Everything you need to know about coeliac disease
Why Gluten Free
What Is The Gluten Free Diet And What You Need To Know Before You Try It. You may have heard the term gluten free, and you may even have a general idea as to what it means to eat a gluten free diet. Most people believe this type of diet is a curse for those who simply cannot tolerate the protein known as gluten, as they will never be able to eat any food that contains wheat, rye, barley, malts, or triticale.
Before adding to the diet, verify with manufacturers that ingredients do not include gluten. Reproduced with permission from Gluten Intolerance Group. 15110 10th Ave. SW, Ste. A, Seattle WA 98166 1987 Table 26-6. Additives and Ingredients Allowed in a Gluten-Free Diet Reproduced with permission from Gluten Intolerance Group. 15110 10th Ave SW, Ste. A, Seattle WA 98166 1987. Table 26-7. Gluten-Free Diet allowed flours (100 potato, corn, arrowroot, soybean) commercial gluten-free baking mixes Cereal Hot or cold cereals made from corn, rice, or Noodles Gluten-free corn pasta special gluten-free and pasta low protein pastas rice pasta or bean pastas Crackers Pure cornmeal tortillas rice wafer or crackers, and snack rice cakes,' popcorn, crackers made with foods allowed flours (100 potato, corn, rice, Low-gluten flours all flours containing wheat, rye. barley, and oats durham wheat, all-purpose flour, white enriched flour, wheat flour, wheat germ, whole wheat flour, wheat starch wheat...
In Walker WA. Durie PR. Hamilton JR. et al. Pediatric gastrointestinal disease. St Louis Moshy 1996. 3. Branski D. Troncone R. Celiac disease a reappraisal. J Pediatr 1998 133 181-7. 4. Trier JS. Celiac sprue. N Engl J Med 1991 325( 24) I 709-19. 5. Kumar PJ. Farthing MG. Oals and celiac disease. N Engl J Med 1995 333( 16) 1075-6. Additional Resources Celiac Disease Support Groups Celiac Sprue Association
It is often possible to correct the cause of the deficiency and thus prevent its recurrence, for example, improved diet, a gluten-free diet in celiac disease, or treatment of an inflammatory disease such as tuberculosis or Crohn's disease. In these cases, there is no need to continue folic acid for life. In other situations, it is advisable to continue the folic acid to prevent recurrence of, for example, chronic hemolytic anemia such as thalassemia or in patients with malabsorption who do not respond to a gluten-free diet.
The ligand of CD94 NKG2A and CD94 NKG2C receptors is the nonclassic MHC class I molecule HLA-E (Braud et al. 1998 Llano et al. 1998) and its Qa-1 homolog in mouse (Vance et al. 1999) combined with conserved leader peptides of MHC class I molecules. In human, CD94 NKG2A and CD94 NKG2C also recognize HLA-E with the HLA-G leader peptide (Llano et al. 1998 Vales-Gomez et al. 1999). Because CD94 NKG2C is poorly expressed by CTLs, ligand induction should generally translate into an inhibitory signal when target cells express normal levels of MHC class I. In disease conditions such as CMV (Guma et al. 2004) and severe celiac disease (manuscript in preparation) CTLs can express CD94 NKG2C, but they do not express CD94 NKG2A, thus avoiding a conflict between these opposite forms of signaling. Intriguingly, human NKG2E and its splice variant H differ significantly from the other mouse and human NKG2 molecules in the putative ligand binding site, suggesting that they may display specificities in...
In developed countries the physician is only allowed to even consider treatment of iron deficiency if its cause is diagnosed, or proper further evaluation is initiated. Treatment of iron deficiency anaemia is rather simple and inexpensive in most subjects and entails oral treatment with ferrous salts. Despite lower absorption of iron, there is renewed interest in therapeutic use of ferric maltose, suggesting that a large influx of Fe(II) from therapeutic doses may cause oxidative damage (Fodor and Marx, 1988 Geisser, 1998). Although treatment failure mostly results from an inadequate dose, persistent blood loss which exceeds iron absorption and poor compliance, failure may also be the result of malabsorption. The cause may be bowel inflammation in the duodenal region, coeliac disease or a genetic defect of one of the proteins involved in intestinal iron absorption. In these patients, parenteral treatment is needed with iron-sucrose or iron-dextran complexes (the latter is not...
Celiac Sprue (Gluten-Sensitive Enteropathy) Celiac sprue, also called gluten-sensitive enteropathy, is a common disease involving a primary lesion of the intestinal mucosa. It is caused by the sensitivity of the small intestine to gluten. This disorder can result in the malabsorption of all nutrients as a result the shortening or a total loss of intestinal villi, which reduces the mucosal enzymes for nutrient digestion and the mucosal surface for absorption. Celiac sprue occurs in about 1 to 6 of 10,000 individuals in the Western world. The highest incidence is in western Ireland, where the prevalence is as high as 3 of 1,000 individuals. Although the disease may occur at any age, it is more common during the first few years and the third to fifth decades of life. In patients with celiac sprue, the water-insoluble protein gluten (present in cereal grains such as wheat, barley, rye, and oats) or its breakdown product interacts with the intestinal mucosa and causes the characteristic...
Although H. pylori is probably the most common association with acquired gastric MALT, it is not the only stimulus to accumulation of lymphoid tissue in the gastric mucosa. The related organism Helicobacter heilmannii is also associated with acquired gastric MALT (21), and MALT-type lymphoid tissue has been described in the stomachs of patients with celiac disease.
Storage Proteins Some plant food-storage organs, such as potato tubers and onion bulbs, store small amounts of proteins in addition to large amounts of carbohydrates. Seeds, in particular, however, usually contain proportionately larger amounts of proteins in addition to their complement of carbohydrates and are very important sources of nutrition for humans and animals. One example of an important protein source in human and animal diets is wheat gluten (to which, incidentally, some humans become allergic). The gluten consists of a complex of more than a dozen different proteins.
Malabsorption may occur, even when digestion is functioning normally, due to defects in the small intestine affecting the absorptive surfaces. There may be a variety of causes, some common ones being bacterial invasion of the gut or sensitization of the gut to dietary components such as gluten, as in coeliac disease. Malabsorption syndromes (often called sprue) are characterized by dramatic changes in the morphology of the intestinal mucosa. The
Growth and weight gain, activity pattern, psychosocial economic issues, smoking, medical history (celiac disease, nephropathy, hyperllpidemia, eating disorder, high blood pressure, asthma, attention deficit disorder, hypothyroidism, and other autoimmune diseases), insulin regimen, oral glucose-lowering medications, blood glucose monitoring schedule
Celiac Disease Celiac disease is a lifelong disease of the small intestine characterized by an abnormal mucosa and associated with a permanent intolerance to gluten. Gluten is a protein that makes up 5()f of the total proteins in wheat, rye. and barley gliadin is the water soluble protein fraction of pro-lamin. The prevalence of celiac disease in the United States is estimated at 1 2.()()() to 3.000. with populations in western Ireland and Italy showing prevalences estimated at 1 300.' Population screening suggests that subclinical or preclinical celiac disease is not uncommon. Clinical symptoms of celiac disease usually present in toddlers but can do so at any age. Exposure to dietary gluten is required for symptoms to occur, and celiac disease is more prevalent in countries where wheat is a staple food. Clinical symptoms vary widely (Table 26-3). Celiac disease has been associated with other autoimmune diseases such as Addison's disease, pernicious anemia, autoimmune...
A thorough medical history should note the symptoms and signs of anorexia nervosa, the intensity of athletic training, and the timing of puberty of both parents (see Fig. 5). In boys with constitutional delay of puberty, one parent often developed late as well. A history of chronic illness, such as celiac disease or inflammatory bowel disease, suggests a temporary or secondary delay of puberty. Stature and height velocity should be evaluated using appropriate growth charts. Height velocity is usually reduced in patients with constitutional delay but is normal in patients with isolated hypogo-
Koster-Kamphuis, L., van Straaten, E. A., Kors, W. A., De Schrijver, J. E. A. R., Bovee-Oudenhoven, I. M. Y., van der Meer, R., Forget, P. Ph., Urinary NOx creatinine ratios during gluten challenge in children with celiac disease, J. Pediatr. Gastroenterol. Nutr., 36, 372-375, 2003.
Surgery is nearly universal, and the sensation of liquids hanging up is not unusual either. The cause of these symptoms postoperatively is likely multifactorial. Distal esophageal edema is seen universally postoperatively, transient esophageal dysmotility has been demonstrated after anti-reflux surgery, and recently performed fundoplication-related hematomas can also cause temporary outflow obstruction from this section of the esophagus. For all these reasons, we recommend that the patients stay on a full liquid diet for the first 5-7 days after surgery, and then follow a special soft diet for the next 3 weeks. This special diet restricts the intake of large bolus foods such as meats, raw vegetables, and high-gluten-containing items such as cakes and breads. This protocol dramatically reduced the incidence of postoperative symptomatic dysphagia, food impaction, and retching that occur when a regular diet has begun too soon after surgery and the associate phone calls expressing alarm...
Some important exceptions to the TCR primacy rule, however, have emerged. For example during CMV infection CTLs were reported to express surface NKG2C, and similar observations were obtained in conditions of chronic T cell activation in vitro (Ortega et al. 2004) or inflammation in vivo (Guma et al. 2004 and unpublished data). These changes, which may effectively convert the CTL into an NK cell, have major physiopathological implications that are discussed later. Although they could transiently benefit the host in case of infection, they are detrimental in the case of chronic inflammation and may lead to severe immunopathology, as suggested in celiac disease.
Organs responsible for development of iron-deficiency anaemia are the uterus (increased menstrual blood loss, pregnancy), the oesophagus (varicose veins in patients with liver cirrhosis), the stomach and bulbus duodeni (hiatus hernia, aspirin and detrimental effects of other non-steroidal antiinflammatory drugs, peptic ulcer, carcinoma, partial gastrectomy), the small intestine (hookworm, coeliac disease, diverticulosis, morbus Crohn, angiodysplasia), the colon and rectum (carcinoma, diverticulosis, angiodysplasia, varices, colitis) and, rarely, the kidney and lung. Increased demands for iron, not met by adequate iron intake, occur in premature infants, during any period associated with increased growth, and during pregnancy. Poor diet is also a cause of iron deficiency in some socioeconomic groups in developed countries. Female blood donors in particular may develop iron deficiency. Self-inflicted blood loss is a diagnosis that should be considered if no cause can be found for severe...
Soreness of the lips, tongue or buccal mucosa has a wide variety of causcs. including iron, folate or vitamin Bl2 deficiency, dermatological disorders, chemotherapy, aphthous ulceration and infective stomatitis (Table 5.2). Gastrointestinal disorders particularly associated with mouth uleers include inflammatory bowel disease and gluten enteropathy. A history of recurrent painful tiny mouth ulcers with its onset at the menarche, exacerbations during menstruation and a family history of mouth ulcers suggests idiopathic aphthous ulceration.
Celiac disease, or gluten-induced enteropathy, is a rare disease characterized by mucosal abnormalities of the small intestine and malabsorption. Association with many autoimmune disorders has been noted, and arthritis occurs in fewer than 50 of patients. B. Treatment. Arthritis usually responds well to a gluten-free diet.
When faced in clinic with a child who is having recurrent episodes of hypoglycaemia, a detailed history should be obtained regarding the timing of hypoglycaemia, insulin regimen, dietary intake and the relation to periods of physical activity. This will enable an assessment to be made of possible risk factors and inform how these may be avoided. If no obvious cause is found then other pathology should be sought, such as coincidental coeliac disease or the possibility of Addison's disease, although these are relatively rare causes of recurrent hypoglycaemia (see Chapter 3).
Is there a family history of Gl disorder, e.g. gluten enteropathy, Crohn's Are there any other Gl symptoms, e.g. adomlnal pain and vomiting Are there symptoms of systemic disease, e.g. rigors or arthralgia The diagnosis of gluten enteropathy (coeliac disease was confirmed by the presence of high titres in the serum of endomysial antibodies and total villous atrophy on duodenal biopsy. 3 months alter strict adherence to a gluten-free diet, all of her symptoms had resolved completely. Dysphagia was attributed to the mucosal changes associated with severe iron deficiency (sideropenic dysphagia) and the musculoskeletal symptoms attributed to osteomalacia. Recurrent mouth ulcers are a typical feature of gluten enteropathy and inflammatory bowel disease.
Perhaps because there is no cure for autism, parents are often drawn to investigate alternative therapies. Current alternate therapies include high-dose vitamin Bf, and magnesium supplementation, dimethylglycine (DMG), a gluten-free casein-free diet, and a yeast-free diet. Further research regarding the efficacy of these therapies is required.