هــذا المــرجــع باللغــة الانجليــزيـة لتســهيل الرجــوع للمعلــومــات لمحبـي هــذه اللغـة
ولطلبــة المدارس الأجنبيـــة
Celiac disease (also known as celiac sprue and gluten senstive enteropathy) is a chronic inflammatory disorder characterized by mucosal damage to the small intestine leading to gastrointestinal illness, nutrient malabsorption, and a wide range of clinical manifestations (NIH, 2004; han, et al. 2002). There is a consensus opinion that celiac disease is caused by an aberrant (T lymphocyte) immune response to dietary glutens predominantly found in wheat, barley, and rye (NIH, 2004). However, there is evidence that at least some persons who have celiac disease may not tolerate oats (Lundin et al., 2003; Arentz-Hansen et al., 2004). Those individuals who have a genetic predisposition to celiac disease react to peptides within the proline- and glutamine-rich protein fractions of the grains (Dewar et al., 2004). For affected individuals, celiac disease is a lifelong condition and, if not treated, is associated with significant morbidity and increased mortality (Fasano, 2003; Corrao et al., 2001; Dewar et al., 2004). There is no cure for celiac disease (NIH, 2004). Strict avoidance of potentially harmful concentrations of glutens in the diet is the only known means of completely preventing the clinical and pathological complications of celiac disease (NIH, 2004; Fasano and Catassi, 2001).
B. Mechanism of Pathogenesis
Celiac disease is characterized by injury to the mucosa of the small intestine and specifically targets the fingerlike projections, called villi, where absorption of key nutrients takes place (Figure III-1). This injury is believed to be due to an autoimmune disorder involving modification of the antigenic presentation of gluten in the intestinal tract of genetically predisposed individuals expressing the major histocompatibility haplotypes HLA-DQ2 or HLA-DQ8 (Farrell and Kelly, 2002; Fasano, 2003). In these individuals, binding of the enzyme tissue transglutaminase (tTG) to wheat gluten (a glutamine rich protein) potentiates uptake and presentation by antigen-presenting cells in the lamina propria, triggering a vigorous T-cell response (Schuppan and Hahn, 2002), leading to production of IgG and IgA antibodies directed to wheat gluten peptides (i.e., gliadins and glutenins) and to tissue transglutaminase (tTG). The activated T-cells are responsible for the mucosal damage seen in celiac disease (Fasano and Catrassi, 2001). This immune-mediated damage occurs in two compartments, the epithelium and the lamina propria (Green and Jabri, 2003). Early intestinal disease is characterized by an increased number of intestinal intraepithelial lymphocytes (IELs). As the disease progresses, increasing numbers of lymphocytes and plasma cells infiltrate the lamina propria. This increase in the numbers of cells leads to elongation of intestinal crypts and shortening of villi, which eventually results in partial or total villous atrophy (James, 2005). Elimination of intestinal gluten results in modification of T lymphocyte and antibody responses and, in most cases, full mucosal recovery (Kaukinen et al., 1999; Fasano and Catassi, 2001).
C. Range of Adverse Effects
The clinical manifestations of celiac disease are highly variable in character and severity. The reasons for this diversity are unknown but may depend on the age and immunological status of the individual, the amount, duration, or timing of exposure to gluten, and the specific area and extent of the gastrointestinal tract involved by disease (Dewar et al., 2004). These clinical manifestations can be divided into gastrointestinal, or “classic,” and non-gastrointestinal manifestations. Gastrointestinal manifestations usually present in children 4 to 24 months old and include abdominal pain and cramping, bloating, recurrent or chronic diarrhea in association with weight loss, poor growth, nutrient deficiency, and (in rare cases) a life-threatening metabolic emergency termed celiac crisis, characterized by hypokalemia and acidosis secondary to profuse diarrhea (Farrell and Kelly, 2002; Baranwal et al., 2003). Non-gastrointestinal manifestations are more insidious and highly variable and are the common presenting signs in older children and adults. These manifestations are frequently the result of long-term nutrient malabsorption, including iron deficiency anemia, short stature, delayed puberty, infertility, and osteoporosis or osteopenia (Fasano, 2003). In children, progressive malabsorption of nutrients may lead to growth, developmental, or neurological delays (Catassi and Fasano, 2004). Extra-intestinal manifestations such as dermatitis herpetiformis, hepatitis, peripheral neuropathy, ataxia, and epilepsy have also been associated with celiac disease (Fasano and Catassi, 2001). Individuals with untreated celiac disease are also at increased risk for potentially serious medical conditions, such as other autoimmune diseases (e.g., Type I diabetes mellitus) and intestinal cancers associated with high mortality (Farrell and Kelly, 2002; Peters et al., 2003; Catassi et al., 2002). For example, individuals with celiac disease have an 80-fold greater risk of developing adenocarcinoma of the small intestine, a greater than two-fold increased risk for intestinal or extraintestinal lymphomas (Green and Jabri, 2003) and a 20-fold greater risk of developing enteropathy-associated T cell lymphoma (EATL) (Catassi et al., Dietary Gluten Tissue Tranglutaminase (tTGA)Antigen Presenting Cells Deaminated Gluten/tTGA Activated T-Cells Symptoms Anti-Gluten and Anti-tTGA IgG and IgA Mucosal Damage
2005a). These are rare intestinal malignancies with a high mortality rate. In addition, the relative risk for developing non-Hodgkin’s lymphomas, intestinal or extraintestinal, is three fold greater than in the general population (Catassi et al., 2002). These cancers contribute to nearly two thirds of deaths due to celiac disease and are a major reason for the nearly two-fold increase in overall mortality of adult patients with celiac disease compared to the general population (Corrao et al., 2001).
Currently, individuals with clinical manifestations, or “symptomatic” celiac disease, are believed to represent a small portion of the total affected population (Mäki and Collin, 1997). A larger number of individuals are believed to have “silent” celiac disease, characterized by positive serology and intestinal mucosal abnormalities in the absence of symptoms or nutritional deficiencies. Mäki and Collin (1997) also suggested that there is an even larger population with “latent” celiac disease, individuals who are positive for serological markers or genetic susceptibility to disease and are entirely asymptomatic. It is generally accepted that individuals with silent or latent disease, although asymptomatic, have the capability to manifest aberrant immune responses following exposure to dietary glutens and are, therefore, at increased risk for both acute and long-term complications of celiac disease (Fasano, 2003; Schuppan, 2000). However, the long-term benefit of strict gluten avoidance for these individuals is unproven (Green and Jabri, 2003).
Until recently, celiac disease was considered to be a rare disorder in the U.S., with an estimated prevalence rate of 1:5,000 (Talley, 1994). However, a large epidemiological study screened more than 13,000 people in 23 states and estimated a prevalence rate of 1:133 within the general U.S. population (Fasano et al., 2003). The National Institutes of Health Consensus Development Conference Statement on Celiac Disease currently estimates that 3 million Americans, a little less than 1 percent of the population, may have celiac disease (NIH, 2004). Celiac disease occurs widely among North American and European populations, where wheat is a staple food, but is infrequent among native descendents of China and Japan and those with an African-Caribbean background, where wheat is not as widely consumed (Farrell and Kelly, 2002).
Precise prevalence data for celiac disease are not available. This disease is often misdiagnosed as another gastrointestinal malabsorptive disorder (e.g., irritable bowel syndrome) due to similarities in their symptoms (Sanders et al., 2001). Due to the existence of silent or latent cases, it is assumed that the incidence of celiac disease is underreported (Mäki and Collin, 1997). These forms of celiac disease may go undetected in individuals for years before they develop symptoms causing them to seek medical attention (Green and Jabri, 2003). Mäki and Collin (1997) postulated that there are many more currently healthy individuals who are genetically predisposed to developing celiac disease in future years than there are individuals who are now affected by celiac disease. Only recently has the medical community become more aware of the need to screen for celiac disease when patients experience health problems that may be associated with the disease or when patients have family members, especially first- and second-degree relatives, who have celiac disease (NIH, 2004).
E. Celiac Foods of Concern
Celiac disease is caused by an immune response in genetically predisposed individuals to specific storage proteins, commonly referred to as “glutens,” that occur naturally in cereal grains (Shan et al., 2002). Technically, “gluten” is a term applied specifically to the combination of the prolamin proteins called “gliadins” and the glutelin proteins called “glutenins” found in wheat (Brown, 2004). However, the term “gluten” has been used generically to refer to prolamin and glutelin protein mixtures found in other cereal grains (Kasarda, 2005, personal communication). Although all cereal grains contain prolamin and glutelin proteins, these proteins are not identical in different grains. These proteins differ in their amino acid sequences in different grains, and not all have been shown to evoke an abnormal immune response that affects the intestinal lining of persons genetically susceptible to celiac disease (Kasarda, 2003). The term “gluten” will be used in this report in the more general sense of the combination of both prolamin and glutelin proteins found in cereal grains.
The grains considered to be capable of producing adverse effects in individuals with celiac disease include the different species of wheat (e.g., durum, spelt, kamut), barley, rye, and their cross-bred hybrids (e.g., triticale, which is a genetic cross between wheat and rye) (Kasarda, 1994; Kasarda, 2004). There is also evidence that some individuals with celiac disease may react adversely to oats (Lundin et al., 2003; Arentz-Hansen, 2004). These grains are all members of the grass family (Gramineae, also known as Poaceae) and are closely related taxonomically. The cereal grains assumed to be safe for persons with celiac disease include amaranth, buckwheat, corn, Indian ricegrass, Job’s tears, millet, quinoa, ragi, rice, sorghum, teff (or tef), and wild rice (Kasarda, 2001; Johnson et al., 2002; Kasarda, 2004b; Kupper, 2004).
The grain prolamins of concern include gliadin in wheat, secalin in rye, hordein in barley (Thompson, 2001; Green and Jabri, 2003; Kagnoff, 2005) and possibly avenin in oats (Arentz-Hansen, et al. 2004; Lundin, et al., 2003). There is substantial evidence that both prolamin proteins (i.e., gliadins) and glutelin proteins (i.e., glutenins) in wheat affect individuals with celiac disease (Shan et al., 2002; Hausch et al., 2002; Vader et al., 2002; van de Wal et al., 1999; Molberg et al., 2003).
Wheat gliadin subtypes alpha, beta, gamma, and omega, have been shown to affect individuals with celiac disease (Ciclitira et al., 1984; EFSA, 2004). Rye, barley and triticale are taxonomically related to wheat, express peptides structurally similar to those found in wheat, and have been reported to affect individuals with celiac disease (Vader et al., 2002; Kasarda, 2001; Kasarda, 2004b). In contrast, the prolamins in other cereal grains (e.g., zein in corn and orzenin in rice) have been shown not to affect individuals with celiac disease (EFSA, 2004; Kasarda, 2004b). However, much is still unknown about which proteins in the different grains can affect individuals with celiac disease (Kasarda, 2001).
Analytical information is not available on the actual amount of gluten proteins in different grain-derived food ingredients or finished foods. For single ingredient foods made from wheat, rye, barley, triticale, and oats, the simple presence of “protein” in that
food may be used as an indicator that gluten proteins are present. The USDA National Nutrient Database for Standard Reference, Release 17 (USDA, 2004), the major source of composition data for foods in the U.S., includes hundreds of food items that contain wheat, rye, barley, triticale or oats as an ingredient. Wheat, in particular, is used to manufacture a wide range of food ingredients and finished foods. Rye, barley, triticale, and oats are used to make substantially fewer food products.
Koehler and FDA (2005) estimated the average amount of total grain and individual types of grain available for consumption per person in the U.S., and the total exposure to gluten-forming proteins that would result from this grain consumption. The estimated mean daily consumption rate was approximately 250 grams of grain per capita. Wheat provided 180 of the 187 grams per person per day of grains that are of concern for individuals with celiac disease.
There is no consensus as to whether oats present a hazard for all individuals with celiac disease. Several studies, including one that lasted 5 years, have reported that most celiac study participants tolerated moderate amounts (e.g., 50-70 grams daily) of oats (Janatuinen et al., 1995; Janatuinen et al., 2000; Janatuinen et al., 2002; Lundin et al., 2003; Arentz-Hansen et al., 2004). The oats used by Lundin et al. (2003) and Arentz-Hansen et al. (2004) were tested to ensure that they did not contain any gluten proteins from wheat, rye, or barley.
F. Gluten Contamination of Grains
In the U.S., most commercially available oat products are believed to contain some gluten proteins from wheat, rye, or barley due to cross-contact with these grains during growth, harvest, transport, storage, or processing (Kasarda, 1999; Kasarda, 2001; AGA, 2001; Thompson, 2003). In a recent study, Thompson (2004) analyzed four lots of three brands of rolled or steel-cut oats commercially available in the U.S. for prolamins from wheat, barley, or rye. For one brand, all samples contained 338 to 1807 ppm gluten (expressed as the mean of duplicate determinations). For each of the other two brands, the level of gluten detected in all but one lot ranged from 12-725 ppm in one brand and 120-131 ppm in the other brand (expressed as the mean of duplicate determinations). Thus, only one lot of these two brands was negative for gluten. Thompson (2004) concluded that none of these three brands could be considered a reliable source of oats free of potentially harmful gluten proteins.
Grains that do not contain gluten can become contaminated with grains that contain gluten at any step in the farm-to-table continuum, particularly if shared equipment is not thoroughly cleaned between uses. It is difficult, if not impossible, to prevent all cross-contact situations, considering the tons of grain handled by farm equipment, bulk storage, and transport containers on a daily basis. In fact, the Official United States Standards for Grains (USDA, 1999) assume that most grains that have an established U.S. standard will contain a small percentage of other grains.
G. Gluten Challenge Studies
There is little information in the literature on minimal disease-eliciting doses of gluten for sensitive individuals. Gluten challenges have generally been performed in individuals where diagnosis is uncertain (e.g., infants, Laurin et al., 2002) or in individuals with unclear intestinal pathology results (Wahab et al., 2001). Challenges have also been performed to determine the time of disease relapse after a prolonged period of gluten avoidance (Mayer et al., 1989). In most cases, gluten challenges have been performed to elicit or confirm disease rather than to measure the level of sensitivity (Farrell and Kelly, 2002).
There is no standard protocol for gluten challenges, and challenge studies have varied greatly in amount and duration of gluten exposure. Although some studies have been designed to determine the acute effects (i.e., after 4 hours) of exposure to gluten (Sturgess et al., 1994; Ciclitira et al., 1984), most challenges consist of an open challenge to a fixed or incremental dose of daily gluten over a minimum period of 4 weeks. Many challenge studies use a high exposure (> 10 g/day) to gluten, because this is believed to shorten time to disease confirmation or relapse and, therefore, to minimize discomfort to subjects (Rolles and McNeish, 1976). However, some studies have shown that low daily exposures to gluten also can elicit a disease response (Catassi et al., 1993; Laurin et al., 2002; Hamilton and McNeill, 1972).
Catassi et al. (1993) reported that children, whose celiac disease had previously been controlled on gluten-free diet, had evidence of intestinal mucosal or immunological changes (changes in intraepithelial lymphocyte counts and the villous height to crypt depth ratio) following 100 mg or 500 mg of daily gliadin over 4 weeks; this corresponds to 200 mg and 1000 mg of daily gluten respectively (Collin et al., 2004). The degree of inflammation was dose dependent. However, this study had several important limitations, which include the short-term follow up (4 weeks), testing in young children, the small number of subjects (n=20), and the lack of control groups. In addition, although gliadin is believed to be the major immunogenic portion of gluten, T cells from the small intestine of celicac disease patients have been shown to be responsive to peptides from the glutenin portion as well (Van de Wal et al., 1999). Thus, the Castissi et al. (1993) study was also limited by the use of gliadin rather than gluten. Estimating potential harm by extrapolating from gliadin levels may not be representative of the harm from total gluten exposure.
A study currently in progress [The Italian Microchallenge Study] has extended the scope of these earlier findings by evaluating the effects of exposure to either 10 or 50 mg of purified gluten per day for 3 months with a population of 36 celiac disease individuals in a double-blind, placebo-controlled study (Catassi et al., 2005b). Preliminary unpublished results suggest that minimal mucosal abnormalities occur with a strict gluten-free diet, that both 10 mg and 50 mg daily gluten are well-tolerated, but that there is a trend for mucosal changes to occur at the 50 mg dose. These results can be compared to estimated gluten exposures from gluten-free diets containing various levels of gluten contamination (Table III-1, from Collin et al., 2004, reproduced below). Fasano (2005 personal communication) used these values to suggest that a
conservative threshold for gluten exposure for sensitive individuals would lie between 20 and 100 ppm.
Table III-1. Estimated Daily Gluten Consumption from Combinations of Different Amounts of Food Containing Different Levels of Gluten
Gluten Content in Food (ppma)
Daily Amount of Gluten-Free Food Consumed (g)
—————-Daily Amount of Gluten Consumed (mg)—————–
The Gluten-free Diet: Some Examples
In 2006, the American Dietetic Association updated its recommendations for a gluten-free diet. The following chart is based on the 2006 recommendations. This list is not complete, so people with celiac disease should discuss gluten-free food choices with a dietitian or physician who specializes in celiac disease. People with celiac disease should always read food ingredient lists carefully to make sure the food does not contain gluten.
Indian rice grass
|Foods To Avoid|
- including einkorn, emmer, spelt, kamut
- wheat starch, wheat bran, wheat germ, cracked wheat, hydrolyzed wheat protein
- triticale (a cross between wheat and rye)Other Wheat Productsbromated flour
- durum flour
- enriched flour
- farinagraham flour
plain flourself-rising flour
white flourProcessed Foods that May Contain Wheat, Barley, or Rye*bouillon cubes
brown rice syrup
cold cuts, hot dogs, salami, sausage
communion wafersFrench fries
saucesseasoned tortilla chips
vegetables in sauce
* Most of these foods can be found gluten-free. When in doubt, check with the food manufacturer.
Source: Thompson T. Celiac Disease Nutrition Guide, 2nd ed. Chicago: American Dietetic Association; 2006. © American Dietetic Association. Adapted with permission. For a complete copy of the Celiac Disease Nutrition Guide, please visit www.eatright.org.
THOSE PPT SLIDES WAS PART OF PRESENTATION HELD FOR DOCTORS AT AMIRI HOSPITAL– KUWAIT
Handbook for School
يســـتطيــع الآبــاء تعبئتــه (ترجمتــه في حالة الرغبة بذلك) كمــرجـع للمـدارس لمعرفة المرض مسبباتـه –أعراضــه-الممنــوعــات-المســموحــات
ليبقــى الطـالب فــي أيدي أميــنة في المدرســة وهـــو بعيـدا عـن ناظري والديــه
-ملاحظـــة: يوجـد مرجع للطلـبة باللغة العربيـة في كتـاب قصتي مع السلياك-
(Teachers, Nurses, Health Assts.)
(Confidential Information – Distributed by Parent(s) only)
Emergency Contact Information
Alternate Contact Information
What is Celiac Disease?
Celiac Disease is an autoimmune disorder that damages or destroys the lining of the intestines
in reaction to gluten, which is the protein found in wheat, barley, rye, and sometimes oats.
What are the Effects?
When a person with Celiac Disease digests food containing wheat, barley, rye and sometimes
oats, the gluten shortens and eventually flattens the villi, which are small finger-like projections
that line the small intestine. The villi produce enzymes and allow nutrients from digested food
to pass into the body. If the villi are flat, the body will not be able to absorb vital nutrients such
as vitamins, minerals, proteins, fats and carbohydrates.
Common Symptoms of Celiac Disease
Although there is no one set of symptoms for Celiac Disease, the following conditions may be
• Slower or poor growth • Diarrhea
• Irritability • Anemia
• Weight loss or slow weight gain • Tiredness or fatigue
• Bloating and cramps • No real interest whether things happen
or not; minor depression
What happens if a Celiac digests gluten – what is the reaction like?
A reaction will vary depending on how sensitive the individual person is and according to how
much gluten was ingested. A visible reaction will usually occur within four hours of ingesting
the gluten and can include:
• stomach cramping
• “fuzzy” or unclear feeling; difficult concentrating
How do you know if food contains gluten?
Most ingredients are obvious. For example, enriched flour. Flour is generally made from
wheat. However, most times it can be very difficult to tell. Even when reading the ingredients
on a label, gluten can be hidden in many forms. Also, FDA labeling requirements do not
require manufacturers to define things like “artificial and natural ingredients” or any ingredient
that comprises less than 2% of the product. These items often contain gluten. See attached
What do you do if gluten is digested by mistake?
Please notify parent(s) as soon as possible. Also, the student may need to suddenly run to
What is the treatment for Celiac Disease?
The treatment for Celiac Disease is quite simple – a diet that excludes gluten. A gluten-free
diet means completely omitting wheat, rye, barley and sometimes oats in any form from the
diet. Although the treatment is simple, it is not always easy. If you have have any questions,
please ask. The following website provides a list of products that are gluten free::
Other Websites if interested in more information:
Acacia Gum Distilled Vinegar Rice
Acorn Quercus Eggs Rice Flour
Alcohol (Spirits-Specific Types) Fish (fresh) Rice Vinegar
Alfalfa Flaked Rice Romano Bean (chickpea)
Amaranth Flax Sago Palm
Adzuki Bean Fruit (including dried) Sago Flour
Agar Gelatin Saifun (bean threads)
Algae Gram Flour (chick peas) Scotch Whisky
Almond Nut Grits, Corn Seaweed
Annatto Guar Gum Seed – Sesame
Apple Cider Vinegar Herbs Seed – Sunflower
Arabic Gum Honey Soba (be sure it’s 100%
Arrowroot Hyacinth Bean Buckwheat)
Artichokes Job’s Tears Sorghum
Astragalus Gummifer Kasha (roasted buckwheat) Sorghum Flour
Baking Soda Kudzu Root Starch Soy
Balsamic Vinegar Lentil Soybean
Beans Locust Bean Gum Spices (pure)
Bean, Adzuki Maize Spirits (Specific Types)
Bean, Hyacinth Maize Waxy Starch (made in USA)
Bean, Lentil Maltodextrin(ˇ) Succotash (corn & beans)
Bean, Mung Manioc Subflower Seed
Bean Romano (Chickpea) Masa Flour Sweet Chestnut Flour
Bean Tepary Masa Harina Tapioca
Besan Meat (fresh) Tapioca Flour
Bicarbonate of Soda Methyl Cellulose (ˇ) Tea
(some contain gluten) Milk Tea-Tree Oil
Buckwheat Millet Teff
Butter (beware of additives) Milo Teff Flour
Canola Oil Mung Bean Tepary Bean
Carageenan Chondrus Crispus Nut, Acorn Tofu-Soya Curd
Carob Bean Nut, Almond Tragacanth
Carob Bean Gum Oats (ˇ) Tragacanth Gum
Carob Flour Oils & Fats Turmeric (Kurkuma)
Cassava Manihot Esculenta Peas Urad Beans
Cellulose(ˇ) Pea – Chick Urad Dal (peas) Vegetables
Cellulose Gum Pea – Cow Urid Flour
Cheeses (except blue & chilton) Pea Flour Vinegars (Specific Types)
Chickpea Pigeon Peas Waxy Maize
Corn Polenta Whey
Cornmeal Potatoes White Vinegar
Corn Flour Potato Flour Wines
Cornstarch Prinus Wine Vinegars (& Balsamic)
Corn Syrup Psyllium Wild Rice
Cowitch Quinoa Xanthan Gum
Cowpea Ragi Yam Flour
Cream of Tartar Rape Yogurt
Gluten-Free Food Additives
Adipic Acid Dioctyl Sodium Polysorbate 60; 80
Acacia Gum Elastin Potassium Citrate
Agar Ester Gum Potassium Iodide
Algin Folic Acid-Folacin Pristane
Alginate Formaldehyde Propolis
Allicin Fructose Propylene Gycol
Aluminium Fumaric Acid Monostearete
Annatto Color Gelatine Propylgallate
Arabic Gum Glutamine (amino acid) Pyridoxine Hydrochloride
Aspartame (can cause IBS Glutamic Acid Rennet
Symptoms) Glycerides Reticulin
Aspic Glyceryl Nono-Oleate Rosin
Ascorbic Acid Glycerol Mono-Oleate Royal Jelly
Benzoic Acid Glycol Sphingolipids
Bentaine Glycolic Acid Sodium Acid Pyraphosphate
BHA Guar Gum Sodium Ascorbate
BHT Hemp Sodium Benzoate
Beta Carotene Hydrogen Peroxide Sodium Citrate
Biotin Iodine Sodium Erythrobate
Butylated Hydroxyanisole Invert Sugar Sodium Hexametaphosphate
Butyl Compounds Keratin Sodium Lauryl Sulfate
Calcium Carbonate Lactic Acid Sodium Nitrate
Calcium Chloride Lactose Sodium Silaco Aluminate
Calcium Phosphate Lanolin Sodium Stannate
Calcium Silicate Lecithin Sorbic Acid
Calcium Stearate Lipase Sorbitol-Mannitol (can cause
Camphor Locust Bean Gum IBS symptoms)
Caprylic Acid Magnesium Carbonate Soy Lecithin
Carboxymethylcellulose Magnesium Hydroxide Stearates
Carnuaba Wax Malic Acid Stearamide
Carob Bean Gum Maltitol Stearamine
Carrageenan Microcrystallin Cellulose Stearic Acid
Casein Mineral Oil Sucrose
Castor Oil Mineral Salts Sulfosuccinate
Cellulose Gum Monosodium Glutamate Sulphites
Cetyl Alcohol MSG (Made in USA) Sulpur Dioxide
Chlorella Monopotassium Phosphate Tallow
Chymosin Musk Tartaric Acid
Citric Acid (Made in USA)ˇ M Vitamins & Minerals TBHQ is Tetra or
Collagen Niacin-Niacinamide Tributylhydroquinone
Corn Sweetener Oleyl Alcohol/Oil Thiamine Hydrochloride
Corn Syrup Solids Parrafin Tolu Balsam
Cortisone Pepsin Tragacanth Gum
Cotton Seed Oil Peru Balsam Tri-Calcium Phosphate
Cysteine, L Petrolatum Tyrosine
Demineralized Whey Phenylalanine Vanillan
Desamidocollagen Polyethylene Glycol Vitamin A (palmitate)
Dextrimaltose Polyglycerol Whey
Dextrose Polysorbates Xanthan Gum
Gluten-Containing Food Ingredients**
Abyssinian Hard (Wheat Germ
Triticum Duran) Glutamate (free) Small Spelt
Alcohol (Spirits-Specific Graham Flour Soba Noodlesˇ
Types) Granary Flour Sodium Caseinate
Artificial Flavoringˇ Gravy Cubesˇ (Contains MSG)
Baking Powderˇ Groats (barley, buckwheat Soy Sauce
Barley Grass (can contain Or oats) Spirits (Specific Types)
Seeds) Ground Spicesˇ Spelt Triticum Spelta
Barley Hordeum Vulgare Gum Base Sprouted Wheat Barley
Barley Malt Hard Wheat Starch (Outside USA)
Beer Hydrolyzed Plant Protein Stock Cubesˇ
Bleached Flour (HPP) Strong Flour
Blue Cheese (made from Hydrolyzed Vegetable Suet in Packets
Bread) Protein (HVP) Tabbouleh
Bran Kamut (Pasta Wheat) Teriyaki Sauce
Bread Flour Malt Textured Vegetable Protein
Brewer’s Yeast Malt Extract (TVP)
Brown Flour Malt Syrup Triticale X Triticosecale
Bulgar (Bulgar Wheat/Nuts) Malt Flavoring Udon (Wheat Noodles)
Bulgar Wheat Malt Vinegar Vegetable Starch
Calcium Caseinate Misoˇ Vinegars (Specific Types)
(contains MSG) Matzo Semolina Vitaminsˇ
Caramel Colorˇ Modified Food Starchˇ Wheat Triticum Aestivum
Cereal Binding Mono and Diglyceridesˇ Wheat Nuts
Chilton MSG (Made outside USA)ˇ Wheat, Abyssinian Hard
Citric Acid (made outside Mustard Powderˇ Triticum Durum
USA) Natural Flavoringˇ Wheat, Bulgar
Couscous Pasta Wheat, Durum Triticum
Dextrinsˇ Pearl Barley Wheat Triticum Mononoccum
Durum Wheat Triticum Rice Malt (contains barley Wheat Starchˇ
Edible Starch Or Koji) Wheat Germ
Einkorn Wheat Rye Wheat Grass (can contain
Farina Graham Semolina Triticum seeds)
Filler Semolina Whole-Meal Flour
Fu (dried wheat gluten) Shoyu (Soy Sauce)ˇ
**Some foods containing one of these ingredients may be gluten-free. However, you should
always check with the manufacturer on the gluten status of a food item if you see one of the
above ingredients listed.
Gluten-Free Snack Ideas
Gluten-Free Snack Ideas
Celery/Carrots Planters Dry Roasted Peanuts
Ruffles Potato Chips Fruit roll-ups
Fruit chews/gushers Orville Reddenbacher Popcorn
Blue Diamond Crackers (Pecan) Mott’s Applesauce
Apples w/Skippy’s or Jiff Peanut
Hunts chocolate & vanilla pudding
Gluten-Free Birthday Treat Ideas
3 Muskateer Bars M&M’s (all flavors EXCEPT rice krispy)
Almond Joy O’Henry candy bars
Baby Ruth Popsicles & Freezes
Butterfinger & Butterfinger BB’s Reese’s Peanut Butter Cups
Caramel Nips – Pearson Candy,
Hersheys caramels also ok
Charm’s Blow Pops Smarties
Dum Dum Lollipops Starbursts
Gum – Bubble Yum Bubble Gum, Big
Skittles – all flavors
Hershey’s chocolate bars Sweetarts
Hershey Kisses Snicker Candy & Ice Cream Bars
Ice Cream – Kemps vanilla &
chocolate. Snickers ice cream bars.
Dairy Queen Starkiss. Snickers Ice
Tootsie Rolls + Tootsie Roll pops
Jelly belly jelly beans York Peppermint Patties
Jolly Ranchers & Jolly Rancher
-Necco Valentine Hearts
-Hershey Caramel Eggs
-Hershey Easter Eggs
-Jelly Belly Jelly Beans
-Peeps marshmallow animals
Life Savers – all flavors + lollipops
This is not food!
1-1/2 cups GF flour
¼ cup salt
1-1/2 tsp. oil
1 pkg. Unsweetened Kool-Aid
1 cup boiling water
Mix and have fun! Will keep for weeks in covered container. Not necessary to
refrigerate. Can be stored in small freezer bags.
NOTE: If there are other medical conditions that you would like school staff to
be aware of, you may complete the following format and include in your
handbook. Otherwise, you may delete this page.
What is _________________________?
What are the effects_____________?
Common Symptoms of _________?
What is the treatment___________?
____________________?Is there a cure
احصل على كود الصفحات المحجوبة
أو أحد الكتب الآن pls Note: "السعر مختلف لكل كتاب"