Molekulare Physiologie und Pathobiochemie ausgewählter Magen ...

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ZIEL Molekulare Physiologie - Pathobiochemie MMalabsorption l b ti (Ursachen (U h von Dünndarmepithelstörungen) Dü d ith l tö ) Erkrankungen g des Dünndarms mit den Leitsymptomen y Diarrhoe und Gewichtsverlust primär: Mucosa morphologisch unverändert; sekundär: Schädigung (Atrophie) der Mucosa oder Behinderung des Abtransportes resorbierter Stoffe durch Blut oder Lymphe. Beispiel: Zöliakie Hematoxylin-eosin stained cross-sections of intestinal villi: normal epithelium (left) and celiac epithelium (right), characterized by infiltration of intraepithelial lymphocytes and flattened villi.
ZIEL Molekulare Physiologie - Pathobiochemie Celiac Disease (Zöliakie=glutensensitive Enteropathie Prävalenz auf 1:500 in Deutschland und Dänemark und etwa 1:110 in den USA und Großbritannien, im weltweiten Durchschnitt ungefähr 1:270 Symptoms of celiac disease are caused by a glutamine and proline rich peptides found in gluten that initiates the inflammatory response when bound to these HLA haplotypes (Shan, (Shan Lu et al, al 2002). 2002) The primary HLA association in most patients with celiac disease is with DQ2 (DQA*05/DQB1*02) and in a minority of patients with DQ8 (DQA1*03/DQB1*0302). Approximately 97% of individuals with celiac disease have the HLA-D2Q or HLA-DQ8, compared to 40% of the general population (NIH, 2006). The x-ray crystal structure of the soluble domain of HLA HLA-DQ2 DQ2 was observed bound to the deaminated gluten epitope alpha- alpha I-gliadin. The HLA association in celiac disease can be explained by a superior ability of DQ2 to bind the repertoire of proline-rich gluten pepties that have survived gastrointestinal digestion and that have been deaminated by tissue transglutaminase (Kim et al., 2004). Celiac disease is diagnosed in about 10% of first degree relatives of an individual with celiac disease (Logan, 1992). Although hereditary factors play a significant role, genetic factors alone do not explain the development of the disease because the disease is concordant in only 60% to 70% of identical twins. All people with HLA DQ2 and DQ8 do not develop into disease, and others without those alleles can develop celiac disease, so more genes may be involved. Additional factors such as hormones and infectious agents may also be involved in linking the ingestion of gluten with a chronic inflammatory reaction in the intestine in genetically predisposed individuals (Fasano,1996).
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Molekulare Physiologie und Pathobiochemie ausgewählter Magen ...

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