Essay: Celiac disease

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  • Celiac disease
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Celiac disease defined as an autoimmune digestive disease where the ingestion of gluten containing substance leads to damage the small intestine causing digestive disorders. When someone with celiac disease eats gluten, their immune system will be stimulated to produce antibodies (ab) against their own cells of the small intestine specifically the villi, small fingerlike projections that line the small intestine and responsible for absorption of the nutrients, vitamins, minerals, fluids, and electrolytes leading to malabsorption (CELIAC DISEASE, 2009).
Celiac disease is hereditary disease meaning that it runs in families. People with a first-degree relative with celiac disease (parent, child, sibling) have a 1 in 10 risk of developing celiac disease (Singh et al., 2015). Celiac disease affects women more than men. women in the general population are diagnosed with celiac disease two to three times more often than men. Current research indicates that 60% to 70% of the diagnosed ones are women. Celiac disease is not only more frequent in women than in men but is also more severe and more rapid (Ciacci et al., 1995). Celiac disease symptoms tend to appear more in children than in adults especially the digestive system symptoms (Kho, 2015). Celiac disease also called gluten sensitivity enteropathy (GSE) which means disease in the small intestine that caused by gluten. Also known as celiac sprue (CS) because it occurs in tropical areas (Langenberg, Wismans and van Genderen, 2014).
Gluten is a Latin word that means glue. It is a mixture of proteins found in wheat and other grains, including barley and rye. Gluten gives elasticity to dough, helping it rise and keep its shape and often gives the final product a chewy texture. It contains two elements Gliadins and Glutenins. Gliadins are soluble in alcohol and water solutions. They are separated into four groups: alpha, beta, gamma and omega which they are contributing to the extensibility of dough whereas the Glutenins are not soluble in alcohol/water solutions, but are soluble in some salt solutions and they are aggregate of high molecular mass(HMW) and low molecular mass (LMW) subunits that are responsible for the strength and elasticity of dough (Wieser, 2007).
When gluten is introduced to the body it will breakdown to Gliadin and Glutenin. The immune system will secrete antibodies against the gliadin that called anti gliadin antibodies. Anti-gliadin antibodies consist of anti-tissue transglutaminase antibodies that are autoantibodies target the destruction of intestinal villous epithelial cells by killer cells and anti endomysial antibodies that are autoantibodies attack the endomysium. The endomysium is a layer of connective tissue that covers the muscle fiber of the small intestine. The antibodies that mainly involve in this process are from IgA class.
The producing of these antibodies will recruit all sorts of lymphocytes and white blood cells into the small intestine that indicates an inflammation in the wall of the small intestine which eventually disrupt the absorption process that takes place in the villi which line the wall of the small intestine. The celiac disease patient’s villi will be blunted, this known as villous atrophy. In addition, there are grooves between the villi called crypts. In the diseased person these crypts will be elongated and become a little bit bigger because various cells are dividing there, this is called hyperplasia (Kupfer and Jabri, 2012).
The two genes that encode for celiac disease are HLA-DQ2 and HLA-DQ8 (Human leukocyte antigen). If someone has one of these genes its risk to developing celiac disease is increased. Up to 99% of patients with celiac disease will have one of these two genes. However, 40% of normal people may have one of these genes but without showing any symptoms of the celiac disease. Instead of genetics factors celiac disease can be influenced by other environmental elements that trigger the occurrence of the disease such as the excessive ingestion of wheat based products (Vijzelaar et al., 2016).

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