Celiac Disease - Nursing School
Running Head: CELIAC DISEASE
Celiac Disease
Introduction
Celicac disease (CD) is defined as an immune mediated malabsorption disorder caused by the ingestion of gluten and related proteins, occurring in genetically predisposed individuals, and characterized by a variable combination of elevated titers of celiac-specific autoantibodies, an inflammatory enteropathy with variable degrees of severity, and a wide range of gastrointestinal and/or systemic complaints” (Rivera, Assiri, Guandalini, 2013).
Pathophysiology
Etiology
Both genetic and environmental factors are important and necessary for development of CD. The presence of human leukocyte antigen (HLA) alleles HLA-DQ2 and the HLA-DQ8 are the best characterized genetic susceptibility serum markers that determine predisposition to the disease; however, not everyone with these genetic markers develop CD (Schmelzer, 2011).
Pathogenesis
When gluten is partially digested in the genetically susceptible individual, “gluten releases prolamine peptides, which are absorbed into the lamina propria in the intestinal submucosa” (Schmelzer, 2011, p. 1050). “Once in the lamina propria, peptides bind to HLA-DQ2 and/or HLA-DQ8 antigens and activate an inflammatory response. “These molecules are expressed on the surface of the antigen-presenting cell in the gut lamina propria and play a central role in celiac disease pathogenesis because they are responsible for presenting modified gluten-peptides to CD4+ T cells, thereby eliciting a gluten-specific immune response” (Rivera et al., 2013, p. 637). As with any chronic inflammatory response, devastating structural changes at the site injury take place in a slow progression. Damage is most severe in the duodenum, most likely due to longer exposure to gluten during digestion. The result is flattening and destruction of microvilli, increased density and hypertrophied crypts by infiltration of lymphocytes in the epithelium of mucosa” (Rivera
Celiac Disease
Introduction
Celicac disease (CD) is defined as an immune mediated malabsorption disorder caused by the ingestion of gluten and related proteins, occurring in genetically predisposed individuals, and characterized by a variable combination of elevated titers of celiac-specific autoantibodies, an inflammatory enteropathy with variable degrees of severity, and a wide range of gastrointestinal and/or systemic complaints” (Rivera, Assiri, Guandalini, 2013).
Pathophysiology
Etiology
Both genetic and environmental factors are important and necessary for development of CD. The presence of human leukocyte antigen (HLA) alleles HLA-DQ2 and the HLA-DQ8 are the best characterized genetic susceptibility serum markers that determine predisposition to the disease; however, not everyone with these genetic markers develop CD (Schmelzer, 2011).
Pathogenesis
When gluten is partially digested in the genetically susceptible individual, “gluten releases prolamine peptides, which are absorbed into the lamina propria in the intestinal submucosa” (Schmelzer, 2011, p. 1050). “Once in the lamina propria, peptides bind to HLA-DQ2 and/or HLA-DQ8 antigens and activate an inflammatory response. “These molecules are expressed on the surface of the antigen-presenting cell in the gut lamina propria and play a central role in celiac disease pathogenesis because they are responsible for presenting modified gluten-peptides to CD4+ T cells, thereby eliciting a gluten-specific immune response” (Rivera et al., 2013, p. 637). As with any chronic inflammatory response, devastating structural changes at the site injury take place in a slow progression. Damage is most severe in the duodenum, most likely due to longer exposure to gluten during digestion. The result is flattening and destruction of microvilli, increased density and hypertrophied crypts by infiltration of lymphocytes in the epithelium of mucosa” (Rivera