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https://www.chrjournal.com/ Published on March 1, 2021 Vol 1
Canadian Journal of Health Research
Oral Allergy Syndrome: An Anaphylactic
Reaction Overlooked
Eby Aluckal,1 Nader Saad,2 Raabia El-Aghoury,2 Sarah Al-Shma,3 Amira Abdullsamad,3
Nilima Sibi Thottumkal, 4,5 Noura Tayan, 3 Mark Gera,6 Natalia Melo, 3 Abe Abraham 3,6,7,8
ABSTRACT
Oral allergy syndrome (OAS) is a type of allergic
reaction in the oral cavity induced by
consumption of food such as raw fruits, nuts,
flavors and vegetables. The common well-known
symptoms are itching of mouth and throat,
beginning and ending in few minutes from the
time food came in contact with oral mucosa. It is
vital that dentists and oral health professionals
identify this allergic reaction within this small
window time of manifestations as it turns
asymptomatic after few minutes and later
manifests as an extreme allergic reaction like
anaphylaxis. Oral health professionals should be
able to capture the symptoms and diagnosis
quickly to prevent a full-blown allergic reaction
and saving the life of a patient. This allergic
reaction occurs mainly due to homology of
proteins of pollen to the proteins of fruits and
vegetables. In OAS, the immune system produces
antibodies that are directed against the proteins
of pollen and structurally similar proteins in food,
hence, resulting in allergic symptoms limited
mainly to the oral cavity. In this review, we have
summarized the etiopathogenesis, clinical
features, diagnosis, and management of OAS as
an update for dentists and all oral health
professionals.
INTRODUCTION
Oral allergy syndrome (OAS) is defined as the
symptoms of IgE- mediated immediate allergy
localized in the oral mucosa, and the
characteristics depend on the lability of the
antigen. Another term used for this syndrome is
pollen-food allergy syndrome (PFS); It occurs
mainly due to homology of proteins of pollen to
the proteins of fruits and vegetables. In OAS, the
immune system produces antibodies that are
directed against the proteins of pollen and
structurally similar proteins in food, hence,
resulting in allergic symptoms limited mainly to
the oral cavity. In addition to PFS, latex-fruit
syndrome is also well-known as the disease
exhibiting OAS. In treating the condition, it must
be noted that most but not all symptoms of PFS
are those of OAS. In many cases, antigens
become edible by heating, but some are resistant
to heating. Also, since the exacerbation of atopic
dermatitis is occasionally observed after the
intake of cooked antigens in asymptomatic
individuals, careful inquiry of the history is
important in designing the treatment.
Immunotherapy against the cross-reacting pollen
has also been attempted in PFS.
HISTORICAL CONFUSION
There used to be controversy over the definition
of OAS. In 1987, Almot et al.1 first reported
allergic symptoms induced by eating a food
yielding a positive skin test that are primarily oral
mucosal symptoms which occasionally spread to
the entire body as OAS. They did not mention
whether the patients had pollinosis, and the
causative foods included shellfish, fish, and eggs.
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At that time, the term OAS did not attract much
attention, but a report by Ortolaniet al.2 in 1988
directed attention toward it. Since the symptoms
observed after patients with birch pollinosis ate
fruits and vegetables were in agreement with
those of OAS reported by Amlot, they reported
262 pollinosis patients who developed symptoms
localized to the oral mucosa caused by the
ingestion of fruits and vegetables as cases of
“OAS”, making the term OAS international. OAS
has become widely known with a new definition,
i.e., localized oral symptoms due to a labile
allergen observed after patients with pollinosis
have eaten a fruit or vegetable. This historical
background led to confusion among researchers
concerning the definition. In 1994, Liccardi et al.3
reported oral symptoms without generalized
symptoms caused by the ingestion of eggs or egg-
containing foods in a patient with no pollinosis as
OAS. In response to this, Kelso4 stated that the
condition might have been usual egg allergy
rather than OAS, because the patient had a
history of egg-induced hypotension. Liccardi et
al.3 responded that the hypotension record was
inappropriate as it was based on the self-
judgment of the patient and argued that no
generalized symptom was observed on any of the
confirmation challenge test using egg. To avoid
such confusion related to the term OAS, food
allergy due to a cross-reaction between pollen
antigen and fruit or vegetable antigen has been
called the more specific term “pollen-food allergy
syndrome (PFS)” 5,6.
ETIOPATHOGENESIS
OAS manifestations occur after the patient who
is allergic to pollen consumes certain fruits,
vegetables, or nuts. OAS belongs to the allergy
type I group, that is, allergic reactions mediated
by immunoglobulin E (IgE). In susceptible
patients, the immune system produces IgE
antibodies against the proteins of pollen which
causes hay allergy. Pollen allergies are caused by
repeated exposure to the pollen of some plants,
which are usually pollinated by air and have such
pollen quantities that inhalation of the pollen
easily reaches the surface of the pulmonary
alveoli. The proteins which are structurally similar
to pollen are also found in food. The OAS patient
is first sensitized by inhaling pollen that contains
the antigens, and then after consuming food that
contains cross-antigens (to the inhaled antigens)
the symptoms characteristic of OAS appear.1
Plant-derived proteins responsible for allergy
include various families of pathogenesis-related
proteins, protease and α-amylase inhibitors,
peroxidases, profilins, seed-storage proteins,
thiol proteases, and lectins, whereas homologous
animal proteins include muscle proteins,
enzymes, and various serum proteins.5 Cross-
reactivity between birch pollen and various fruits
and vegetables is due to homology among
various pathogenesis-related proteins, which are
important in the defense against plant diseases.
For example, Mal d 1, the major apple allergen, is
63% homologous to the major birch pollen
allergen, Bet v 1. Other birch pollen-related,
pathogenesis-related proteins have been
identified in hazelnut and celery (Api g 1).
Similarly, the birch pollen profilin, Bet v 2, cross-
reacts with profilins found in apple (Mal d 2),
celery (Api g 2), and potato.6 The same immune
system can trigger allergic symptoms in two
different ways: in the presence of pollen it leads
to rhinitis and in the presence of a particular food
it leads to symptoms of food allergy. Different
allergens vary in their stability, with differences in
digestion survival, storage, high temperature,
cold, and cooking or pasteurization survival. As
important drivers of anaphylaxis, the lipid
transporting proteins play an important role,
since they cannot be easily denatured by
digestion or cooking. Antibodies can react to
linear amino acid sequences of the protein or a
conformational epitope. Persons who respond to
the linear sequence of the protein can tolerate
neither raw nor cooked food, while those that
respond to a conformational epitope can
consume cooked food but not the raw
food.1Certain foods like peanuts are able to
sensitize and elicit reactions after oral exposure
and could trigger responses that generalize to
related foods (legumes). In other groups of foods
like apples, sensitization to homologous proteins
encountered through respiratory exposure (e.g.,
birch pollen) may mediate reactions to cross-
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reacting proteins in the food.5 IgE mediated food
allergy is classified as classes 1 and 2. This
distinction is based on clinical appearance, the
predominantly affected group of patients
(children or adults), and disease-eliciting food
allergens. Primary (class 1) food allergy starts in
early life and often represents the first
manifestation of the atopic syndrome. The most
common foods involved are cow’s milk, hen’s
egg, legumes (peanuts and soybean), fish,
shellfish, and wheat. The allergens contained in
these foods not only elicit allergic reactions in the
gastrointestinal tract but also often cause
urticaria, atopic dermatitis, and bronchial
obstruction. With a few exceptions, most
children outgrow class 1 food allergy within the
first 3 to 6 years of life.7 Secondary (class 2) food
allergy describes allergic reactions to foods in
mainly adolescent and adult individuals with
established respiratory allergy, for example, to
the pollen of birch, mugwort, or ragweed. This
form of food allergy is believed to be a
consequence of immunological cross-reactivity
between respiratory allergens and structurally
related proteins in the respective foods. OAS
belongs to this group.7 Food allergens that induce
OAS rapidly dissolve in the oral cavity and are
readily broken down by digestive enzymes.8
Preservatives in foods may also trigger the
manifestation of the disease. Due to the
structural similarity of individual protein
molecules, a large number of allergens that exist
in nature can be classified into groups as
follows1,8 (Table 1). Among the allergens in each
group there is a possibility of cross-reactivity of
IgE antibodies, that is, antibodies binding to one
of two or more allergens. The reaction may start
with one type of food, and subsequently allergies
to other food types can develop.1
Latex allergens can also sensitize patients to
cross-react to the protein found in some foods.
One of the most notable features of latex allergy
is the patients’ cross-reactivity to various fruits
and vegetables, a condition often called latex-
fruit syndrome. The first report of an allergic
reaction to banana in a latex allergic patient was
published in 1991.9,10 Structurally similar proteins
in many kinds of plants must be responsible for
such extensive cross-reactivity.11 Commonly
reported cross-reactive foods include banana,
avocado, kiwi, chestnut, potato, and papaya, and
numerous latex allergens cross-react with food
and pollen proteins.5 Rarely OAS is induced by the
ingestion of other foods in subjects without
pollen sensitization, for example, shellfish and
pork.12,13 Honey is considered to be another food
which can cause OAS. During collection, grains of
pollen are admixed to this raw material which
retains their allergenic properties during the
honey making process.14More and coworkers
reported that some patients presented with OAS
symptoms after eating foods cooked over
mesquite wood and individuals were positive to
skin prick test with mesquite pollen extract.15
DIAGNOSIS
Food allergy diagnostics are one of the most
difficult tasks in allergology, especially when
there is no clear connection between the
development of the clinical features and the
ingested food or when food allergy takes an
atypical or chronic course. The diagnostic
methods can be divided into two groups: clinical
and laboratory. Among the group of the clinical
method’s, clinical history, eating habits
investigation, skin tests, and challenge tests are
used for their high informative value. Trial
elimination diets are also applied. The specific IgE
antibodies assay is the most important among
the laboratory methods.22
Skin testing for IgE mediated reaction can be
carried out using different methods: the prick
method (prick test), the application of
allergens via scratching the skin (scratch test),
and rarely an intradermal test (application of
allergens into the skin by a needle). Commercial
extracts are used for prick tests, determining
allergy to peanuts, hazelnuts, and peas. Prick
tests are not carried out in areas of dermatitis or
in areas where dermo corticosteroids or
immunomodulating creams have been applied.22
The skin prick test is performed with commercial
extracts of pollens and food on the forearm or
the back, measuring the wheal after 15 minutes,
and is considered positive if the diameter of the
wheal is greater than 2 mm of the negative
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control sample.3 The commercially available fruit
extracts used in allergy testing are not usually
reliable indicators of allergy in patients with oral
allergy syndrome, because the cross-reactive
epitopes have been destroyed by the
manufacturing process. Prick-plus-prick testing
(prick the fruit and then prick the skin) with
freshly prepared fruit extracts is more sensitive in
detecting allergen specific igeantibody.23 If the
history is positive and the prick test is negative, a
provocation test with a fresh food should be
conducted. An oral provocation test represents
the safest confirmation of the presence of the
disease. In doing so, the person first consumes a
suspected food, and subsequently the onset of
symptoms is recorded. To set up an accurate
diagnosis, it would be necessary to keep a diary
of food consumption as the basis for
determination of which food tests to undertake.
Good history can focus the testing on a specific
type of food, and thus the doctor can act more
rationally.1 Blood tests are mostly performed as
RIST (Radio Immunosorbent Test) for the
determination of total igeand RAST
(Radioallergosorbent Test) for the determination
of specific IgE antibodies to a particular allergen.
A blood test is usually used when there is no
possibility of skin tests.23Extensive research has
led to the identification of principle allergens in
cross-reactive food. Many allergenic components
have been produced in a recombinant form
maintaining their immunoreactivity and
allergenic epitopes. These allergens are applied
to a chip-based microarray that uses small
quantities of serum and provides igeantibody
profiles to over 100 food and pollen allergens.
However, most of the in vitro diagnostic tests are
expensive and the cost factor limits its use.24
Radioallergosorbent testing is more sensitive
than skin prick testing with commercial extracts
but is less sensitive than skin prick testing with
fresh extracts.25 CAST-ELISA (cellular antigen
stimulation test in combination with enzyme-
linked immunosorbent assay) is more specific
diagnostically for allergy to celery, hazelnut, and
carrot when compared to commercial skin prick
tests and allergen-specific IgE analysis. The CAST-
ELISA is a method for assessing IgE- and non–IgE-
mediated allergies. The test measures
sulfidoleukotriene release by sensitized
leukocytes after specific allergen stimulation.26
The released leukotrienes are measured by an
ELISA test. A concentration of sulfidoleukotrienes
greater than 200 pg/mL above the spontaneous
production level is a positive result. Component-
resolved diagnosis using microarray techniques
has also been used in the diagnosis of IgE-
mediated allergens, yet its utility in discriminating
between sensitization versus real allergy is
questionable.27
MANAGEMENT
A multidisciplinary approach in patients with OAS
is necessary, which involves different professions
(ear-nose-throat specialists, oral pathologists,
immunologists, dermatologists, pediatricians,
gastroenterologists, and various other
specialties). There is no standard treatment
established for OAS except avoiding implicated
food.28 The OAS should be managed according to
the clinical presentation.23 The easiest and safest
way to treat oral allergy syndrome is to
recommend that the patient avoid the foods that
cause the problem. Cross reactivity varies among
patients. Only those foods causing the clinical
allergy need to be avoided. Most patients with
seasonal allergic rhinitis can be treated with a
combination of allergen avoidance and
pharmacotherapy.9 Immunotherapy may be
beneficial if a single allergen is
implicated.8 Pollen-specific immunotherapy can
be used to treat rhinosinusitis, conjunctivitis and
asthma resulting from exposure to birch or tree
pollen.8,10 Since many of the immunogenic
proteins in fruits and/or vegetables are unstable
(heat-labile), patients will tolerate food cooked
and canned well and fresh or raw foods badly. It
has been shown that cooking food can
sometimes eliminate allergens in certain species
like apples, while it is impossible to destroy
allergens in celery and strawberries. For some
types of food (e.g., nuts) that contain more than
one allergen, heat treatment will destroy certain
allergens, while some of them can cause a
reaction even after that.1 Education is the key
pillar of an effective long-term elimination diet.
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Patients, their families, close relatives, and
caregivers should be aware of risk situations and
should be instructed in reading labels and how to
avoid the relevant food allergens both inside and
outside the home.29 Most patients with OAS can
be treated with a combination of allergen
avoidance and pharmacotherapy. The most
important therapy includes antihistamines. Oral
antihistamines such as cetirizine 10 mg or
intramuscular aqueous epinephrine at the dose
of 0.01 ml/kg of 1 : 1000 dilution can alleviate
allergic symptoms by blocking specific immune
pathways.30 Patients with a history of anaphylaxis
should always carry a shot with a dose of
epinephrine with them. In the event of a reaction,
the patient is advised to stay calm, rinse their
mouth with plain water, and rest. The patient can
use hot beverages that can inactivate residual
allergens. This usually leads to withdrawal of the
sensation of prickling, itching, and swelling, which
stops within 30 minutes to an hour (before the
antihistamine makes an effect). When the patient
is able to swallow a dose of antihistamines, they
definitely need to be taken. However, severe
symptoms are rare in patients with OAS.1 In
patients with suspected OAS, preemptive caution
is necessary because the preparation of food can
be connected to reactions. Wearing gloves and
masks can help prevent contact with allergens. It
is also recommended to avoid latex (rubber
gloves) that can cause cross-allergic reactions to
foods of plant origin. If the patient avoids areas
of certain types of pollen, the syndrome usually
relieves after two to three years.1Desensitization
to the pollen with immunotherapy is
recommended in some cases and can sometimes
help minimize cross-reactions.2 Immunotherapy
may be beneficial if a single allergen is
implicated.23 Subcutaneous specific
immunotherapy (SIT) has been tried and has
significantly reduced OAS symptoms associated
with ingestion of the responsible fruit and
vegetables.24 According to a study by Asero, at
least in some patients pollen SIT can exert a long-
lasting effect on pollen-associated food allergies
(patients sensitized to birch pollen were still able
to eat apples without any complaints as long as
30 months after the end of SIT).31 A study by
Bergmann et al. Also suggested that pollen-
specific SIT can reduce OAS triggered by pollen-
associated foods in patients with pollen-induced
rhinoconjunctivitis.32
CONCLUSION
Allergy or intolerance to the food we eat may be
a problem routinely encountered. Though OAS is
mainly managed in allergy clinics, it is equally
important for the oral physicians to be aware of
the symptoms and clinical features of OAS. It is
equally important to record patient’s history
accurately regarding previous episodes of
allergies. An orderly approach should be followed
in managing the patients with OAS. The dentists
should pay attention especially to the individuals
with a history of asthma, atopy, or any other
allergic problems during the dental treatment
procedures. Even though the symptoms of OAS
are mild in most of the cases, they can manifest
life-threatening complications occasionally.
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Table 1: Types of pollen and food associated with oral allergy syndrome
Pollen
Fruit
Vegetable
Nuts
Grains
Birch
Kiwi, apple, pear, plum,
peach, nectarine, apricot,
cherry, banana, fig,
avocado, strawberry, dried
plum, mango
Celery, carrot, parsnip, parsley,
dill, cumin, cilantro, fennel,
potato, tomato, pepper
(green), chicory
Hazelnut,
almond,
walnut,
peanut
Soybeans,
wheat,
lentils, peas,
beans
Ragweed
Banana, watermelon,
melon, honey dew,
cantaloupe
Squash, pepper, cucumber,
artichoke, hibiscus, zucchini,
chamomile tea
Sun
flower seeds
Weeds
Melon, watermelon,
orange, kiwi
Tomato
Wormwood
Apple, watermelon, melon
Celery, carrot, parsley, pepper,
cilantro, fennel
Parietaria
Cherry, melon
Grass
Fig, melon, orange, kiwi,
watermelon
Tomato, potato
Peanut
Alder
Apple, cherry, peach,
pear, strawberry,
raspberry
Celery, parsley
Hazelnut,
almond,
walnut
Japanese
cedar
Tomato
Mugwort
Mango
Celery, carrot
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Plane
Apple
Lettuce, corn
Hazelnut,
peanut
Chickpea
Table 2: List of reported cases on various food items causing OAS symptoms.
S. No.
Food
Manifestation
1
Jackfruit
Itching and burning in the mouth and throat
2
Salami
Mild pruritus in oral mucosa
3
Pork
Itching and angioedema of the lips and oral mucosa
4
Honey
Itching in the mouth, gastrointestinal symptoms, and angioedema
5
Tomato juice
Dyspnea, swelling of the oral and nasal mucosa, and congestion of the bulbar
conjunctiva
6
Raw fish
Oropharyngeal irritation and facial angioedema
7
Peanut
Lip tingling, oral itching, lip swelling, and throat itching
8
Cashew nut
Sialorrhea, perioral urticarial rash, tongue swelling, and immediate vomiting
9
Grapes
Flushing of the face and neck, followed by local itchy skin rash, itching and edema of
the oral and perioral mucosa, and moderate dyspnea
10
Sapodilla plum
Lip edema, accompanied by itching in the lips, tongue, and throat, as well as a
feeling of dryness and hardness in the throat (glottic edema)
11
Cooked
aubergine
Oral itching and significant perioral urticaria
12
Pistachio nuts
Oral and lip itching and swelling
13
Royal jelly
Lip, tongue edema, and palate itching
14
Mango
Oropharyngeal itching, tiredness, dizziness, and swelling of the face