Coeliac Disease Essay

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A working diagnosis of coeliac disease has been made for patient MJ, in this report I will explain and analyse the patient’s immune responses and attempt to suggest several treatments. Coeliac disease is usually triggered by the ingestion of gluten which contains the peptide gliadin found in wheat, alternatively other peptides in the prolamin family are able to elicit an immune response in CD sufferers (C. Gianfrani, 2005). The gliadin antigen works by enlarging tight junctions, allowing larger proteins to permeate through the membrane (Lammers, K.M., 2008), thus inducing an immune response and leading to small intestine enteropathy (C. Gianfrani, 2005). CD is a relatively common disease, it’s estimated that 1% of the population in the US and in Europe suffer from the condition (Catassi, C., et al., 2001). It is a multifactorial disease hence depending upon several aspects such as environmental and genetic input (Sollid, L.M., 2000).

The HLA regions of the gene are responsible for coeliac disease, patients with HLA-DQ2 or the DQ8 variants are most at risk of having the disease, with most sufferers having the DQ2 serotype (Sollid, L.M., 2000). Rye, barley, as well as wheat create similar responses in coeliac patients (Meresse, B., et al., 2012). The usual advice for CD suffers is to maintain a gluten free diet for the rest of their lives (Van de Kamer et al., 1953). The gliadin antigen causes an adaptive immune response, and more recently it’s been found to cause a response in the innate system also. The gliadin epitope is recognised by CD4+ cells of the adaptive immune system and are signalled to create pro inflammatory cytokines (C. Gianfrani, 2003). CD8+ T lymphocytes infiltrate the mucosa of the intestine, their role in the ...

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...n, the body is able to regenerate villi and gut physiology and functions should return to normality. However more research is being done on alternative treatments. Enzyme therapy is currently being studied, the treatment relies on enzymes such as gluten-specific endopeptidases and endoprotease reducing the antigenicity of gluten (Zingone, F., et al., 2010). tTg and inhibitors are also being investigated, although several gliadin epitopes have been shown to mount an immune response without being deaminated (Sollid, M.L., 2005). Another method that was under clinical trials depended on desensitising the body to gluten via a course of vaccines gradually increasing the concentration of gluten, (Zingone, F., et al., 2010) however none of the above methods have passed clinical trials so the only common treatment for coeliac disease remains leading a gluten free lifestyle.

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