Celiac disease is a lifelong autoimmune inflammatory disease in the small intestine, due to an abnormal immune response to Gluten products when ingested. Those affected by CD have an abnormal reaction during digestion of gluten products, leading to gastrointestinal complications and is also linked to the development of several other health problems. Roughly 60,000 Americans are diagnosed each year with this disorder, while scientist believe that 1 in 140 people have this disease and are unaware of it. Ultimately, researchers believe that more than 2 million Americans have celiac disease. Physicians in the early 1900s rarely considered CD as a diagnosis to those suffering from common gastric pains and colitis symptoms, but with today’s upscale
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Clinical signs and symptoms of CD vary from person to person, but the most common among patients is the gastrointestinal symptoms such as abdominal pain, anorexia, persistent fatigue and chronic diarrhea. A constant exposure to gluten causes the reoccurring symptoms and inflammation in the small intestine, causing gastrointestinal damage and malnutrition in patients. Malnutrition is caused by the disruption in absorption, which primarily occurs in the small intestine. These common symptoms can be linked to several gastrointestinal disorders, which can delay a diagnosis in patients (6). Dermatitis herpetiformis ( Shown in Figure 1), a manifestation of grouped papulovesicles on the skin are also a symptom physician’s use for diagnoses in individuals with absent or minor signs of typical CD symptoms. Autoimmune disorders are commonly linked to CD, as well as the duration of gluten exposure the patient has had. The duration of the exposure is directly proportional to the number of autoimmune disorders that follow in CD patients, including hepatitis, thyroid disease, diabetes mellitus and even development of neurologic disorders. (1) Causes of CD have been extensively studied throughout the years, showing …show more content…
When CD patient ingests gluten, it is broken down into Gliadin which is resistance to the enzymes used to breakdown food. Once Gliadin reaches the small intestine it binds to secretory IgA in the mucosal membrane. In normal digestion, when a substance binds to IgA it is marked for cell destruction, but in Celiac Disease the IgA gliadin complex binds to the TFR (transferrin receptor) and is then transported across the cells to the lamina propria, where gliadin is deamidated by tTG(transglutaminase) and then consumed by macrophages. MHC II (Major Histocompatibility Complex) presents Gliadin on its surface for T-helper cells (CD4), where Patients with celiac disease have specific deaminated gliadin such as HLA-DQ2 or HLA-DQ8, which in response CD4 cells release inflammatory cytokines to initiate inflammation. This reaction alone causes damage to the epithelial cells of the small intestine. T-cells stimulate B cells to release IgA, tTG and EMas antibodies against gliadin, as well as initiate killer T cells to attack the cells that are undergoing inflammation. Researches are unsure why EMas are released, but they are important for diagnostic testing. Because of the destruction of epithelial cells in the small intestine, gliadin is easily able to cross over into the lamina propria causing a simultaneous reaction. Because the small intestine is the primary site for
Clinical signs and symptoms of CD vary from person to person, but the most common among patients is the gastrointestinal symptoms such as abdominal pain, anorexia, persistent fatigue and chronic diarrhea. A constant exposure to gluten causes the reoccurring symptoms and inflammation in the small intestine, causing gastrointestinal damage and malnutrition in patients. Malnutrition is caused by the disruption in absorption, which primarily occurs in the small intestine. These common symptoms can be linked to several gastrointestinal disorders, which can delay a diagnosis in patients (6). Dermatitis herpetiformis ( Shown in Figure 1), a manifestation of grouped papulovesicles on the skin are also a symptom physician’s use for diagnoses in individuals with absent or minor signs of typical CD symptoms. Autoimmune disorders are commonly linked to CD, as well as the duration of gluten exposure the patient has had. The duration of the exposure is directly proportional to the number of autoimmune disorders that follow in CD patients, including hepatitis, thyroid disease, diabetes mellitus and even development of neurologic disorders. (1) Causes of CD have been extensively studied throughout the years, showing …show more content…
When CD patient ingests gluten, it is broken down into Gliadin which is resistance to the enzymes used to breakdown food. Once Gliadin reaches the small intestine it binds to secretory IgA in the mucosal membrane. In normal digestion, when a substance binds to IgA it is marked for cell destruction, but in Celiac Disease the IgA gliadin complex binds to the TFR (transferrin receptor) and is then transported across the cells to the lamina propria, where gliadin is deamidated by tTG(transglutaminase) and then consumed by macrophages. MHC II (Major Histocompatibility Complex) presents Gliadin on its surface for T-helper cells (CD4), where Patients with celiac disease have specific deaminated gliadin such as HLA-DQ2 or HLA-DQ8, which in response CD4 cells release inflammatory cytokines to initiate inflammation. This reaction alone causes damage to the epithelial cells of the small intestine. T-cells stimulate B cells to release IgA, tTG and EMas antibodies against gliadin, as well as initiate killer T cells to attack the cells that are undergoing inflammation. Researches are unsure why EMas are released, but they are important for diagnostic testing. Because of the destruction of epithelial cells in the small intestine, gliadin is easily able to cross over into the lamina propria causing a simultaneous reaction. Because the small intestine is the primary site for