A. Case study
B. More information
C. Editors' comments
E. CPD questions (South Africa)
A. Case study
A 20-month-old girl was referred with a diagnosis of wheat allergy after
not improving on a "wheat-free" diet. She was still experiencing
gastrointestinal symptoms such as diarrhoea and abdominal cramps approximately
2-3 times per week. The girl was breast-fed until the age of 1 year,
and solid foods were introduced at 6 months. Wheat, however, was introduced
only at 14 months, whereafter the symptoms started presenting. Skin
prick tests were negative for wheat, but wheat allergy was diagnosed
because of a strong clinical history of adverse reactions to wheat.
WHAT ARE THE POSSIBLE REASONS FOR THE CHILD
- The diagnosis made was not correct
- Non-compliance by the mother or caretaker
- Hidden allergens that the mother or caretaker is not aware of are
still included in the diet
- There is another food or substance that the child is reacting to
as well, in addition to the wheat
What are the possibilities that one needs consider at this point?
- Is the reaction caused by wheat, gluten, or either plus another
- Is there any other underlying allergic condition such as hayfever
or asthma that could be a further indication that an allergy is present?
In this case there was not.
- Type of reaction:
These symptoms can be the result of allergic or non-allergic causes.
Allergy symptoms can involve the gastrointestinal tract (abdominal
cramps, nausea and vomiting, oral allergy syndrome), but gastrointestinal
problems are evident in children with Celiac Disease (CD) as well.
These problems can manifest as abnormal stools (ranging from diarrhoea,
to soft and bulky, clay-coloured, foul-smelling stools and constipation),
abdominal distension, pain, flatulence, nausea, vomiting and intestinal
malabsorption. (Symptoms can also be mild, presenting as iron deficiency,
failure to thrive or poor school performance - discussed below.) If
we compare CD with wheat allergy, both have separately typical sets
of symptoms, but some symptoms are quite similar to each other. Wheat
intolerance was unlikely, as flatus and bloating were not prominent
- Onset of symptoms:
Onset of symptoms is usually delayed in CD, compared to an allergy,
in which symptoms can be either acute or delayed.
Although it was not relevant in this case, in general the ethnic background
of the child might provide a strong indication of CD being the cause,
as it primarily affects caucasians of northwestern European descent
and rarely affects Africans, people of Mediterranean extraction or
- Family history:
CD and allergies can both be inherited. A child is more likely to
have either if there is a family history present, especially if one
or both parents had/have it. Wheat allergy may be present in the absence
of a family history, but CD is probably always inherited. However,
as coeliac disease can be silent or latent, a family history is not
always reliable. There was no apparent family history of either in
SO, WHAT CAN WE DO AT THIS POINT?
- Reassess the patient's diagnosis.
- Repeat the skin prick test or do an IgE blood test, unless suspicion
of CD is prominent, in which case an antigliadin IgA test should be
done. (Endomysial antibody and/or transglutaminase are more specific/accurate
tests, and IgA can eliminate IgA deficiency.)
- Implement a food-symptom diary to identify a pattern between ingested
food and the symptoms experienced.
- Always refer for endoscopy/biopsy before an elimination diet if
blood tests are positive. (Negative blood tests despite positive family
history can indicate latent coeliac disease. The disease may develop
at any stage triggered by stresses or aging.)
- Go directly onto an elimination diet and challenge with wheat.
Reassessing the diagnosis is always important, as aspects can easily
be overlooked and some conditions can change or become more apparent
over time. A thorough clinical history was done. Up to this point the
mother was convinced that the reaction was to wheat, but was confused
about the cause of the persisting symptoms.
Should we consider doing another skin prick
test or do a blood test?
First, we need to consider the possible reasons for the initial skin prick
test having been negative:
- The reaction is to wheat, but is a non-IgE cellular response.
- The reaction is due to CD (which is not IgE mediated).
- The reaction is due to wheat intolerance (unlikely, as mentioned
- The patient was on antihistamines (which suppress skin histamine
response) at the time of the skin prick test, or the skin prick test
failed to pick up intestinal allergy.
- Techniques used were flawed.
- The reaction is not to wheat at all.
- Presence of parasitic infection
- Post-enteritis syndrome
- Carbohydrate intolerances such as lactose or fructose intolerance
The benefit of redoing a skin prick
test is that one can ensure that the correct techniques are used and
that the child is not on any medication that can influence the results.
The benefit of doing a blood test is that one can determine the total
serum-IgE level (to find out if there is any IgE-mediated reaction taking
place - even if it is not to wheat; this is only the case if parasitic
infections, etc., have been ruled out, as total IgE can be elevated
in these cases - but not specific IgE), as well as the serum-specific
IgE level to wheat. Blood tests were therefore done, but the total serum-IgE
and the serum-IgE levels for wheat were not elevated. What can this
mean? The reaction that is taking place is non-IgE mediated, which still
includes the possibility of non-IgE cell-mediated allergy as well as
CD. As noted, both of these can have delayed reaction times, and symptoms
can be diarrhoea and abdominal cramps (as in this patient).
As a further step to identify the cause
of symptoms, the mother was asked to keep a food-symptom diary. The
problem with implementing an elimination diet at this stage is that,
if further diagnostic tests for CD are done, the results can appear
normal. For example, the avoidance of gluten by CD patients results
in a decrease in the serum-antigliadin IgA and IgG levels, which thus
may be at normal levels on elimination diets.
The food-symptom diary was scrutinized,
and it was confirmed that the mother and other caretakers were complying
well with a wheat-free diet. Also, notably, the child was not ingesting
any rye or barley. She was receiving oat porridge some mornings, but
was not reacting with any acute or noticeable delayed reactions. Symptoms
commonly appeared approximately 1 day after the ingestion of "wheat/gluten-free"
There are many studies that suggest that
oats are safe in CD. Thus, the oats in the girl's diet would probably
not exacerbate CD, unless she was ingesting excessive amounts or there
was contamination by other gluten-rich foods present.
The mother was sure that she had done thorough
research on the "wheat/gluten-free" pasta and that it was
obtained from a reputable source. After obtaining more information on
the product, it was determined that the pasta was, in actual fact, made
from spelt. The manufacturing company was marketing it on their website
as a "wheat/gluten-free" pasta that had been "used successfully,
under physicians' supervision, as a wheat substitute for people who
have wheat allergies". This is incorrect, as spelt (and also dinkel)
is in actual fact non-hybridized wheat and is not tolerated by wheat-allergic
persons. This type of mistake is widespread.
CD and wheat allergy are thus still possibilities.
CD and wheat allergy can also be present at the same time. What would
be the next step at this point? As mentioned above, an elimination diet
is not recommended before antigliadin IgA and IgE is measured. An endoscopy
with intestinal biopsy may be required for certainty. Antigliadin IgA
and IgG antibodies to gliadin were found to be at normal levels, which
indicates that CD is unlikely. CD should, however, not be excluded as
a possibility yet. An intestinal biopsy can be done if one needs to
rule CD out totally. But when spelt was excluded from the diet, the
child improved rapidly. This rapid response would be more in line with
an allergy response than with CD, as CD symptoms take longer to improve.
After a symptom-free period, the child
was challenged with wheat, rye and barley one by one and reacted only
with wheat. This confirms the diagnosis of a non-IgE cell-mediated wheat
|TIP for Allergy Advisor users:
For assessing the diet history and food-symptom diary, the
"Hidden allergens" function under the Management
bar can be used to search for possible hidden allergens that
might be present in the diet. The program also has wheat-free
and gluten-free diet sheets that can be adapted to the individual
and printed out. The diet sheets include foods allowed, foods
restricted, ingredient items to avoid on labels (hidden allergens)
and examples of substitutes that can be used. Also under the
Management bar, "Substitutes and Recipes" enable
you to print out recipes and substitutes for the patient to
Adverse reactions to wheat can be divided into:
|A.) Immune reactions:
- Allergic immune reactions
- Non-IgE-mediated cellular response
- Non-allergic immune reactions
- Celiac Disease (CD) (producing IgA and IgG antibodies)
- Non-CD enteropathy
A wheat allergy involves an immune reaction
in response to an allergen that the body is exposed to. The production
of IgE antibodies can be involved or not. The reaction can be IgE-mediated,
or it can be a non-IgE-mediated cellular response.1
Intolerance does not involve the immune
system, and the mechanisms responsible for wheat intolerance include:
- an enzyme deficiency
- undigested food as a result of malabsorption syndromes or retrogradation
(starch has changed in such a way that the digestive enzymes cannot
digest it any longer), which result in bacterial fermentation in the
colon, causing specific symptoms.2 Under normal circumstances
also, some starch escapes digestion and becomes a bacterial substrate
in the colon.
- abnormal colonic bacterial flora present as a result of antibiotic
therapy, post gastroenteritis or an inappropriate diet, causing fermentation
with associated symptoms
The body's different mechanisms
of defence involved in each type of adverse reaction to wheat cause
symptoms which may be quite different from or confusingly similar to
each other. The severity of symptoms can vary considerably within each
type of adverse reaction, but the patterns are distinct. An allergy
can cause very mild to quite severe reactions (such as life-threatening
anaphylaxis), compared to wheat intolerance, which can cause significant
discomfort, but is never dangerous. CD can lead to serious long-term
complications if left untreated (discussed below).
Wheat allergy may be present in the absence
of a family history, but CD is probably always inherited. However, as
CD can be silent or latent, a family history is not always reliable.
Proteins and allergens in wheat
Wheat, like all other foods, contains a number of proteins (more than
100), of which some have been identified as allergens. Some are major
allegens (more than 50% of wheat-allergic persons react to these allergens)
and others minor (less than 50% of wheat-allergic persons react to these
allergens). The type and proportions of proteins in a cereal have a major
impact in determining the quality and end use properties of the cereal.3
Wheat proteins can be characterized by their solubility:
and by their type of protein:
- albumins (water-soluble) (These albumins are not similar to egg
or milk albumin.)
- globulins (salt-soluble, water-insoluble)
- glutens which are a mixture of 2 proteins:
- gliadins (28-42%), the major prolamin protein in wheat (soluble
in 70-90% alcohol)
- glutenins (42-62.5%), the major glutelin proteins in wheat (soluble
in dilute acid or alkali solutions)2,5,6,7
Prolamins are alcohol-soluble storage
proteins of cereal grains.3
The gliadin proteins are divided into alpha,
beta, gamma (all three are toxic to persons with CD) and omega gliadins
(non-toxic to persons with CD).5,8
The major proteins in wheat (albumin, globulin,
gliadin and glutenin) vary in proportion according to the type of wheat,
and this variability is one reason reactions to different wheat products
are not consistent.4,9,10
More about gluten:
|Wheat flour contains between 7 and
12% gluten proteins by weight.1 Gluten is composed of
two protein groups, namely gliadins, which give wheat dough its
flow characteristics, and glutenins, which provide the elasticity
in finished wheat products. These occur in approximately equal amounts,
but it is only the gliadin fraction, and in fact only some gliadins,
that cause adverse reactions.1,7 Gliadin is a type of
prolamin (a group of proteins with similar protein structures).
Other grains such as rye, barley, oats and triticale (wheat-rye
hybrid) each contain their own prolamins, which cause the same intestinal
damage in CD that gliadin causes. This is due to the similarity
in protein structure.
gluten is found only in wheat, although the term is commonly
used to refer to any similar prolamin protein in any grain
that is harmful to a person with CD.1,5,11,12
The following is a list of the type of prolamin in each
grain and the percentage that the prolamin contributes to
the grain's protein content:
- Wheat: Gliadin (69%)
- Corn: Zein (55%)
- Barley: Hordein (46-52%)
- Sorghum: Kafirin (52%)
- Rye: Secalinin (30-50%)
- Millet: Panicin (40%)
- Oats: Avenin (16%)
- Rice: Orzenin (5%)5
|Because the type and proportion of
prolamin proteins in these grains vary, the kind of reaction (if
any) they are likely to cause also varies.2,9,10,13,14
Corn, rice, other cereal grains such as sorghum, millet, teff, ragi
and Job's tears as well as buckwheat, quinoa and amaranth can safely
be ingested by a person with CD. Spelt and kamut, however, should
be avoided in CD.12,15
What about oats?
The safety of the ingestion of oats is still controversial. The amount
of avenin in oats is relatively small compared with the amounts of relevant
prolamins present in wheat, barley and rye. Therefore, the quantity
of oats consumed may be critical. Although many studies have proven
this grain safe to consume, there are still certain factors that need
to be considered. Most commercial oat products contain wheat flour or
gluten. Contamination of oats with wheat may occur due to the sharing
of equipment in grain processing and the rotation of crops (wheat may
be grown on the same field as oats were). Therefore, contamination may
be the cause of adverse reactions to oats often reported by gluten-sensitive
One should bear in mind that gliadins and
other prolamins are only some of the many proteins found in wheat, rye
and barley, and that the origin of an adverse reaction to these foods
is not necessarily a prolamin.
Wheat allergy refers specifically to adverse immune reactions to one
or more of the proteins/allergens found in wheat. When exposed to an
allergen in wheat, an allergic individual's immune system responds through
the release of IgE antibodies or through a non-IgE-mediated cellular
immune mechanism.4,16 Inflammatory mediators are released
and the allergic symptoms that are experienced result from the specific
effect of each inflammatory mediator on the body. If inflammatory mediators
are released or their levels enhanced by mechanisms that are independent
of the immune system, the reaction is due to an intolerance.9
As noted before, allergic reactions to
wheat can result from a wide range of proteins/allergens or a combination
of these. The majority of wheat allergies involve the albumin and globulin
fractions of wheat, but even gluten may also, rarely, induce IgE-mediated
Wheat allergy may be caused by the ingestion
of wheat-containing foods or by inhalation of or contact with flour
containing wheat (e.g., Baker's asthma: see below).2,4
have been identified as the culprits in certain allergic conditions:
- Baker's asthma: gliadin (a major allergen), alpha-amylase
inhibitors from the globulin fraction (a major allergen), acyl
coA oxidase, peroxidase, fructose-biphosphate aldolase, and
a polysaccharide containing mannoglucan
- Atopic dermatitis: gluten (a major allergen)
- Wheat-dependent exercise-induced anaphylaxis (WDEIA): gliadin
(a major allergen)
- Wheat allergy: alpha-amylase inhibitors
- Asthma: alpha-amylase inhibitors17,18,19,20
a. How common is wheat allergy?
Clinical experience suggests that it is a relatively common allergy,
but there are no accurate figures for prevalence. It is, however, more
prevalent in certain groups: for example, wheat allergy is responsible
for occupational asthma in up to 30% of individuals in the baking industry.4
Wheat allergy is most common in young children,
of which the majority will outgrow it within five years. This occurs
more quickly if the wheat-containing food is completely avoided. Those
who develop the allergy later in life will probably retain it.4,16
b. What are the symptoms?
Allergic reactions to wheat can be acute or delayed, occurring within
minutes or a few hours after eating or inhaling wheat. The symptoms
can involve the skin (urticaria, eczema, angioedema, atopic dermatitis),
the gastrointestinal tract (abdominal cramps, nausea and vomiting, oral
allergy syndrome) and the respiratory tract (asthma or allergic rhinitis).4,9,16
Wheat is one of the allergens causing Baker's asthma and has also been
associated with wheat-dependent exercise-induced reactions (see below).
Contact with or inhalation of wheat flour proteins is one of the
causes of baker's asthma (an occupational allergy), but allergens
other than the wheat itself (e.g., storage mites, yeast and baking
additives) may also be causes. Symptoms that may present include
rhinitis, skin itching/rash, ocular symptoms (including tearing,
itching and conjunctival injection), respiratory symptoms (including
coughing, wheezing, shortness of breath and sputum production)
and "grain fever".21,22
reactions: Exercise within 3 hours of wheat consumption can
induce an adverse reaction in susceptible individuals. In some
cases, this can also occur when wheat is consumed directly after
exercise. Typical symptoms experienced include asthma, urticaria,
angioedema, dyspnoea, syncope and anaphylaxis. A diet excluding
wheat, rye, and barley is indicated due to cross-reactivity.17,23
Coeliac Disease (gluten-sensitive
CD is a hereditary disorder of the immune system. A key mechanism of
the disease is immune-mediated T-lymphocyte activation in the gastrointestinal
mucosa following gluten ingestion. Inflammation of the intestinal mucosa
and atrophy of the villi occur, and can result in the inadequate absorption
of nutrients such as proteins, carbohydrates, fats, vitamins, minerals,
and, in some cases, water and bile salts. Undigested foods (including
protein and fats) that reach the colon are fermented by bacteria, possibly
causing some of the symptoms such as bulky, foul-smelling stools. CD
is caused by IgA- and IgG-mediated responses to gluten, and thus is
not IgE-mediated, like wheat allergy. The disease is permanent, and
damage to the small intestine will occur every time gluten is consumed,
regardless whether symptoms are present or not.2,4,9,10,11,13,14,24
It has been reported that as little as 0.1 grams of ingested gluten
can trigger symptoms.1
There are at least four mechanisms involved
at bowel level:
- glutaminase (an intestinal enzyme) deficiency
- increased permeability of the bowel to macromolecules, including
- the production of antibodies to the relevant prolamin, or a fragment
- increased production of inflammatory mediators
The onset of noticeable symptoms
of CD seems to be dependent on the following: exposure to wheat, as
when an infant is weaned (introduction of solids); predisposition through
family history; and some kind of "trigger" mechanism. Little
is known about this "trigger" but suspected factors include
physical or emotional stress, trauma such as surgery or pregnancy, over-exposure
to wheat, viral infection, other diseases, and even antibiotics.13,24,25
a. How common is CD?
CD is one of the most common life-long disorders in certain countries.
CD is frequently under-diagnosed, particularly in adults, who may present
with only subtle symptoms.2,4 In some countries the incidence
is as high as 1 in 200 (Sweden).4
Although there is a definite genetic component,
CD is apparently a multigene disease, and is not completely understood.17
As coeliac disease can be silent or latent, a family history is not
always reliable. It primarily affects caucasians of northwestern European
decent and rarely affects Africans, people of Mediterranean extraction
or Asians. It affects twice as many females as males.13,25
CD usually develops in childhood but can
begin at any age. Typically the disease presents at the age of 6-24
months, after wheat has been introduced into the diet, and in early
adult life (30's and 40's).4,13,16,25
b. What are the symptoms?
The clinical manifestations of the disease vary markedly with the age
of the affected person, the duration and severity of the disease and
the presence of extra-intestinal pathologic conditions.14
There is no typical set of symptoms. However,
there are "classic" symptoms (diarrhoea, bloating, weight
loss, anemia, chronic fatigue, bone pain, and muscle cramps), but CD
frequently presents with other symptoms. In some cases only one symptom
may be experienced (e.g., anemia, a run-down feeling, or behavioral
In infants and young
children: Symptoms usually arise after weaning and with
the introduction of cereals into the diet. In children,
gastrointestinal problems are more evident;2
they include abnormal stools (ranging from diarrhoea, to
soft, bulky, clay-coloured, foul-smelling stools, to constipation),
abdominal distension, abdominal pain, flatulence, nausea,
vomiting and intestinal malabsorption. Children also present
with irritability, apathy, loss of appetite, weight loss,
poor weight gain, short stature, muscle wasting, hypotonia,
general failure to thrive, poor school performance, bone
and joint pains, and occasionally rickets.2,4,9
It is not uncommon for symptoms
experienced during infancy to disappear during later childhood
or adolescence, and then to reappear later in life. The
disease does not disappear; the small intestine damage still
occurs during these years even though no symptoms are experienced.13
In older children and
adults: The symptoms may be quite varied, from severe
weight loss, diarrhoea and bulky, offensive stools to less
severe symptoms that may lead to a missed diagnosis. Subtle
complaints of abdominal bloating, cramping, flatulence and
constipation are often mistakenly attributed to irritable
bowel syndrome. Symptoms such as recurrent mouth ulceration,
miscarriages or failure to conceive may lead to further
investigations with an eventual diagnosis.
Some individuals present with
only anemia-related fatigue and have no gastrointestinal
symptoms. CD in these patients is likely to be limited to
the proximal small bowel where iron is normally absorbed,
with the rest of bowel being unaffected. This results in
otherwise adequate nutrient and fluid absorption. Other
manifestations of the disease include osteopenic bone disease,
infertility, tetany, ataxia and neurologic disorders. Recent
studies show the presence of ataxia in persons with serological
evidence of gluten sensitivity but without overt gastrointestinal
symptoms or evidence of small-bowel inflammation. The sole
manifestation of disease in such patients may be ataxia.2,4,9,25,27
What is dermatitis herpetiformis?
Dermatitis herpetiformis is a form of CD. It is a skin reaction to gluten
(granular IgA is deposited under the skin). Dermatitis herpetiformis
manifests as a blistering, burning, itchy rash on the extensor surfaces
of the body (mainly the back, sacrum, face, trunk, elbows, knees and
buttocks, but also inside the mouth) in strikingly symmetrical patterns.
In most of these individuals, intestinal biopsies are characteristic
of CD regardless of whether gastrointestinal symptoms are present. The
treatment is the same as for CD, but it may take two or more years after
the initiation of the diet before the rash clears.1,2,4,24
||compiled by Karen du Plessis
Food & Allergy Consulting & Testing Services (FACTS)
PO Box 565
by our editors
Prof Janice M. Joneja Ph. D.,
This case study brings
up a number of very important issues in the management of adverse
reactions to foods:
1. The correct identification of the culprit food(s) is crucial
for successful treatment of the problem. Skin tests and blood
tests, such as RAST and ELISA, are almost invariably the first
diagnostic procedures carried out in the search for a cause
of symptoms when allergy is suspected. However, as all of us
involved in the clinical practice of allergy know only too well,
tests for food-specific IgE, and skin tests in particular, are
only accurate in about 30% of cases. All such tests, even when
they are positive, must be followed by elimination of and challenge
with the incriminated foods before a definite diagnosis of allergy
to that food can be made.
2. In the case under discussion, all the tests for food-specific
IgE were negative. However, subsequent elimination and challenge
identified wheat as the culprit. This emphasizes the fact that
in many cases of adverse reactions to foods, we lack the research
data that would allow us to identify the etiological mechanism
responsible for the reaction. Therefore, it is very important
that a food and symptom record, together with a careful history,
should be used in identifying the likely culprits, especially
when skin and blood tests for the suspect food(s) are negative.
Each suspect food should then be eliminated and challenged as
part of the process of accurately identifying all causes of
the patient's symptoms.
3. Even though gluten was obviously suspect when the mother
had identified wheat as a trigger for the child's reaction yet
the child's symptoms persisted, it was very important that all
gluten not be removed from the child's diet before tests for
gluten-sensitive enteropathy (celiac disease) had been carried
out. Too often, when gluten sensitivity is suspected, people
remove gluten entirely from their diet before seeing their doctor,
because information about celiac disease is readily available
in many non-professional publications. Unfortunately, this means
that when such a patient presents to a doctor with suspected
gluten sensitivity, anti-gliadin antibody tests and intestinal
cytology will often be normal. Tissues and indicators of the
immune response quickly return to normal in celiac disease when
gluten has been removed from the diet. In such cases, the patient
will need to consume gluten-containing grains for a minimum
of four weeks before tests for celiac disease become positive,
during which time symptoms will be expected to recur.
4. Identification of spelt as a second trigger when all sources
of wheat had been eliminated from the diet indicates another
important aspect of correct management of food allergy. It is
not sufficient to eliminate only the obvious sources of the
allergen, but to be aware of all of the alternative terms and
hidden sources of the food. In the case of wheat, we have several
pitfalls to consider:
· There are many varieties and hybrids of wheat on the
market, which appear under several different names: spelt, triticale,
kamut, durum, bulgur, and semolina are just a few that the average
consumer may not be aware of as being potential sources of the
wheat allergen or wheat gluten.
· Some manufactured foods contain wheat flour, which
may not be included on a product label. It is especially difficult
to detect if the food is obtained from a bulk food bin. For
example, buckwheat noodles often contain wheat flour. Buckwheat
is not related to wheat, and is allowed on a wheat- and gluten-free
diet. Japanese soba noodles are traditionally made with buckwheat,
but the soba noodles sold in some stores and restaurants may
actually be made from wheat flour, or contain wheat flour. Likewise,
soy noodles and pasta often contain wheat flour as an ingredient.
Careful education and label reading is essential in the management
of all food allergies, but when the food is a common ingredient
and takes a multiplicity of forms in the diet, as is the case
with wheat sensitivity, awareness on the part of the consumer
is even more important.
Sabine Spiesser B.Sc. Dip.
When a person presents with a possible wheat sensitivity, it is
vital that blood tests, endoscopy and biopsy precede any dietary
intervention to ensure that a CD diagnosis is not missed. Adequate
quantities of wheat must be consumed prior to the procedures to
prevent false negative results. Sometimes CD presents with patchy
lesions, which are easily missed on endoscopy unless several biopsies
are taken. In some individuals CD is clinically silent. The patients
are asymptomatic and apparently healthy. Such cases of CD are
usually picked up when relatives of an active CD patient are screened.
The blood tests are positive for antigliadin and endomysial antibodies.
Occasionally IgA deficiency can be the cause of false negative
blood tests. IgA levels should ideally be determined. Patients
need to discontinue anti-inflammatory, immunosuppressive and cytotoxic
drugs prior to biopsy.
Failure to respond to a gluten free
diet could be due to accidental ingestion of hidden gluten, or
the presence of other food allergies or intolerances. Many patients
newly diagnosed with CD have concomitant lactose, sucrose and/or
disaccharide intolerance. Some may suffer from small intestinal
In wheat-allergic patients (positive
SPT), grass pollen allergy may be a cause of allergen exposure
when a patient's condition does not improve despite strict wheat
| Dr. Harris Steinman M.B.Ch.B.
Wheat allergic persons may also be affected by grass pollen. In
our experience, specific IgE to wheat can be raised in 70-80% of
children, but fewer among adults.
For more information on this subject and
other allergy and intolerance related topics, visit:
To join a professional food allergy discussion
list where this subject can be discussed further, go to http://groups.yahoo.com/group/AllergyDietitian
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Questions (for South African dietitians only)
PLEASE ANSWER ALL THE QUESTIONS
1. True or false: A wheat allergy may or may not involve the immune
2. Which of the following is not a mechanism
responsible for wheat intolerance?
(a.) An enzyme deficiency
(b.) Malabsorption syndromes
(c.) The release of inflammatory mediators
3. True or false: The alpha, beta and gamma
gliadin proteins are toxic to persons with Celiac Disease, but the omega
gliadins are not.
4. Which one of the following is toxic
to a person with Celiac Disease?
5. Which of the following fractions of
wheat does not cause an IgE-mediated allergy?
(d.) None of the above
6. True or false: If inflammatory mediators
are released or their levels enhanced by mechanisms that are independent
of the immune system, the reaction is due to an intolerance.
7. Wheat-dependent exercise-induced reactions
occur when wheat is ingested
(a.) Within 3 hours after exercise
(b.) Within 3 hours before exercise
8. Which of the following are adverse reactions
related to Celiac Disease?
(a.) Bulky, foul-smelling stools
(b.) Anemia-related fatigue
(d.) All of the above
|1. a [ ] b [x]
||2. a [ ] b [ ] c [x] d
||3. a [x] b [ ]
|4. a [ ] b [ ] c [x] d
||5. a [ ] b [ ] c [ ] d
||6. a [x] b [ ]
|7. a [ ] b [x]
||8. a [ ] b [ ] c [ ] d
1. b. False
2. c. The release of inflammatory mediators
3. a. True
4. c. Kamut
5. d. None of the above
6. a. True
7. b. Within 3 hours before exercise
8. d. All of the above