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Query: UMLS:C1291077 (bloating)
1,674 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Celiac disease is an autoimmune enteropathy, triggered by ingestion of gluten in genetically predisposed individuals. Since the use of anti-transglutaminase and anti-endomysium antibodies in the early 1990s, two main groups of clinical presentation can be identified: patients with a symptomatic form of the disease, and patients with a pauci (a)-symptomatic form detected during the work-up of another autoimmune disease or due to a family history of celiac disease. The prevalence of both forms of the disease is currently estimated between 1/100 and 1/400. Classical form of the disease is characterized by occurrence of diarrhoea, failure to thrive, and abdominal bloating in young infants in the months following gluten introduction. Serological tests show high level of anti-transglutaminase and anti-endomysium antibodies. Until recently, the diagnosis required duodenal biopsies that show villous atrophy. HLA genotype can help for diagnosis: the absence of the HLA-DQ2 or DQ8 alleles has a high negative predictive value. European guidelines recently proposed to reconsider the need for systematic endoscopy in typical symptomatic forms with high level of anti-transglutaminase and positive anti-endomysium. These recommendations are being assessed now. Currently, the gluten-free diet remains the only effective treatment for celiac disease. Children with celiac disease have to exclude from their diet all products containing wheat, barley and rye. Gluten-free diet causes clinical remission within a few weeks, but normalization of the small bowel mucosa and negativity of anti-transglutaminase antibodies are obtained in several months or even years. Gluten-free diet is useful to obtain clinical assessment, but also to prevent long-term complications of celiac disease, mainly osteoporosis, other autoimmune diseases, decreased fertility and cancers.
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PMID:Celiac disease in children. 2618 78

Coeliac disease is an immune-mediated systemic disorder caused by ingestion of gluten. The condition presents classically with gastrointestinal signs including diarrhoea, bloating, weight loss and abdominal pain, but presentations can include extra-intestinal symptoms such as iron-deficiency anaemia, faltering growth, delayed puberty and mouth ulcers. Some children are at higher risk of developing coeliac disease, for example those with a strong family history, certain genetic disorders and other autoimmune conditions. If coeliac disease is suspected, serological screening with anti-tissue transglutaminase titres should be performed and the diagnosis may be confirmed by small bowel biopsy while the child remains on a normal (gluten-containing) diet. Modified European guidelines recommend that symptomatic children with anti-tissue transglutaminase titres more than ten times the upper limit of normal, and positive human leucocyte antigen (HLA)-DQ2 or HLA-DQ8 status, do not require small bowel biopsy for diagnosis of coeliac disease. Management of the disease involves strict adherence to a lifelong gluten-free diet, which should lead to resolution of symptoms and prevention of long-term complications. Healthcare professionals should be aware of the varied presentations of coeliac disease to ensure timely screening and early initiation of a gluten-free diet.
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PMID:Coeliac disease in children. 2624 21

Celiac disease (CD) is the most common autoimmune enteropathy worldwide. In CD, dietary gluten triggers a T cell driven small intestinal inflammation in a subset of genetically predisposed subjects, expressing the HLA DQ2 and/or DQ8 genes on their antigen presenting cells. HLA DQ2/DQ8 can bind gluten peptides after their prior modification by the CD autoantigen, tissue transglutaminase (TG2). This process leads to the activation of gluten reactive T cells, small bowel villous atrophy, crypt hyperplasia and intraepithelial lymphocytosis, the histological hallmarks of CD. The clinical picture of CD is extremely heterogeneous including intestinal (especially diarrhea, abdominal pain, bloating) and extraintestinal (especially associated autoimmune diseases, anemia, osteoporosis) manifestations. The prevalence of CD in most parts of the world is estimated at 1:100-1:150 and its diagnosis is based on the presence of circulating autoantibodies (anti-TG2) and the histological detection of villous atrophy. Treatment is a lifelong gluten free diet but adjunctive therapies are in development. Although CD is a well-characterized disease, it is grossly underdiagnosed, despite the severe consequences of long-term gluten ingestion in CD, such as enhanced autoimmunity, refractory CD and intestinal T cell lymphoma. The aim of the presented review is to provide a clinical guide and to summarize the most recent clinical progress in CD research.
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PMID:Management of celiac disease in daily clinical practice. 3059 47