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Secondary One Biology: Cooperative Learning @ AsknLearn Forum FORUM 10: COELIAC DISEASE Done By: Low Yi Mei (20) Kimberly Ng (21) Nicolette Wong (22) Samantha Phey (23) Rose Ow (24) Ruth Tai (25) Sarah Khan (26)

ÿ Causes of coeliac disease Coeliac disease is caused by intolerance to gluten, a protein that is found in foods such as bread, pasta, cereals and biscuits. For certain people, eating oats may also trigger the symptoms. If one has coeliac disease, any gluten that he/she eat is attacked by their immune system when it reaches the intestines (gut). This happens because coeliac disease is an autoimmune condition, in which the immune system mistakes gluten for a harmful substance and produces antibodies against it. When the antibodies attack gluten, they can also damage the lining of your gut, causing inflammation. Normally, the surface of the gut lining is covered with millions of tiny tube-shaped growths called villi, which increase the surface area of your gut, helping it to digest food more effectively. However, in coeliac disease, the damage and inflammation to the lining of your gut flattens the villi, reducing their ability to aid digestion. As a result of this, your gut can no longer digest all of the nutrients that you need from the food you eat. ÿ Diagnosis, signs and symptoms Classic symptoms of coeliac disease include diarrhoea, weight loss and fatigue, but while coeliac disease is primarily a bowel disease, bowel symptoms may also be limited or even absent. Some patients are diagnosed with symptoms related to the decreased absorption of nutrients or with various symptoms which, although statistically linked, have no clear relationship with the malfunctioning bowel. Given this wide range of possible symptoms, the classic triad is no longer a requirement for diagnosis. Children between 9 and 24 months tend to present with bowel symptoms and growth problems shortly after first exposure to gluten-containing products. Older children may have more malabsorption-related problems and psychosocial problems, while adults generally have malabsorptive problems. Many adults with subtle disease only have fatigue or anaemia. There are several tests that can be used to assist in diagnosis. The level of symptoms may determine the order of the tests, but all tests lose their usefulness if the patient is already taking a gluten-free diet. Intestinal damage begins to heal within weeks of gluten being removed from the diet, and antibody levels decline over months. For those who have already started on a gluten-free diet, it may be necessary to perform a re-challenge with 10 g of gluten per day over 2–6 weeks before repeating the investigations. Those who experience severe symptoms (e.g. diarrhoea) earlier can be regarded as sufficiently challenged and can be tested earlier.

ÿ Treatment • Diet: Presently, the only effective treatment is a life-long gluten-free diet. Currently, here is no medication which exists that will prevent the body from attacking the gut when gluten is present. • Refractory Disease: A minority of patients suffer from  refractory disease, which simply means that they do not improve on a gluten free food. This may be because the disease has been present for too long that the intestines are no longer able to heal on diet alone, or because the patient is not adhering to the diet, or because the patient is consuming food that are inadvertently contaminated with gluten. If alternative causes have been eliminated, steriods or  immunosuppressants (such as  azathioprine) may be considered in this scenario. • Experimental treatments -Genetically Engineered wheat species have been selectively bred to be minimally immunogenic. -A combination of enzymes ( prolyl endopeptidase and a barley glutamine-specific cysteine  endopeptidase that degrade the putative 33-mer peptide in the duodenum. This combination would enable  coeliac disease patients to consume gluten-containing products. -Inhibition of zonulin, an endogenous signalling protein linked to increased permeability of the bowel wall and hence increased presentation of  gliadin to the immune system. -Other treatments aimed at other well-understood steps in the  pathogenesis of coeliac disease, such as the action of tissue  transglutaminase and the interaction that may be involved in the killing of enterocytes. ÿ Prevention and control There is significant debate as to the benefits of screening. Some studies suggest that early detection would decrease the risk of osteoporosis and anaemia. In contrast, a cohort studied in Cambridge suggested that people with undetected coeliac disease had a beneficial risk profile for cardiovascular disease (less overweight, lower cholesterol levels). Due to its high sensitivity, serology has been proposed as a screening measure, because the presence of antibodies would detect previously undiagnosed cases of coeliac disease and prevent its complications in those patients. Serology may also be used to monitor adherence to diet: in those who still ingest gluten, antibody levels remain elevated. In the United Kingdom, the National Institute for Health and Clinical Excellence (NICE) recommends screening for coeliac disease in patients with newly diagnosed chronic fatigue syndrome and irritable bowel syndrome. Other clinical scenarios in which screening may be justified include type 1 diabetes, unexplained iron-deficiency anaemia, Down's syndrome, Turner's syndrome, lupus, and autoimmune thyroid disease. Although celiac disease cannot be prevented, symptoms and damage to the small intestine can be reversed by maintaining a strict gluten-free diet. At first, you may also have to avoid milk and milk products. After you stop eating gluten, the intestines begin to heal and you likely will be able to gradually reintroduce milk products into your diet without triggering symptoms. Some adults with celiac disease have a poorly functioning or non-functional spleen, which is a risk factor for developing a pneumococcal infection. For this reason, your doctor may recommend that you get immunized with the pneumococcal vaccine. ÿ In summary Coeliac disease is an autoimmune disorder of the small intestine that occurs in genetically predisposed people of all ages from middle infancy on up. Symptoms include chronic diarrhœa, failure to thrive (in children), and fatigue, but these may be absent, and symptoms in all other organ systems have been described. A growing portion of diagnoses are being made in asymptomatic persons as a result of increased screening. Coeliac disease is caused by a reaction to gliadin, a gluten protein found in wheat. Upon exposure to gliadin, the enzyme tissue transglutaminase modifies the protein, and the  immune system cross-reacts with the small-bowel tissue, causing an  inflammatory reaction. That leads to flattening of the lining of the small intestine, which interferes with the absorption of nutrients, because the intestinal villi are responsible for absorption. The only known effective treatment is a lifelong gluten-free diet. While the disease is caused by a reaction to wheat proteins, it is not the same as wheat allergy.

ÿ Bibliography • http://en.wikipedia.org/wiki/Coeliac_disease • http://www.streetdirectory.com/travel_guide/26899/medical_conditions/a_guide_to_understanding_coeliac_disease.html • http://www.coeliac.org.uk/coeliac_disease/default.asp • http://images.google.com.sg/images?hl=en&q=coeliac%20disease&um=1&ie=UTF-8&sa=N&tab=wi • http://images.google.com.sg/images?hl=en&um=1&q=coeliac+disease&sa=N&start=18&ndsp=18

ÿ Interesting videos • http://www.youtube.com/watch?v=4v-9U8GbLu0 • http://www.youtube.com/watch?v=AxBZ5E8Ilf8