both the EpiPen and the Anapen. We encourage people to practise with the adrenaline autoinjector
training devices, no needle, no medication, regularly. This, however, is a live device, live EpiPen that has expired and I’m about to inject it
into the orange and not the outer aspect of my thigh. We ask people to put their fist
around the EpiPen, to move their fingers and thumb
away from both ends. At the blue end is the safety end
and the orange end is the needle end. Blue to the sky, orange to the thigh. Remove the safety release.
You place it on the… Don’t imagine for a moment
that injecting an orange is going to help the child
with the anaphylactic reaction? No, you would inject the kid’s thigh. It can be injected through clothing but you would frisk the child’s leg to make sure they haven’t got
a Matchbox car in their pocket. This orange is about to get
the shock of its life. You place it on the outer aspect
midway between the knee and the hip. You place and you push. (Click!)
– You hear the click. You hold it there for ten seconds. Meanwhile someone’s calling
an ambulance. The ten seconds are up, you remove it. As you go to remove the device, the orange end actually extends
over the needle, so you can’t see the needle. We tell people to take that to the
hospital once the ambulance arrives. Rub the site of the injection
straight after. Rub the orange.
Tell me about the Anapen. The Anapen we’ve had in Australia
for about three years. Again, you would put your fist
around the device. It has a grey end and a black end. The black end is your needle shield,
the grey end is your safety end. You remove the needle shield. You remove the safety cap. You place again on the thigh. And you place your thumb
over the red button. (Click!)
– And you hear a click. You hold it there for ten seconds. Once the ten seconds is up,
you remove it and rub the thigh. And Rob, you’ve got to be careful
what you choose to use as a GP, given what’s commonly available
or understood in child care centres or schools? ROB: Yes. That’s true. Most of the schools have been trained
initially in the use of the EpiPen. Because the Anapen works
in a different way, it’s easy to get confused
about what to do in an emergency, people can panic. I think it’s safer to stick with
the one device in the school setting. Once they leave school
and they’re out in the world, they can make their own choice about
what they want to use, that’s fine. But I did want to emphasise there are
two different doses available for both the EpiPen and the Anapen. The EpiPen and Anapen Junior,
150 microgram. Sorry the green one. They’re both colour-coded
in the same way. You just happen to have forgotten
the colour code for a moment there, Dr Loblay! – Sorry.
ALYSON: It says ‘Junior’ on it. The yellow one is 300 microgram
in both devices. And the transition in Australia
is at 20kg. So when a child reaches 20kg, they’re
ready to switch over to the full dose. Although the product information
in the package says 30kg. So internationally,
30kg is the switchover, in Australia, 20. Between 20 and 30,
probably doesn’t matter all that much. Very briefly, Maria, there’s all sorts
of nice ways to carry your EpiPen? MARIA: Yep. It’s really important if you’re
prescribed an EpiPen or an Anapen you must always have it with you and in the case of children,
in close proximity. So we have this little bumbag
that Mum can pass to teacher at school. Teenagers don’t like the world knowing
that they’re carrying it, so this is a slimline belt
that you can put under your shirt. NORMAN: This is the one your son uses?
– This is the one my son uses. He puts it on his ankle and it actually
has space there for two devices. You might be lucky
and never have to use it but you might forget how to use it
so you need a refresher. Really important to practise regularly. So if you’re going to see the GP,
the GP should remind you. Let’s move on to another case study. Wendy is aged 18, she is quite obese. She has recently moved
to a rural town. She has come into your practice, Rob,
after developing an allergic response to being stung by a bee in the backyard. She describes a very painful sensation,
local swelling, which was followed by the development of
a red and itchy rash all over her body. What are you going to do for Wendy? Well, based on the story, I’d be suspecting
that she’s allergic to the sting. And so I’d be skin-testing her. I normally do both the blood
and the skin tests to get an idea of the antibody
specificities and level. And then a discussion needs to be had
about whether or not to embark on immunotherapy. – So to prevent another reaction?
ROB: To prevent anaphylaxis. Is this somebody who needs an EpiPen
or an autoinjector for the likelihood of another bee sting? That would be advisable. Particularly if they live
in a remote area. The difficulty is, if somebody
hasn’t had full-blown anaphylaxis, they’ve been stung, they might’ve had
a large local reaction, maybe involving an arm or leg
or the face, you can’t be sure that they really are
at risk of anaphylaxis. About a third of reactions
the next time round are less severe, about a third the same
and about a third more severe. It’s hard to predict. Sometimes the only way of knowing
is to actually do a sting challenge and see what reaction they have. NORMAN: With a real bee?
– Yep. With a real bee. NORMAN: You’re kidding? Really?
MARIA: First, catch your bee. MARIA: I’ve done it.
(Laughter) And of course, if they’re
in a particularly high-risk group, if they’ve got asthma, if they’ve got other allergies
that might make them more prone to be more reactive
at certain times of the season… NORMAN: So a full allergic history. If they live in remote areas,
you play it safe. If they work with bees, if they are
bee lovers and work with bees, then they should almost certainly
be undertaking immunotherapy. And it works very effectively. About 90% can be fully protected. – Through immunotherapy.
ROB: Yes. – Is that permanent?
– It probably is permanent. I mean, do you have to keep
on having it to keep it down? Like the milk, if you’re on this cooked
milk treatment for milk allergy, that’s probably got to be maintained. The usual immunotherapy course
goes from three to five years. Most people would probably err on
the conservative side and say five years but studies have shown that
after five years if you stop, almost everybody fails to react
to bee sting challenges. – Can you tolerise to penicillin?
– You can acutely. So if somebody needs penicillin
because they have a serious infection and that’s the only drug available
or the drug of choice, and they’re known
to be allergic to penicillin, they can undergo
what’s called rapid desensitisation. It can be done either orally
or parenterally, giving tiny doses increasing every
20 minutes or so under observation, should be done in hospital
under careful observation. And within six or eight hours, they can get up to the full dose and they’ll tolerate that dose
while they’re having the drug. But as soon as they stop,
within a few days, the drug is gone
off all the IgE receptors, and they’re then susceptible
to anaphylaxis once again. This is what you were talking
about earlier, Alyson, for some allergens
you’ve got to keep on them? You do.
And this is particularly important. I’ll just give an example of, say, a young child who has eczema,
atopic eczema, and skin-prick tests may be done. And unfortunately,
in the context of atopic eczema, the skin-prick tests are not really that they have to be interpreted
very carefully, because many children will come up
positive to certain foods, but they will actually
be already eating these foods. And sometimes people
will take them off those foods, such as egg and cow’s milk, in the hope that
that will improve their eczema. The problem is that those children
have been tolerant to those foods, so the risk is when they actually ingest
the foods again that they will have a very serious
acute allergic reaction. So if you take them off,
you could make them worse? So you don’t want to fiddle
with their diets? No, unless you know what you’re doing. With eczema, you want to treat it
properly, don’t you, Deryn? DERYN: Yes. The biggest thing
with all people with eczema is to actually be using
enough moisturiser. And within Australia and worldwide, the majority of people
do not use enough moisturiser. For example, an adult or a teenager
should be using about 500g of moisturiser a week. That’s the thick moisturiser,
not in a pump pack, so when you tip the top upside down
it doesn’t come out. – It should be thick.
NORMAN: And non-perfumed. Brand is not important,
it’s the thickness of the moisturiser. And a child such as the little ones, a baby about 125g and a child
about 250g a week of moisturiser. – And an adult that whole tub a week?
– That whole tub a week. And a teenager. And also have baths rather than showers? A non-soap-based wash in the bath. I usually suggest people get it from the
pharmacy, rather than the supermarket. There’s a bit more guidance there
on the non-soap-based things and no bubbles
and no lovely smells of products. And not that baby smell. And you were saying to me
before we came on air that when people do treat properly
and moisturise they’re less tempted to fiddle
with the diet? Yes. It tends to take the focus
away from the diet because the skin’s improving. Basically with eczema
we’ve got skin like a brick wall and people with eczema
don’t have enough mortar in between the bricks. And the person has to be replacing that. We haven’t got any drug
that will fix that yet. We put that barrier across the top. And that stops the irritants
and potentially perhaps allergens, the jury is out on that at the moment, but there is increasing research
suggesting that that may be a factor. And this will keep those things
on the outside. Cecil is aged 45. He is a farmer, lives about 35km
out of town on a large sheep station. He’s come to the practice
saying he might have hayfever. He complains of constant sneezing, coughing, itchy eyes,
a runny nose and headaches. He also feels tired and run down. There’s been an increasing problem
over a number of years getting worse particularly
in springtime. He has recently noticed a bit of
wheezing and tightening in his chest. He has brought this to you, Rob,
to get sorted out. Well, the first thing to tease out
from his history is whether he gets symptoms
all year round, as well as an exacerbation
in the springtime. Seasonal symptoms
are almost always pollen-related. Perennial all-year-round symptoms
almost always dust mite, sometimes mould-related. But often there’s a combination
of things. Maybe he’s sensitised
to several allergens. Maybe both pollen and dust mite. And also worth remembering
that dust mites proliferate more in the warm humid weather, and so there can be a seasonal element
to people with dust mite allergy. So he needs to be tested. Again, skin prick, not patch? Yes. Normally we’d start
with skin-prick tests. With a standard range
of pollens and dust mites. The particular pollens will vary
geographically around the country. So it’s important for people to be aware which are the predominant
pollen allergens in their region and to make sure that those are the ones
that are tested for in those patients. Once you’ve made the diagnosis… How does it change your management
if you find out that buffalo grass
is what you’re reacting to? You can hardly protect yourself
against it? Yeah. Pollen allergy
is very difficult to avoid, to avoid the pollen exposure. We have to breathe, pollen’s in the air,
not much you can do about it. There are measures, people talk about floppy hats
and all that sort of thing, staying indoors, but people who live out in the country,
it’s not possible. So really… How does it change the management
knowing that it’s pollen? Well, you would probably be more
inclined to start immunotherapy in somebody with a pollen allergy. NORMAN: And that works for rhinitis? ROB: It certainly does, yes. – Not in every case.
NORMAN: Is that an oral… It can be done orally but injection immunotherapy
is generally the preferred method. It’s thought to be slightly more
efficacious. And that’s done in a similar way
over a period of several weeks, gradually building up… Is it a surface reaction? Why wouldn’t you treat
the mucosa rather than the… Well, of course, you should be treating
the mucosa with sprays, usually a steroid spray
to cut down the inflammation. – The immunotherapy not.
– Sorry? The immunotherapy not. In food allergy, you are treating
orally, not by injection? ALYSON: That is absolutely true. However, in this case, if you can think it’s an allergy
to bee venom immunotherapy, what you’re doing is actually trying
to induce the immune system to tolerate these pollen allergens, so what you’re doing is injecting
subcutaneously a small amount of the specific pollen. Why doesn’t immunotherapy work
for house dust mite? ALYSON: It does.
ROB: It does. NORMAN: Oh, does it?
ROB: It does. The old preparations that were around
20 or 30 years ago were not as highly purified
as the current ones. And now we have standardised allergens
for a whole range of things, including dust mite, bee venom,
pollens and so forth. It’s the same deal –
five years of treatment? Three to five years. I mean, a lot of people would stop
after three or four years and say, ‘Let’s see what happens.’ And there’s no benefit from going nuts
in the house ripping up all the carpets, wrapping every mattress in polythene? Well, people have different opinions
about that. I have to confess I’m a dust-mite nazi. NORMAN: I thought that had been tested
in randomised trials and was found to be useless? The problem is it’s a package deal. When you only test one approach
on its own, nothing can be shown
to be that effective but when you do the whole package, I think quite often you can get
much better control over symptoms. And that package may include
pulling up the carpets, putting covers on the bed, it might include much more frequent
washing of the sheets. You’d be surprised
how many people wash their sheets once every three or four weeks. – Too much detail here, I think.
(Laughter) ALYSON: However, there is a lot, you’re right, Norman,
there is a lot of controversy about the environmental control. And a lot of the studies
we’ve done in environments such as very high up
where there is very little dust mite. In Sydney, for instance, you can really not get the level
of house dust mite down to a level that’s actually possible. NORMAN: In Wagga there’s almost none.
ALYSON: Well, that’s true. But you know, a lot of money is spent on a lot of this house dust mite
control measures which I think is probably
not well spent. What we advise actually
in young children who have house dust mite contributing
for instance to their eczema, is to say concentrate
on the bedding, the bedroom. ‘Cause that’s where
your bang for your buck goes. And there are some really good… You have a relatively new mattress
and a new pillow – if you’re using a pillow at all – and you can get very good quality covers
that enclose the mattress and the pillow and the doona and so on. I think that’s probably
where the effort should be put, rather than buying leather furniture
and ripping up all your carpets. ROB: I don’t disagree with that. The bedroom is the place to focus and the bed is the place in the bedroom
where the mites breed, where the droppings are. Every time you roll over in bed, there’s a little microscopic cloud
of mite droppings in the air… NORMAN: I’m getting itchy. ALYSON: It doesn’t bother
those of us who are not allergic. Unfortunately
this is the nature of allergy. NORMAN: What did you say, Deryn?
DERYN: Hot water washing. You have to wash the sheets
and child or person’s pyjamas in water that’s 55 or 60 degrees. – That unglues the eggs from the sheets.
NORMAN: Right. ROB: And there are little issues
to worry about such as damp. A lot of houses have got damp
under the floor, rising damp in the walls
or in the bathroom. So the environment is humid. The mites proliferate
more rapidly when it’s humid. Kids got eczema, he’s got shedding
little skin flakes in the bed, the mites feed on that. NORMAN: Oh, God!
(Laughter) – Eugh!
ROB: It becomes a vicious circle. ALYSON: They don’t sleep very well.
NORMAN: I’m itching already. OK… This has been fascinating. We were going to get on
to drug allergies but I think we’ve covered them. I’m interested in what your takeaway
messages are, Deryn? Mine largely would be that the nurses
out working in general practice and in rural communities, that they utilise
and look for the resources that are on the ASCIA website, which is the Australasian Society
of Clinical Immunology and Allergy. A great number of evidence-based
resources there for nearly every manifestation
of allergic disease. NORMAN: There are some useful resources
here which we have on the screen now. DERYN: Yes, very useful resources there. Anaphylaxis Australia, etc. And then the College of GP. But the ASCIA ones
are updated very regularly on good evidence-based resources. There are also things there
that dispel myths and misconceptions. And then of course, the registered
nurses that might want to go on and further their qualifications… You got your ad at the beginning,
you’re not allowed a second one. DERYN: So a combination of both. The patients will be well ahead. NORMAN: Maria? My take-home message is I guess that
for most allergies there is no cure, that people need
to learn to live life with it. There are more questions
than we have answers at present. And with education and support, people can manage
and have a great quality of life. NORMAN: Rob? I think doctors ought to bear in mind that people can often forget
how to use their EpiPen or their Anapen. So when they come into the surgery and there’s someone you know
that’s at risk of anaphylaxis, first thing to do is say,
‘Where’s your EpiPen? Why didn’t you bring it?
Should go with you everywhere.’ And then show them the trainer
and say, ‘Do you know how it works?’ Within a couple of years of being shown,
they’ve forgotten. And so they might say, ‘Yeah, I know.’ ‘So show me.’ Often they’ll be fiddling
and won’t know what end is what. So then they need to be re-educated
to have a refresher course, if you’ve got a practice nurse, you can get her to train them
and bring them up to date. The other thing I think is useful,
there are these kits, they’re free. Each of the autoinjector companies have an online membership thing
where you can register. And they’ve got DVDs
that can be shown to relatives. NORMAN: Thanks, Rob. Alyson? I think what I’d like to emphasise is that with the rapid growth
in the rate of allergic diseases particularly food allergy
and particularly in children, that we all have to work together,
actually, and help each other
to manage this real crisis. We cannot possibly manage all
these children in the tertiary centres, we have to engage
the help of our rural colleagues and we have to educate
and we have to learn and we have to help each other. NORMAN: Shared care.
– Yep. And briefly, Kim? I think for dieticians, we have
to take our advice from our doctors on what comes out of the diet. Don’t try to interpret anything,
it’s up to the doctors to do that. Once we know what comes out of the diet, it’s very important that the diet
for that child becomes balanced and you’re watching their growth
all the way through. Again, the same sorts of website,
the ASCIA website, the Anaphylaxis Australia website have some fantastic handouts
that can be used to teach people to read
the food labels, what are the tricky things to avoid. Make use of them. Thank you all very much indeed. If you’re interested
in obtaining more information about the issues raised in the program
or want to watch it again, please visit our website – – and click on
Allergic Disease: On The Increase. If you’re a health professional, don’t forget to complete
your CPD evaluation form which can be completed online. You’ll receive a certificate of
attendance, and if eligible, points. Our thanks to
the Department of Health and Ageing for making this program possible and thanks for you to taking the time
to watch our discussion today. We’d appreciate your feedback
on the program and your comments
are very important to us. Let us know you watched
by sending an email, text or tweet. And feel free to share your views,
we’d love to hear them. I’m Norman Swan. Bye for now. Join us again soon
on the Rural Health Channel. Captions by CSI Australia Funded by the Australian Government
Department of Families, Housing, Community Services
and Indigenous Affairs.

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