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Contents A. Case study B. More information C. Editors' comments D. References E. CPD questions

Index

A. Case study
The following case presentation was loosely modified and adapted from the following article in order to maximise the reader’s learning experience: Biagi et al. A milligram of gluten a day keeps the mucosal recovery away: a case report. Nutr Rev. 2004 Sep; 62 (9): 360-3 & Nutr Rev 2004 Dec; 62 (12): 490-491

A 36-year-old nun was admitted to hospital complaining of diarrhoea, abdominal pain and weight loss. On admission her BMI was 19 kg/m² (normal BMI range for >35 years: 21-27 kg/m²). She had a history of iron deficiency anemia over the past 10 years, with fatigue, hair loss and koilonychia (thin, concave nails with raised edges, a clinical feature of iron deficiency anaemia), which was treated with intravenous iron supplementation. When questioned further about her medical history, she reported failure to thrive in childhood and late menarche.

Laboratory tests revealed the following:
• Hemoglobin: 10 g/dL (normal: 12 – 15.5 g/dL)
• Serum iron: 3.7 µmol/L (normal: 10 – 30 µmol/L)
• Ferritin: 5 µg/L (normal: 12 – 150 µg/L)
• Liver function tests: mildly raised transaminases

She still therefore demonstrated iron deficiency anemia. Levels of folate were not reduced, and vitamin B12 was normal, ruling out other causes of anaemia.

QUESTIONS AT THIS POINT:
It is necessary to establish the extent and time frame of weight loss. More than 10% weight loss over 3-6 months is considered significant. If the patient does not know the exact amount, the following questions may be asked to gauge the severity of weight loss and the risk of undernutrition:

• What is your normal weight?
• Have you unintentionally lost weight recently?
• A drop in clothes size or looser belt (change in belt notch) may indicate weight loss:
______- A drop in 1-2 clothes sizes or tightening of 1-2 belt notches would indicate 3-6 kg weight loss
______- >2 clothes sizes or >2-3 belt notches could indicate > 6 kg weight loss
• Have you been eating less than usual?
• Do you experience difficulties in eating, or are you able to eat normally?
• Do you experience any diarrhoea or vomiting?
• Do you have a good appetite?
• How many times a day do you eat, and how much of the plate of food do you eat?

On questioning, it was established that the patient had experienced severe, ongoing weight loss.
The next step was to eliminate causes of iron deficiency anemia:
• Chronic loss of blood due to GIT bleeding or excessive menstrual loss
• Inadequate iron intake due to poor diet
• Impaired iron absorption
• Unmet increased requirements, as seen in children, adolescents, and pregnant and lactating women
• Inadequate utilisation of iron due to chronic inflammation or disease
• Defects in release from iron stores

The patient revealed a history of chronic diarrhoea (>4 loose or watery stools daily), which she had never been able to diagnose but through the years had managed to cope with. She had started menstruating after the age of 16 years and had an irregular cycle, with no marked losses. A diet history revealed inadequate iron intake.

WHAT DOES A PRACTITIONER DO AT THIS STAGE?:
Stools need to be tested for occult blood and pathogenic organisms. Malabsorption syndromes such as celiac disease should be ruled out.

Celiac disease screening tests, including endomysial and gliadin antibody tests, were found to be positive, and the diagnosis was confirmed with a duodenal biopsy, which revealed villous atrophy and a flat small bowel mucosa.

Guidelines for a gluten-free diet as well as appropriate dietary sources of iron and vitamin C were given by a dietitian. Iron and vitamin C supplementation were prescribed.

The patient returned to hospital 15 months later. Her diarrhoea and abdominal pain had stopped, and weight loss had reversed. Transaminases were normal, revealing good liver function; however, iron deficiency anemia, fatigue and endomysial antibodies were still present.

QUESTIONS AT THIS POINT:
Although many symptoms have improved, the ongoing anemia, fatigue and positive celiac disease screening test could imply the following:
• Poor compliance in gluten-restricted diet, as well as continued inadequate dietary intake of iron
• Possible hidden sources of gluten in the diet
• Suboptimal iron supplementation, and therefore a lack of improvement in serum levels

A thorough dietary assessment revealed that she had adequate iron sources but had in fact not been following a strict gluten-free diet. She was taking a daily communion wafer (made from wheat flour) and had had several dietary lapses, as she did not want to inconvenience others. Analysis of various products in her present diet that were thought to be gluten-free, e.g., the oats she ate every second morning, showed wheat contamination. It was therefore felt that her lack of improvement could be attributed to her incorrect diet.

Unfortunately, she refused to stop taking a daily fragment of communion wafer, despite suggestions of alternative gluten-free wafers and discussions on the importance of complete gluten avoidance. According to the Catholic Church, the wafers must be made with wheat flour. It was decided to assess how much gluten was in the wafer, as certain patients with celiac disease may have a tolerance threshold. Hidden sources and contaminated foods were identified, and she was advised to eliminate them. The monastery was contacted to ensure that gluten-free meals could be prepared for her.

Investigation of the communion wafer fragments revealed a weight of 30 mg each, and an ELISA test was used to measure the amount of gliadin. The mean amount was found to be 1.76 g gliadin/100g. This corresponded to 3.52 g gluten/100g. A 30 mg fragment of communion wafer therefore contained approximately 0.5 mg gliadin (1 mg gluten). It was felt that this small amount could be tolerated.

Eighteen months later, the nun returned for a routine follow-up and a second duodenal biopsy to reveal histological recovery. Mucosal repair is important in celiac patients, as ongoing atrophy and damage leads to an increased risk for developing intestinal lymphoma.

A dietary intake diary revealed that she was following a strict gluten-free diet apart from the daily intake of the communion wafer fragment. Her diet consisted almost entirely of natural foods and a few approved gluten-free commercial products. Her anemia had disappeared, and celiac antibodies were negative. Multiple duodenal biopsies, however, revealed persistence of severe villous atrophy and an increased number of intraepithelial lymphocytes.

WHAT COULD THE CAUSE BE?
• The intake diary may be inaccurate, and she may actually be eating more gluten-containing foods than recorded.
• She may still not be adhering to a gluten-free diet.
• She could be sensitive to even the small amount of gluten in the communion wafer.
• She may have refractory/complicated celiac disease.

WHAT CAN WE DO?
Her diet may have been contaminated by undetected gluten; however, examination of the foods recorded showed very little to no contamination in the products. This showed that contamination was an unlikely cause of the lack of mucosal recovery. Her diet was also found to be gluten-free in other respects, except for the communion wafer. The good dietary adherence as well as the patient’s remarkably good clinical condition made it highly unlikely that she was affected by complicated celiac disease and suggested that the daily intake of 0.5 mg gliadin for a 2 year period was the reason for poor mucosal recovery.

Only the withdrawal of the fragment of the communion wafer followed by a duodenal biopsy would confirm whether such a small amount of gluten was responsible for the lack of mucosal recovery.

SUGGESTIONS:
Permission could be obtained for the nun to be allowed to eat gluten-free communion wafers, made without wheat flour.

TIP for Allergy Advisor users: To distinguish between the various adverse reactions a person can have to wheat and/or gluten, Allergy Advisor has developed an information sheet. To find it in the program, click on the “Management” bar, choose “Patient information sheets”, click on “Food” and then “Adverse reactions to wheat and gluten”. There is a part I and II that follow on each other.

B. More information:
Adverse reactions to wheat can be divided into the following:¹
i. Immune reactions:
• Allergic immune reactions
_____- IgE-mediated responses
_____- Non-IgE-mediated cellular responses
• Non-allergic immune reactions
_____- Celiac Disease (CD) (producing IgA and IgG antibodies)
_____- Non-CD enteropathy
ii. Intolerance

The focus of this newsletter is the non-allergic immune reaction of Celiac Disease.

Epidemiology and pathogenesis of Celiac disease
Celiac disease is widespread, occurring on 0.5-1% of the population, and has been called the most common ‘food intolerance’ in the world. A disease traditionally associated with European countries, particularly Scandinavia, it is now commonly seen in populations of European ancestry (North and South Americas, Australia), and in North Africa, the Middle East and South Asia.^{4, 5, 6, 7, 8, 9} In adults, the prevalence appears to be 1 in 250-300, while in children it may be as common as 1 in 100.^{4, 5, 10}

Celiac disease may occur at any age. In infants, symptoms will usually appear only a few months after the introduction of foods containing gluten into the diet (6-12 months); in adulthood, the onset is usually between 30-40 years.^{11, 12, 13, 14} After onset, it is a life-long disorder. It tends to affect twice as many females as males.^{12, 13}

Celiac disease is a disease resulting from an inappropriate T-cell-mediated immune response against ingested gluten in genetically pre-disposed individuals. It is caused by IgA- and IgG-mediated immune responses, and approximately 90-95% of cases are linked to the HLA-DQ2 gene complex, while 5-10% are seen in those with HLA DQ8 gene complexes. Sensitisation and activation of the T-lymphocytes lead to inflammation and structural alteration of the mucosal lining. The enzyme tissue transglutaminase is one of the targets of the autoimmune response in celiac sprue. The enzyme converts particular glutamine residues in gluten peptides into glutamic acid, which results in a higher affinity of these peptides for HLA-DQ2 or HLA-DQ8 (negative charges are preferred at anchor positions in the peptide-binding groove of this molecule).^{3, 4, 6, 15, 16, 17, 18, 19, 20, 21, 22, 23}

Clinical manifestations and symptoms
Celiac disease can be considered a systemic immunological disease as well as a gastrointestinal disorder with a wide spectrum of clinical presentations. Classical, atypical, silent and latent forms of the disease have been identified. Only 20-30% patients suffer from active-classical form of the disease, while approximately 70-80% of cases in adults will fall within the non-diagnosed, inactive forms. Celiac disease is usually characterised by damage to the small intestinal mucosa. Symptoms vary from mild gastrointestinal disturbances to severe growth impairment, failure to thrive, foul-smelling diarrhoea, iron-deficiency anaemia, oedema and signs of malabsorption.^{8, 15, 18, 23, 24}

The resulting gastrointestinal abnormalities differ in different gastrointestinal regions. Oesophageal transit and gastric and gallbladder emptying are delayed, while colonic transfer is faster. Gut motility disorders may predispose the individual to bacterial overgrowth, contributing further to symptoms in some undiagnosed celiacs, and to the persistence of symptoms after initiation of a gluten-free diet. All gastro-intestinal disturbances should, however, ultimately disappear with continued gluten avoidance.²⁵

A vast majority of sufferers (adults and children) demonstrate atypical symptoms and may well remain undiagnosed. Symptoms could include recurrent apthous stomatitis (mouth ulcerations 3), herpetiformis dermatitis (a skin reaction to gluten; a form of celiac disease with or without gastrointestinal symptoms; symmetrical blistering, burning, itchy rash on various body surfaces^{1, 3, 11, 26 27, 28, 29}), unexplained elevated liver enzyme levels, sensory neuropathy and dental enamel hypoplasia. These manifestations often occur in the absence of any ‘typical’ gastro-intestinal symptoms.^{10, 30, 31, 32} The disease is also associated with an increased risk of osteoporosis, infertility, autoimmune diseases such as diabetes mellitus (type 1) and malignancy diseases, especially lymphomas.⁹

The onset of noticeable symptoms of Celiac disease seems to be dependent on the following:
• Exposure to wheat when an infant is weaned (introduction of solids)
• Familial/genetic predisposition
• A “trigger” mechanism. Suspected factors are emotional stress, trauma such as surgery or pregnancy, over-exposure to wheat, viral infection, other diseases, and even antibiotics.^{12, 13, 22, 28}

Summary of clinical disorders associated with celiac disease ³³

Diagnosis and screening
The availability of more-sensitive and more-specific serological tests (antigliadin, antiendomysial and antitransglutaminase antibodies) has facilitated non-invasive screening methods and early intervention in well-defined risk groups.^{4, 23}Despite the high frequency of false positives in at-risk adult groups, IgA gliadin antibodies are still the best marker of celiac disease in children under 2 years. A positive biopsy of the small intestine (duodenum/jejunum), revealing a flattened small bowel mucosa in serologically positive individuals, is still, however, the gold standard for diagnosis. In response to a gluten-free diet, a subsequent biopsy should demonstrate healing of the mucosa.^{6, 15, 18, 23, 24, 34, 35}

Treatment & management
The most effective treatment for celiac disease in both adults and children is complete elimination of gluten from the diet. Intestinal mucosa should heal totally after removal of the aggravating gluten. Further damage to the small intestine will occur every time gluten is consumed, regardless whether symptoms are present or not.^{11, 12, 22, 27, 28, 29, 36, 37}

Poor or no response to gluten avoidance could indicate incorrect diagnosis, inappropriate adherence to the diet or an unresponsive phase of the condition, requiring more-intensive medical intervention, perhaps including corticosteroid treatment. Occasionally, the lack of response could indicate development of complications, including ulcerative jejunitis or enteropathy-associated T-cell lymphoma.³⁸

The failure to treat and manage celiac disease (whether overt symptoms are present or not) by means of a strict gluten-free diet will place individuals at risk of developing life-threatening lymphoma. It is in this light that the dietary management of this disease should be viewed as essential.

What is gluten, and where is it found?
Wheat, like all other foods, contains a number of proteins (more than 100, in this case).³⁹ Wheat proteins can be characterised by the following:
i. Solubility:
• water-soluble
• salt-soluble
• alcohol-soluble
• alcohol-insoluble^{11, 40}
ii. Type of protein:
• albumins (water-soluble – differing from egg and milk albumin)
• globulins (salt-soluble and water-insoluble)
• glutens, which are a combination of 2 protein fractions/epitopes, namely:
_____- gliadins (28-42%), the major prolamin (alcohol-soluble storage proteins of cereal grains with ______similar structures) protein in wheat (soluble in 70-90% alcohol); the prolamin fractions of wheat, ______rye and barley are gliadin, secalin and hordein respectively.^{39, 41}
_____- glutenins (42-62.5%), the major glutelin proteins in wheat (soluble in dilute acid or alkali ______solutions)^{6, 27,}

Gluten is found in various grains, including wheat, barley and rye.5 The major proteins in wheat (albumin, globulin, gliadin and glutenin) may vary in proportion according to the type of wheat.17, 11, 36, 37 Wheat flour contains between 7 and 12% gluten proteins by weight.13

Gluten is found in various grains, including wheat, barley and rye.⁵ The major proteins in wheat (albumin, globulin, gliadin and glutenin) may vary in proportion according to the type of wheat.^{17, 11, 36, 37} Wheat flour contains between 7 and 12% gluten proteins by weight.¹³

The gliadin fractions in gluten are responsible for the viscous consistency when wheat flour is mixed with water to form dough. The glutenins provide the elasticity in wheat baked products.⁴² Although gliadins and glutenins occur in similar amounts, it is certain of the gliadin fractions of wheat gluten and similar prolamins found in other grains (barley, triticale [wheat-rye hybrid], rye and oats) that are responsible for the characteristic small intestine mucosal damage seen in celiac disease.^{24, 29}

The gliadin proteins are divided into alpha, beta, gamma (all three being toxic to persons with CD) and omega gliadins (non-toxic to persons with Celiac disease).^{6, 40, 43, 44} Recently, in vitro studies have suggested that the immunodominant gliadin fraction may lie within the region of amino acids 57-75 of alpha-gliadins. The toxicity of these peptides was also confirmed in vivo when adults on a gluten-free diet, challenged with the peptide, demonstrated significant deterioration in biopsy morphology.¹⁷

In the future, knowledge of the specific wheat gliadin fractions that exacerbate the condition may allow for the development of immuno-modulatory peptides and cereals with the baking and nutritional qualities of wheat, rye and barley but without harmful effects on susceptible individuals.¹⁷

Although true gluten is found only in wheat, the term gluten is used to refer to any similar prolamin proteins in other grains.

The following shows the percentage of specific prolamins in other grains:

How much gluten is safe?
Controversy has existed as to whether small amounts of gluten would be detrimental to a celiac sufferer and still cause symptoms after a period of gluten avoidance. It has been reported in the past that as little as 0.1 grams of ingested gluten can trigger symptoms.¹

Gluten contamination in gluten-free products cannot be totally avoided; this fact helps render the safe threshold for gluten still obscure. Individual countries tend to show different amounts of residual gluten in gluten-free products. In a recent study in Finland, an attempt was made to estimate the reasonable limit for residual gluten, based on the current literature and the measurement of gluten in ‘gluten-free’ products on the market. A number of both naturally gluten-free and wheat starch-based ‘gluten-free’ products analysed contained gluten, from 20 to 200 ppm (20-200 mg/kg). The median flour consumption of the adults in the study (n=76) following a gluten-free diet was 80g (range 10-300). Within these limits, long-term mucosal recovery was good.^{7, 18, 47}

The study concluded that the threshold for gluten contamination could be safely set at 100 ppm (100 mg/kg) gluten per day. If the daily flour intake is 300g, a level of 100 ppm results in 30 mg gluten (gliadin) intake. This amount still allowed improvement in histology in both clinical and challenge studies. It is a level of ingestion that can be faciliated by proper controls in the food industry and does not make the diet too cumbersome.⁴⁷

According to the old Codex Alimentarius standard, for a product to be considered gluten-free, it must contain less than 200-300 ppm (200 mg/kg) gluten. There is, however, evidence to demonstrate that even smaller amounts of gluten ingested on a regular basis by individuals with celiac disease can lead to mucosal changes on intestinal biopsy. Controversy surrounding what constitutes a ‘gluten free diet’ is the result of inaccurate techniques for detecting gluten and the lack of sound scientific evidence for a threshold of gluten consumption below which no harm occurs. As a result, a new limit of 20 ppm (mg/kg) is being considered as defining gluten-free in the proposed Codex Alimentarius,⁴⁸ a level already implemented in Canada and in draft legislation in South Africa.

Ultimately, the safe limit in a diet should be evaluated individually. When mucosal recovery is evident after 1 year on an apparently gluten-free diet, the diet can be assumed to be strict enough. The diet must be practical and realistic, as it is poor dietary compliance in the treatment of celiac disease that seems to be more deleterious and common than the adverse effects of trace amounts of gluten in otherwise gluten-free products.⁴⁹

How safe are oats – what does the literature say?
The case for…..

Whether oats should be included in a gluten-free diet has been debated for half a century. The amount of avenin in oats (10%) is relatively small compared with the amounts of relevant prolamins present in wheat, barley and rye (40-50%).16

It has been established that gluten contains a number of T-cell stimulatory peptides leading to the inflammatory events in the pathogenesis of celiac disease. In 2003, a study attempted to identify similar T-cell stimulatory peptides in barley, rye and oats in order to establish the actual toxicity of these grains in the disease. It was possible to demonstrate T-cell cross-reactivity between gluten peptides and related peptides in hordeins and secalins, thus explaining toxicity of barley and rye respectively in patients with celiac disease (all contain high amounts of glutamine and proline residues).^{16, 41}

Regarding avenin in oats, differences were found between the peptides – avenin lacks certain proline molecules, making it more susceptible to degradation by proteases in the gastrointestinal tract. In a comparison of the identified peptides of hordein, secalin and avenin, it was only avenin peptides that were sensitive to breakdown. This rapid degradation of the potentially harmful avenin peptides may help prevent initiation of an immune response against oats in the small intestine. These findings may pave the way for treatment of gluten enteropathy with an enzyme specific for proline-rich sequences, to destroy the toxic properties of gluten.^{16, 41}

In 1995, in the largest and most scientifically robust study on the safety of oats, investigators found no adverse effects associated with regular consumption of moderate amounts of oats. Subsequent studies have concluded without exception that intake of oats in varying quantities (range: 24-63g/day) in adults with celiac disease is safe.⁴¹

The case against…..
Although oats themselves may be considered safe, it is of major concern that they may often be contaminated with wheat, barley or rye. The extent to which contamination of commercial oat products occurs is unknown, and the quantity of oats consumed may be critical. It is estimated that 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).^{1, 41}

On histological grounds, no differences have been described between patients on a traditional gluten-free diet and those on a more rigorous, non-detectable gluten diet. A dose of 100 mg/day of gliadin administered for 1 month is toxic to duodenal mucosa in susceptible individuals; however, there is little known about the effects of smaller gliadin doses ingested over a longer period of time. In recent case reports and a literature review regarding the safety of commercial oats and the minimal amount of gluten that could be harmless to celiac patients, it was shown that, although most patients with celiac disease tolerated oats (controlled for contamination) in their diet, a few patients exposed to food challenges with pure oats developed changes in bowel habits and abdominal discomfort or dermatitis.^{41, 50, 51}

It was also concluded that as little 1 mg of gluten ingested every day for 2 years prevented histological/mucosal recovery in spite of satisfactory clinical and serological responses. Mucosal recovery is the main protection against the development of intestinal lymphoma, and therefore it is suggested that a second duodenal biopsy should be done in all cases following gluten restriction, to identify those patients with persistent villous atrophy despite appropriate clinical and serological data.^{41, 50, 51}

Practically…..
Authorities on celiac disease, however, are still reticent to advise the safe intake of oats as an alternative to wheat. The Finnish Celiac Society advocates the safe consumption of oats; in the UK, only healthy adults on well-established gluten-free diets are told they can consume oats, with amounts not exceeding 50g/day; all organisations in North America continue to advise against the use of oats. Reasons include methodological limitations in studies that have observed the lack of toxicity of oats; observed immune response to oat prolamins in vitro, and the possible contamination of commercial products with wheat, barley and rye.⁴¹

In patients likely to use oats, it is therefore advised that only products tested and found to be free of contamination, or those within acceptable limits for residual gluten, should be consumed. Practically, an amount of approximately a half a cup of dry whole-grain rolled oats per day is recommended. Ways to reduce chances of consuming contaminated oats include avoiding oats sold in bulk from bins, and determining from the manufacturers whether a dedicated line or facility is used for processing^{1, 41}

C. Comments by our editors

Prof Janice M. Joneja Ph. D., RDN It is extremely important that celiac disease be accurately diagnosed. Undiagnosed disease can have significant adverse consequences in a variety of organ systems, as this excellent article clearly makes evident. On the other hand, an incorrect diagnosis, or assumption based on insufficient evidence can result in a lifetime of unnecessary dietary restriction. In my practice I have encountered a number of patients who have made the assumption that they have celiac disease, based on their reading of articles on the subject, and advice from friends. They have thenceforth strictly avoided gluten-containing foods, sometimes for a number of years. The problem has then arisen that any tests for celiac disease will be invalid, since histological and immunological markers will be absent as long as gluten is avoided. In order to make a valid diagnosis the patient must consume gluten for about four weeks prior to testing. I have found that after several years of avoiding gluten, and adjusting to a specific type of diet, the majority of self-diagnosed patients are extremely reluctant to do this and elect to maintain a gluten-free diet rather than take what they consider to be an unacceptable risk by consuming what they now consider to be “poison”.

Dr. Harris Steinman M.B.Ch.B. Because of the often non-specific symptoms of coeliac disease, it is crucially important that health professionals bear this disease in mind when evaluating patients for food related conditions. Any patient with unresolved symptoms should alert the clinician to reflect on this diagnosis similar to the way a doctor always asks a patient whether they are penicillin allergic before prescribing this antibiotic.

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48. Hill et al. Guideline for the Diagnosis and Treatment of Celiac Disease in Children: Recommendations of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition. J Ped Gastroenterol Nutr 2005;40(1):1-19.
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50. Biagi F, Campanella J, et al. A milligram of gluten a day keeps the mucosal recovery away: a case report. Nutr Rev. 2004 Sep; 62 (9): 360-3 & Nutr Rev 2004 Dec; 62 (12): 490-491.
51. Lundin K, Nilsen E, et al. Oats induced villous atrophy in celiac disease. Gut 2003; 52: 1649-1652.

E. CPD Questions (For South African dietitians only. Australian dietitians: where you have relevant learning goals, CPD hours related to this resource can be included in your APD log.)

2. The gold standard for diagnosing celiac disease is:
(a.) Antiendomysial antibodies
(b.) Anti transglutaminase antibodies
(c.) Skin prick test
(d.) Serum blood tests
(e.) Small bowel biopsy

3. Which one of the following is toxic to a person with Celiac Disease?
(a.) Corn
(b.) Rice
(c.) Quinoa
(d.) Spelt

4. Identify which of the following clinical manifestations could be associated with gluten sensitive enteropathy:
(a.) Iron deficiency anaemia
(b.) Short stature and failure to thrive
(c.) Recurrent mouth ulcerations
(d.) Neuropathy
(e.) All of the above

5. The prolamins present in barley, rye and oats are:
(a.) Hordein, secalin and avenin
(b.) Glutenin, avenin and secalin
(c.) Avenin, hordein and secalin
(d.) Hordein, secalin and gluten

6. Studies have concluded without exception that intake range of oats in adults with celiac disease in the following quantities is safe:
(a.) 63-100 g/day
(b.) 24-63 g/day
(c.) 10-25 g/day
(d.) 100-110 g/day

7. True or false: As little as 1 mg of gluten ingested every day for 2 years prevented histological/mucosal recovery in spite of satisfactory clinical and serological response.
(a.) True
(b.) False

8. In patients likely to use oats, only products tested and found to be free of contamination or those within acceptable limits for residual gluten should be consumed. An amount of approximately 2 cups of dry whole-grain rolled oats per day is recommended.
(a.) True
(a.) False

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