January 2008
Food
Allergies: Type II, III, and IV Hypersensitivities
By Janice M. Vickerstaff Joneja, PhD, RDN,
and Dale Ames Kline, MS, RD, CNSD, LD
Today’s Dietitian
Vol. 10 No. 1 P. 10
CDR Learning Codes: 2000, 2060, 5110; Level
III
Editor’s Note: This is the second
of a two-part series on food allergies and the immune system.
The first part, “Food Allergies: The Immune Response,”
appeared in the July 2007 issue of Today’s Dietitian
and is available as a free download at www.todaysdietitian.com/tcpeexam.shtml.
The previous article discussed the difference
between a food allergy, which is an immunologic response to
ingested food, and a food intolerance, which is the result of
nonimmunologic mechanisms. The immune mechanisms that cause
the most common food allergy, immunoglobulin E (IgE)-mediated
hypersensitivity, and its symptoms were explained. This article
will pick up where Part 1 left off and discuss other types of
food allergies and intolerances.
Type II and III
Hypersensitivities
Type II and III hypersensitivity reactions resemble the type
of immune response triggered by an invading pathogen—a
virus or bacterium likely to cause disease if not effectively
eradicated from the body. This reaction is initiated by Th1
lymphocytes. The foreign antigen is processed by antigen-presenting
cells and recognized by T-helper cells, a reaction described
as Th1-mediated. This leads to the production of antigen-specific
antibodies of the immunoglobulin M (IgM) isotype, followed by
an isotype switch to immunoglobulin G (IgG) antibodies.Unlike
IgE, IgG does not directly initiate degranulation of mast cells.
Instead, the coupling of IgG and its homologous (specific) antigen
leads to a complex series of reactions involving triggering
the complement cascade. In this, a specific sequence of reactive
proteins is activated, designed to lead to the final destruction
of the invader by a process of cell lysis.1
As a consequence of the activities of the complement
system proteins, several newly formed proteins emerge, two of
which (C3a and C5a) are powerful anaphylatoxins that are able
to degranulate basophils and possibly mast cells without the
mediation of IgE. In addition, complement protein C5a and at
least one other complement system protein complex act as chemotaxins
and attract granulocytes to the reaction site to augment the
local response with their own inflammatory mediators.
The IgG-mediated “allergy” to drugs
is a recognized phenomenon.2 Penicillin-induced, Coombs-positive
hemolytic anemia is an example of a type II hypersensitivity
reaction. Penicillin causes the body to produce IgG antibodies
to the drug. The body attacks its own red blood cells containing
the IgG antibody to penicillin, causing red blood cell destruction.
The difference between a type II and III hypersensitivity
reaction is that a type III reaction can be caused by not only
external sources but also antigens to “self.” The
damage in a type III hypersensitivity reaction is from immune
complexes and complement. Immune complexes are formed when antigens
bind to antibodies and form a complex, which can cause an immune
reaction, damaging organs or tissues. Type III hypersensitivity
reactions to antibiotics such as penicillin have been identified,
with symptoms such as serum sickness, rash, painful joints,
and hives.
Systemic lupus erythematosus is another example
of a type III hypersensitivity reaction in which the body attacks
“self” cells and immune complexes are formed. As
a result of the formation of the antigen/antibody complexes,
the complement cascade is active and anaphylatoxins are released,
which mediate the degranulation of mast cells. Consequently,
inflammatory mediators are released, which results in inflammation
and widespread tissue damage.
IgG-mediated reactions are sometimes called
anaphylactoid reactions to distinguish them from IgE-mediated,
or anaphylactic, responses.3
Can IgG Hypersensitivity
Cause Food Allergy?
It is relatively easy to measure the level of antigen-specific
IgG in blood, and many laboratories now offer “food-allergy
blood tests” that measure the IgE and IgG antibodies against
specific foods (antifood IgE and IgG). Some practitioners believe
that food allergy symptoms that occur from one to several hours
(up to 24) after consumption of the allergenic food (delayed
food allergy) represent IgG-mediated food allergy, especially
when allergen-specific IgE is low or absent.
Theoretically, the release of inflammatory mediators,
either by the action of anaphylatoxins or direct bonding of
antifood IgG to IgG receptors on basophils, may occur.4 IgG-mediated
allergy to egg whites and fish have been reported.5
The delay in the onset of symptoms is thought
to be due to the increased time required for activation and
progress of the complement cascade prior to release of the inflammatory
mediators responsible for the symptoms. However, the mere presence
of antifood IgG, even at high levels, does not necessarily indicate
that the food is the cause of the reaction.
It is common to find antifood IgG antibodies
circulating in blood, even in people who have no signs or history
of adverse reactions to foods. In fact, an increase in antifood
IgG in some cases may be indicative of successful treatment
of an IgE-mediated allergy.6
The subject of IgG-mediated food allergy is
complicated because of the antibody’s nature and the immunological
reactions associated with it.
Food Allergy-associated
IgG
Four distinct subclasses of IgG have been identified: IgG1,
IgG2, IgG3, and IgG4. Of these, IgG4 seems to be the subclass
with a high affinity for food antigens. IgG4 represents a very
small proportion of total IgG in normal sera, but reports of
the level of IgG4 differ from laboratory to laboratory (range
of 0.7% to 4.9%).7
In a newborn baby, IgG1 and IgG3 levels rise
rapidly, and IgG1 may reach concentrations close to the adult
level at the age of 8 months. In contrast, IgG4 is still only
a fraction of the adult level at the age of 2 and may not reach
adult levels until the age of 12.8 IgG4 differs from all other
IgG subclasses in that it does not trigger the complement cascade
by the classical pathway and therefore is least likely to lead
to an inflammatory response.7
There is some evidence that antifood IgG may
represent some protection from IgE-mediated food allergy. In
a 1978 study, symptom-free children had higher levels of IgG
antibodies to milk and egg proteins than those who developed
allergic symptoms.9 Results from a later study suggested that
a high IgG/IgE ratio in cord blood was a good prognostic sign,
suggesting a decreased risk for food allergy.6
In contrast, other studies suggest that increased
levels of antifood IgG, especially IgG4, may be associated with
allergy, particularly IgG4 antibodies to the milk protein beta-lactoglobulin
in atopic dermatitis (eczema) in children.10
IgE-mediated food allergy in infants is frequently
associated with an increase in gut permeability, which may allow
antigenic food molecules to pass into circulation, triggering
production of antifood IgG. Therefore, it is logical to expect
to find higher-than-normal levels of antifood IgG in these infants.
It is possible that these antifood IgG antibodies would represent
a protective mechanism rather than a source of allergic pathology.11
Future research needs to determine the role of IgG, especially
IgG4 antifood antibodies, in allergy.
Type IV Hypersensitivity
The type IV hypersensitivity reaction is commonly known as a
contact allergy. It involves cell-to-cell contact between the
antigen (allergen) and T-cell lymphocytes, usually in the skin.
Some of the T cells respond to the antigen by producing soluble
inflammatory mediators while others develop cytotoxicity, causing
damage to cells in the surrounding tissue. The reaction continues
as long as the antigen is in contact with body cells; thus,
it is often referred to as a cell-mediated response. No antibodies
are produced. The reaction appears to be mediated by cytokines
such as interleukin 1, interleukin 2, and interferon-gamma released
by T cells.12
The allergen involved in a type IV hypersensitivity
reaction is usually a simple chemical called a hapten that would
normally be unable to elicit an immune system response. By linking
with a body protein (usually in the skin), it becomes antigenic.
A type IV hypersensitivity reaction is typically a delayed response
visible 24 to 72 hours after the skin’s exposure to the
allergen and is normally diagnosed by means of patch tests.
The suspect allergen is applied to the skin and covered by an
adhesive bandage, and the site is examined after a delay of
up to 72 hours for development of the characteristic reddened
wheal.
Although a type IV hypersensitivity reaction
can cause damage to intestinal cells in animals, there is no
clear evidence that food can mediate such a reaction in the
human digestive tract.13 However, a type of dermatitis on the
hands of sensitized individuals in contact with raw foods such
as a potato, tomato, apple, watermelon rind, or carrot has been
linked to a type IV hypersensitivity response. Speculation has
followed that if such a reaction occurs on the hands, a similar
response may be expected in the gut epithelium when the food
is eaten. At present, there is no good evidence for this, since
there are no methods available for assessment of such a reaction
within the intestinal epithelial tissue.14
Oral allergy syndrome (OAS) and latex allergy
are examples of conditions in which contact with the offending
allergen results in local reactivity. Both conditions can lead
to severe allergic reactions, and latex allergy is becoming
an increasing problem among healthcare workers. Although latex
allergy is thought to be initiated by a type IV hypersensitivity
reaction, IgE-mediated type I hypersensitivity is the reaction
responsible for the acute symptoms in both OAS and latex allergy.
Nickel Contact Dermatitis
and Food Allergy
An association between food and contact allergy has emerged
from observations of nickel-associated dermatitis. Contact allergy
to nickel, often suspected when dermatitis develops at sites
where nickel-containing jewelry, watchbands, and other metal
objects touch the skin, occurs in approximately 10% of females
and roughly 3% of males.15 Since the mid-1970s, a number of
reports have indicated that dermatitis, especially on the hands,
can be aggravated by oral administration of nickel.16-18
Since nickel occurs in many foods to varying
degrees, it was assumed that a diet low in nickel may cure or
reduce the severity of dermatitis in people who responded positively
to oral nickel challenge.17 However, there are differing opinions
about what constitutes a low-nickel diet and the degree to which
symptom improvement can be achieved on such a regimen.15
Nevertheless, nickel-associated dermatitis serves
as an example of the possible association between food constituents
and the immune system that differs from the more familiar protein/glycoprotein
antigen in an IgE-mediated reaction. Future research will no
doubt elucidate the nature of the reaction and possibly uncover
other similar interactions.
Allergy: An Inflammatory
Process
Regardless of the hypersensitivity reaction involved, allergy
symptoms result from the release of inflammatory mediators that
act on body tissues and cause the clinical condition. In other
words, allergy is an inflammatory process, and each inflammatory
mediator released in the hypersensitivity reaction has its own
effect.
For example, histamine increases the permeability
of small blood vessels (capillaries), so fluid moves from the
vessels into tissues and causes swelling in various body sites.
Histamine is the only known mediator of itching and also causes
a widening of blood vessels (vasodilation) and constriction
of smooth muscle (eg, around major organs such as the lungs).
These effects result in symptoms such as rhinitis (nasal congestion),
earache (sometimes with itching and effusion), urticaria (hives)
on the skin, and swelling, often of facial tissues (angioedema).
Other effects from histamine are flushing or
reddening, headache, hypotension (decreased blood pressure),
tachycardia (increased heart rate), bronchospasm due to contraction
of smooth muscle around the lung, and mucosal edema (swelling
and irritation in mucus membranes).
Prostaglandins, on the other hand, mediate both
vasodilation and vasoconstriction. Leukotrienes cause contraction
of smooth muscle and are largely responsible for the bronchospasm
of asthma. Bradykinin, in conjunction with prostaglandins, causes
pain.
Allergy is the result of the combined effect
of all of the inflammatory mediators. Treatment usually involves
symptomatic relief with drugs designed to combat the local effects
of each type of mediator.
Nonallergenic
Mast Cell Degranulation
The definition of allergy as an immune system-mediated
process becomes a little unwieldy, considering there are mechanisms
that lead to the degranulation of mast cells that do not require
initial stimulation by an allergen.19
Nevertheless, because the inflammatory mediators
are released, the resulting symptoms are the same whether or
not their release was allergen mediated. The key event is the
degranulation of the mast cell. Since the mast cell is an essential
immune system component, these reactions should be included
under the umbrella of immune-mediated reactions.
Two important factors that can stimulate mast
cell degranulation are substance P and vasoactive intestinal
peptide. These are neuropeptides and are frequently detectable
in the gastrointestinal tract.19 It is possible that they may
stimulate the degranulation of intestinal mast cells, resulting
in inflammatory mediators being released into the area and contributing
to a chronic inflammation, which may present as irritable bowel
syndrome.20
Physical factors can also lead to mast cell
degranulation. The abrasion of the skin leading to reddened
wheals in dermatographia, inhaled cold air passing over the
surface of hypersensitive airways in asthma, and cold-induced
urticaria are examples of this type of physical degranulation
mechanism.21
Some medications such as codeine and morphine
can induce mast cell degranulation. Biologically active chemicals
such as interferon, phospholipase, and chymotrypsin and certain
serum factors and basic polypeptides involved in other physiological
processes can likewise release inflammatory mediators from mast
cells.19,22
A great deal of research is required in this
field, which is presently poorly understood, but recognizing
that factors other than the well-known inhaled, ingested, and
injected antigens can lead to symptoms resembling allergy should
alert practitioners to the fact that sometimes the search for
an external allergenic cause for an adverse reaction may be
futile.
Prevalence
Accurate statistics on the prevalence of food allergy in the
general population are difficult to obtain. Consumer surveys
in North America and Europe indicate that one third of the population
believes they have food allergies.23,24 However, the medical
literature suggests that true food allergy (defined as an immediate,
IgE-mediated type I hypersensitivity reaction) is uncommon.
Based on double-blind, placebo-controlled food
challenges, skin tests, and blood tests to detect antifood antibodies,
the consensus seems to be that food allergy affects up to 8%
of children under the age of 5 and 1% to 2% of the adult population.11,25-27
Food allergy is more common in children than
adults, and the majority of children with food allergies experience
symptoms of food-related allergy during the first year of life.28
Most children with food allergies outgrow their early ones,
especially to cow’s milk and egg proteins, by the age
of 5, but some IgE-mediated food allergies may persist throughout
life.27,29
The most severe allergic response to a food,
a life-threatening anaphylactic reaction, mediated by a type
I hypersensitivity reaction, is very rare. Estimates indicate
that approximately 100 fatal cases of food-related anaphylaxis
occur in the United States each year.30 However, because it
may result in deadly anaphylactic shock, such a reaction to
a food is always treated aggressively. Extreme precautions to
avoid the allergen are crucial.31,32
Statistical studies of the incidence of food
allergy may not be representative of the incidence of adverse
reactions to foods that are mediated by mechanisms other than
type I hypersensitivity. In adults, non–immune-mediated
intolerance seems to be much more common than food allergy.
Due to the lack of definitive, objective tests, it is impossible
to provide reliable statistics. Some practitioners estimate
that up to 50% of the total population may experience some degree
of food-related reaction.
Allergenic Foods
Every food contains potentially allergenic proteins, but some
are more likely to cause an allergic reaction than others.33,34
In general, the top eight foods that are more frequent causes
of allergy are peanuts, tree nuts, shellfish, fish, eggs, milk,
wheat, and soy. Children under the age of 5 are more vulnerable
to the development of food allergies because of their immature
immune and digestive systems. Cow’s milk proteins, egg
proteins (especially ovalbumin), and peanuts are the most common
foods causing type I hypersensitivity in children. Although
there are many more food allergens, the top eight account for
approximately 90% of food allergies. See Table 1 for a list
of the food sources of tree nuts and foods to avoid with a tree
nut allergy.
In January 2006, the Food Allergen Labeling
and Consumer Protection Act began requiring that foods containing
ingredients with the top eight allergens list those ingredients
in common terms or “plain English.” Thus, the new
law will make it easier for consumers to determine whether a
food contains an allergen. In the past, a food label might have
used the word “albumin,” and a consumer would not
know that the ingredient came from egg. Now, the manufacturer
must state albumin (egg) or casein (milk).
Food allergens that come from spices, spice
blends, and food colorings or flavorings are included in this
law. If the label states natural flavoring, it must state natural
flavoring (egg, soy, nuts) if that is the source of the flavoring.
In addition, it must state which fish, shellfish, or tree nut
is in the food product.
As mentioned previously, early food allergies
are often outgrown by the age of 5, but certain allergies to
foods—peanuts, nuts, shellfish, and sometimes fin fish—can
last a lifetime. These foods are most frequently implicated
in life-threatening anaphylactic reactions.31 Sometimes, inflammatory
mediators are released, or their levels are enhanced by food
components or food additives acting through mechanisms that
are independent of the immune system. This is presently classified
as food intolerance rather than allergy.
The Dietitian’s
Role
Understanding the mechanics of allergic reactions and intolerances
can help dietitians explain to their clients why identifying
allergenic foods is difficult and time-consuming. There are
many bogus “allergy tests” being offered to susceptible
clients. Dietitians can play a supporting role in treatment
by carefully monitoring clients’ participation in valid
testing and helping them provide the detailed information required.
They can also provide detailed dietary and nutritional advice
to avoid the culprit food(s).
Determining the foods responsible for clinical
symptoms requires elimination of the suspect foods for a trial
period in which the symptoms of concern should disappear. This
is followed by careful challenge of each individual food component
in a precisely selected and controlled fashion so that its effects
on the body can be monitored. This is the only way in which
the role of foods in the disease process can be determined accurately.
The laborious elimination and challenge process may be used
to confirm or refute any prior allergy tests or establish the
most appropriate therapeutic diet in managing specific food-related
conditions.
To determine which elimination diet is the most
appropriate, several pieces of information are required, including
the following:
• a careful medical history, ideally supplied
by the patient’s doctor (It is especially important that
any anaphylactic reactions suspected to be due to food be recorded.);
• exclusion of any other cause for the
symptoms, determined by diagnostic tests and procedures, carried
out by the patient’s medical advisors; and
• results of any allergy tests previously
carried out.
Dietitians can assist by carefully interviewing
the client to compile a detailed diet history (at least seven
days) and symptom record. Additional information should include
an assessment of the patient’s financial situation, living
conditions, cultural and religious food practices, and lifestyle
so that appropriate adjustments can be made in the directives
for substitute meals in the elimination phase of the program.
Additional information required in the choice
of the appropriate elimination diet is provided by a seven-day
food intake and symptom record, which the patient is instructed
to complete before attending the clinic. The patient should
record the following:
• all foods, beverages, medications, and
supplements ingested;
• approximate quantities of each;
• composition of compound dishes and drinks
(ingredient list);
• the time at which each was taken;
• all symptoms experienced, graded on
a four-point scale from mild to severe;
• time of onset and duration of the symptoms;
• whether medications were taken to control
the symptoms;
• symptom status on awakening in the morning;
and
• any sleep disturbance due to specific
symptoms.
Beyond these intake procedures, the dietitian
can assist in monitoring and advising the client during the
ensuing elimination and challenge regime and help plan a nutritionally
adequate diet once the test results are determined.
— Janice M. Vickerstaff Joneja, PhD,
RDN, is a researcher, an educator, and a clinical counselor
with more than 30 years of experience in food allergies and
intolerance. She holds a doctorate in medical microbiology and
is an RD/nutritionist with the Dietitians of Canada and the
American Dietetic Association. She has directed the Allergy
Nutrition Program at the Vancouver (British Columbia) Hospital
& Health Sciences Centre and taught in the School of Family
and Nutritional Sciences at the University of British Columbia.
A frequent presenter at worldwide symposia on allergies, she
is also in private practice in Kamloops, British Columbia.
— Dale Ames Kline, MS, RD, CNSD, LD,
is president of Nutrition Dimension Inc. A former hospital chief
clinical dietitian and nutrition educator in the Women, Infants,
and Children Program, she has written and edited continuing
education home study courses since 1984.
Table 1
Food Sources of Tree Nuts
• Almonds
• Artificial nuts
• Brazil nuts
• Caponatanut meat
• Cashews
• Chestnuts
• Filberts/hazelnuts
• Gianduja (a nut mixture in some chocolate)
• Hickory nuts
• Macadamia nuts
• Mandelonas (peanuts altered to look and taste like tree
nuts)
• Marzipan/almond paste
• Nan-gai nuts
• Natural nut extract (eg, almond, walnut)
• Nougat
• Nut butters (eg, cashew)
• Nut meal
• Nut oil
• Nut paste (eg, almond)
• Nut pieces
• Pecans (Mashuga Nuts)
• Pesto
• Pine nuts (Indian nuts, pinon nuts, pignoli nuts, pignon
nuts, pigñolia nuts)
• Pistachios
• Pralines
• Walnuts
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16. Kaaber K, Veien NK, Tjell JC. Low nickel
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Examination
1. Which of the following antibodies is produced in a type II
hypersensitivity reaction?
a. Immunoglobulin A
b. Immunoglobulin D
c. Immunoglobulin E (IgE)
d. Immunoglobulin G (IgG)
2. The tissue damage from a type III hypersensitivity
reaction is caused by which of the following?
a. IgE and mast cells
b. Immune complexes and complement
c. IgG and basophils
d. Degranulation of mast cells
3. The presence of antifood IgG always indicates a food allergy.
a. True
b. False
4. A family member develops a rash 24 to 72
hours after coming in contact with a chemical. The doctor diagnoses
it as an allergy. Which type of allergy is it?
a. Type I hypersensitivity
b. Type II hypersensitivity
c. Type III hypersensitivity
d. Type IV hypersensitivity
5. Clinical symptoms of a food allergy such
as rhinitis, earaches, hives, and swelling are caused by which
of the following?
a. Histamine
b. Cytokines
c. IgE
d. T lymphocytes
6. Based on double-blind, placebo-controlled
food challenges, skin tests, and blood tests, what is the prevalence
of food allergies in children and adults?
a. Up to 8% of children under the age of 5; 1% to 2% of adults
b. 10% to 12% of children under the age of 5; 3% to 6% of adults
c. Up to 8% of children under the age of 10; 2% to 4% of adults
d. 8% to 12% of children under the age of 10; 3% to 6% of adults
7. What are the most common food allergies in
children?
a. Shellfish, peanuts, and cow’s milk proteins
b. Egg proteins, wheat, and soy
c. Cow’s milk proteins, egg proteins, and peanuts
d. Egg proteins, shellfish, and peanuts
8. If an individual has a tree nut allergy,
which of the following foods should be avoided?
a. Peanuts, walnuts, pralines, and soy
b. Pesto, marzipan, walnuts, and pralines
c. Almonds, wheat, cashews, and pesto
d. Cashew butter, soy, marzipan, and peanuts
9. Which of the following statements about the
Food Allergen Labeling and Consumer Protection Act is true?
a. All foods that cause a food allergy must appear on the food
label in plain English.
b. Allergenic foods must be identified on all food labels, except
if they are found in miniscule amounts.
c. The source of flavoring and spices do not need to be listed,
even if they are an allergic food.
d. The top eight allergenic foods must be listed on the food
label in plain English, including flavorings and spices.
10. The optimal method for determining foods
responsible for clinical symptoms related to a food allergy
is:
a. a skin prick test.
b. blood testing.
c. elimination and challenge dieting.
d. hair analysis.
