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Effectiveness of nutrition intervention in Celiac disease - Essay Example

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This essay describes in detail the pathology of the Celiac disease in relation to the nutrition of specific substances and how diet efficacy would affect the pathology of this disease. The author investigates the major causes of the disease and thus the best preventive measures of the disease…
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Effectiveness of nutrition intervention in Celiac disease
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Celiac Disease Celiac disease which is also known as the celiac sprue is a disease related to the small intestine. In it the epithelium of small intestine is affected as the mucosal cells lining it are destroyed. This causes difficulties in nutrient absorption from the small intestine. It usually occurs in white skinned people and lesser in Japanese, Africans and Mongolians. The prevalence of the disease in the last years has increased significantly to alarm the medical world of its importance in pathology. It is usually caused by gluten which is an alcohol soluble component of protein. This composite of protein is also insoluble in water. The disease is successfully cured by treatments related to a gluten free diet or by enzymatic therapies. But the most successful intervention is that of a gluten free diet. This essay would further describe the pathology of the disease in relation to the nutrition of specific substances and how diet efficacy would affect the pathology of this disease (Robbins et al 2005). The disease is characterized by a marked sensitivity to gluten which is an important composite of proteins. Gluten can usually be found in grains and is alcohol soluble. This sensitivity can lead to the secretion of T cells from the bone marrow and can thus cause inflammation. It is usually caused because of hereditary features and environmental factors. Usually people suffering from it show a deposition of major histocompatibility complex class II HLA DQ2. Gliadin which is a protein containing gluten leads to the formation of the enzyme known as transglutaminase and this enzyme then deamidates gliadin into its deamidated form. This deamidated gliadin then attaches to DQ2 and DQ8. And further the CD8 and T cells then recognize the stress induced on the epithelial cells which then secrete the antibody interferon gamma which acts on the mucosa of the epithelium and hence destroying it. Thus it can be said that celiac sprue is a disease caused by the autoimmune component of T cell which produces antibodies against the body’s own mucosal cells. The disease can be diagnosed if the antibodies of gliadin and transgluataminase are detected in the body. Moreover definitive diagnosis can be achieved only if malabsorption is witnessed in the body, small bowel biopsy is done so as to show the lesion and betterment of the condition is witnessed if a gluten free diet is followed. Celiac disease in the long term can cause malignant diseases which may be lymphoma in the small intestine, adenocarcinoma in the small intestine and esophageal squamous cell carcinoma. If the histological features of the small intestinal mucosa are seen it would be witnessed that the mucosa is flat and is going through atrophy. The surface epithelium of the tissue would be degenerated because of the destruction of the mucosa (Robbins et al 2005). It is seen that the disease is mostly prevalent in Europe and the siblings of celiac disease show more tendency of getting the disease from each other because of the genetic similarities (Bourgey et al 2007). The antideamidated gliadin peptide antibody test has proved to be more effective in diagnosing Celiac disease (Rashtak et al 2007, Kaukinen et al 2007, Villata et al 2007 & Leffler et al 2007). The most effective treatment for this disease is by intervention in the nutritional intakes of the individual. It is seen that gluten should be avoided the most in this disease so that the mucosa can recover properly. It is recommended that gluten intake should be reduced to less than 10mg in a day. Fatigue is commonly caused in this disease and to recover from this one has to get treated by L-carnithine. Gluten products should greatly be avoided in this disease as wheat contains a great amount of gluten. Moreover another treatment for this disease can be those of enzymes in which the toxin gluten epitopes should be removed before they actually reach the epithelium of the intestine. This should be achieved by detoxifying wheat flour and fermenting it with a specific mixture (Rizello et al 2007 & Gianfrani et al 2007). Celiac disease can cause serious diseases if not cured in a proper span of time. These complications can be related to cancers in the small intestine ulcerative jejunoilietis, collagenous celiac disease and pancreatitis. Individuals who suffer from celiac diseases may develop cancers or lymphomas in the small intestine. The individuals who are more at risk from the celiac disease are the ones who are having it for a long time. Moreover these individuals can also develop these carcinogens in the esophagus too. These carcinogens can thus cause the person to lose weight and get anemic. It can be diagnosed by running a Computed Tomography test. Ulcerative jejunoileitis is another complication caused by celiac disease. Such a complication can cause the intestinal lumen to get obstructed and thus can lead to blood loss. Similarly a person with celiac disease for a long time can also develop collagenous celiac disease in which collagen fibers get stored abnormally under the lining of intestine. Pancreatitis is rarely caused by celiac sprue however because of its effect on the absorption rate it can cause the disease. Celiac sprue would result in the person changing his diet to a gluten free diet in which he would not be able to consume enough magnesium and this would further cause pancreatitis (Robbins et al 2005). Here however the treatment of nutrition intake would be discussed in more detail. Gliadin is the main cause of the disease to occur and thus the best prevention of the disease is to consume a gluten free diet. Oats although are controversial when relating to the gluten free diet but even then they are at times said to be a safe source of gluten free diet. They are not usually recommended to the people as they may cause significant increase in the level of gluten. It is found that oats help to increase the individuals intake of iron fiber thiamine and zinc (Storsud 2003). Wheat starch although an important source for gluten is not necessarily causing celiac disease if taken in the amounts recommended by the Codex. This is because usually wheat starch produced in the UK contains only about 0.3 % proteins in its dry matter. This is further proved by several studies conducted by Selby and Kaukinen et al which show that this wheat starch allowed to the patients does not greatly affect the submucosal lesion in the small intestine. Moreover it was also seen that the villous in the patients consuming these wheat starch products under the codex standards was not affected. (Selby et al 2003, Kaukinen et al 1999 & Lohiniemi et al 2000). Similarly another study conducted by Peraaho et al showed that mucosal lesion did not occur on people who followed the standards of codex when consuming a gluten free diet. By gluten free diet it is not usually meant that the diet be completely free of gluten. Worldwide it is seen that patients suffering from celiac disease have been allowed to intake gluten but the amount that has to be taken varies but is quite less. It is necessary for the patient to visit his/her doctor continuously so as to check the submucosal lesion with every diet he/she is suggested. On the other hand the celiac disease can not be completely treated by gluten free diet intervention (Perri et al 2000, Bona et al 2002, Jameson 2000 & Hallert et al 2002). This gluten free diet intervention can lead to other diseases to develop in the patient and eventually lead to death if not diagnosed. It can lead to the increase of lipids, decreased micronutrients to the health and weight management problems. As gluten free diet contains less vitamins magnesium and zinc it would lead to vitamin deficiencies. And these deficiencies would further cause increased cardiovascular diseases and problems in blood formation. Cholesterol would not be absorbed in the intestine and this would lead to high cholesterol levels. And these cholesterol levels would thus lead to more cardiovascular diseases to arise ((Hallert 2002, Kupper 2005 & Mariani 1998) Although gluten free diet has its own complications but it is still the best proved treatment for celiac sprue. In order to raise the efficiency level of a gluten free diet it is necessary to consult the doctor frequently at times while being on such a diet. The level of gluten in the diet should strictly be measured so that it neither goes high nor low enough to cause other diseases. It is seen that gluten free diet best works if the codex standards are applied and one consumes gluten as per the recommended daily allowance for the celiac sprue patients. By applying such a standard they would be able to avoid the complications of malabsorption of other vital substances in the body which can lead to even more disease and eventually cause death. Bibliography Kumar, Vinay, Abul K. Abbas, Nelson Fausto, Stanley L. Robbins, and Ramzi S. Cotran. Robbins and Cotran Pathologic Basis of Disease. Philadelphia: Elsevier Saunders, 2005. Bourgey M, Calcagno G, Tinto N, et al. HLA related genetic risk for celiac disease. Gut 2007; 56:1054–1059 Rashtak S, Ettore MW, Homburger HA, et al. Comparative usefulness of deamidated gliadin antibodies in the diagnosis of celiac disease. Clin Gastroenterol Hepatol 2008; 6:426–432. Kaukinen K, Collin P, Laurila K, et al. Resurrection of gliadin antibodies in celiac disease. Deamidated gliadin peptide antibody test provides additional diagnostic benefit. Scand J Gastroenterol 2007; 42:1428–1433. Villata D, Alessio MG, Tampoia M, et al. Testing for IgG class antibodies in celiac disease patients with selective IgA deficiency. A comparison of the diagnostic accuracy of 9 IgG antitissue transglutimase, 1 IgG antigliadin and 1 IgG antideaminated gliadin peptide antibody assays. Clin Chim Acta 2007; 382:95–99. Leffler DA, Edwards George JB, Dennis M, et al. A prospective comparative study of five measures of gluten-free diet adherence in adults with celiac disease. Aliment Pharmacol Ther 2007; 26:1227–1235. Rizello CG, De Angelis MD, Di Cagno R, et al. Highly efficient gluten degradation by lactobacilli and fungal proteases during food processing: new perspectives for celiac disease. Appl Environ Microb 2007; 73:4499–4507. Gianfrani C, Siciliano RA, Facchiano AM. Transamidation of wheat flour inhibits the response to gliadin of intestinal t cells in celiac disease. Gastroenterology 2007; 133:780–789. Størsrud S, Hulthén LR, Lenner RA. Beneficial effects of oats in the gluten-free diet of adults with special reference to nutrient status, symptoms and subjective experiences. Br J Nutr 2003;90:101–107. Selby WS, Painter D, Collins A, Faulkner-Hogg KB, Loblay RH.Persistent mucosal abnormalities in coeliac disease are not related to the ingestion of trace amounts of gluten. Scand J Gastroenterol 1999;34:909–914. Kaukinen K, Collin P, Holm K, et al. Wheat starch-containing gluten-free flour products in the treatment of coeliac disease and dermatitis herpetiformis. A long-term follow-up study. Scand J Gastroenterol 1999;34:164–169. Lohiniemi S, Maki M, Kaukinen K, Laippala P, Collin P. Gastrointestinal symptoms rating scale in coeliac disease patients on wheat starch-based gluten-free diet. Scand J Gastroenterol 2000;35:947–949. Perri F, Pastore M, Zicolella A, Annese V, Quitadamo M, Andriulli A. Gastric emptying of solids is delayed in celiac disease and normalizes after gluten withdrawal. Acta Paediatr 2000;89:921–925. 32. Bona G, Marinello D, Oderda G. Mechanisms of abnormal puberty in coeliac disease. Horm Res 2002;57(Suppl 2):63–65. 33. Jameson S. Coeliac disease, insulin-like growth factor, bone mineral density, and zinc. Scand J Gastroenterol 2000;35:894–896. 34. Hallert C, Grant C, Grehn S, Grännö C, Hultén S, Midhagen G Ström M, Svensson H, Valdimarsson T. Evidence of poor vitamin tatus in coeliac patients on a gluten-free diet for 10 years. Aliment Pharmacol Ther 2002;16:1333–1339. Hallert C, Grant C, Grehn S, et al. Evidence of poor vitamin status in celiac patients on a gluten-free diet for 10 years. Alimentary Pharmacolology & Therapeutics 2002;16:1333-1339. Kupper C. Dietary guidelines and implementation for celiac disease. Gastroenterology2005;128(4 Suppl 1):S121-7. Mariani P, Viti M, Montouri M, et al. The gluten-free diet: a nutritional risk factor for adolescents with celiac disease? Journal of Pediatric Gastroenterology and Nutrition1998;27:519-523. Peräaho M, Kaukinen K, Paasikivi K, Sievänen H, Lohiniemi S,Mäki M, Collin P. Wheat-starch-based gluten-free products in the treatment of newly detected coeliac disease: prospective and randomized study. Aliment Pharmacol Ther 2003;17:587–594. Read More
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