Abstract
Celiac disease is a chronic intestinal disease caused by intolerance to gluten. It is characterized by immune-mediated enteropathy, associated with maldigestion and malabsorption of most nutrients and vitamins. In predisposed individuals, the ingestion of gluten-containing food such as wheat and rye induces a flat jejunal mucosa with infiltration of lymphocytes. The main symptoms are: stomach pain, gas, and bloating, diarrhea, weight loss, anemia, edema, bone or joint pain. Prevalence for clinically overt celiac disease varies from 1:270 in Finland to 1:5000 in North America. Since celiac disease can be asymptomatic, most subjects are not diagnosed or they can present with atypical symptoms. Furthermore, severe inflammation of the small bowel can be present without any gastrointestinal symptoms. The diagnosis should be made early since celiac disease causes growth retardation in untreated children and atypical symptoms like infertility or neurological symptoms. Diagnosis requires endoscopy with jejunal biopsy. In addition, tissue-transglutaminase antibodies are important to confirm the diagnosis since there are other diseases which can mimic celiac disease. The exact cause of celiac disease is unknown but is thought to be primarily immune mediated (tissue-transglutaminase autoantigen); often the disease is inherited. Management consists in life long withdrawal of dietary gluten, which leads to significant clinical and histological improvement. However, complete normalization of histology can take years.
Highlights
Celiac disease (CD) in children and celiac sprue in adults are probably the same disorder with the same pathogenesis
Since celiac disease can be asymptomatic, most subjects are not diagnosed or they can present with atypical symptoms
It is characterized by immune-mediated enteropathy, resulting in maldigestion and malabsorption
Summary
Firm diagnosis of CD can only be established after small intestinal biopsies confirming a flat jejunal mucosa with absence of normal intestinal villi [2,3]. Gliadin-reactive CD4+ T cells were isolated from the intestinal mucosa of patients with celiac disease [97] These T cells can elicit a B cell response with production of autoreactive antibodies against gliadin peptides or tTG. Whether the role of these antibodies is significant [104] or whether they have a pathogenic role in celiac disease remains unknown [105] It remains unknown why tTG or gliadin complexes are recognized only by T cells from celiac patients and not by those from healthy HLA-DQ2 positive subjects. This gliadin fragment is rich in proline http://www.OJRD.com/content/1/1/3 and contains multiple short amino acid sequences, which were previously shown to stimulate T cell lines [106,111113] This peptide was completely resistant to the breakdown of endogenous proteases and peptidases, indicating that the full length fragment can reach the small intestine and stimulate mucosal T cells. The question of how much gluten is toxic (e.g. trace amounts of contaminated gluten) is a matter of discussion in both Europe and USA
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