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Celiac Disease & Gluten Intolerance Research
New research clarifies the mechanics driving crypt hyperplasia in celiac disease, and suggests that PRC2-dependent fostering of epithelial stemness is a common aspect of intestinal diseases marked by epithelial hyperplasia or neoplasia.
Fecal gluten peptides show limits of monitoring gluten-free diet in celiac disease patients
If kids with celiac disease go on a gluten-free diet, how quickly does their serology return to normal?
New research shows that most patients with SNVA, especially non-white patients, do not have celiac disease.
Transglutaminase 2-specific celiac disease autoantibodies cause morphological changes and inflammation in the small-bowel mucosa of mice.
Could the amount of gluten matter more than breast-feeding or the timing of the introduction of gluten as a trigger for celiac disease?
Celiac disease is an autoimmune disease in genetically susceptible individuals and is triggered by adverse immune reactions to gluten, a protein found in wheat and other grains.
Older people often show clinically atypical symptoms of celiac disease, which can delay diagnosis.
Sufferers of clostridium difficile infection have new hope in fecal transplants. Doctors understand better why they work.
A new study looks at intestinal cell damage and systemic immune activation in individuals reporting wheat sensitivity, but no celiac disease.
Does the season or region of birth influence celiac disease risk? New science says yes.
Although serological tests are useful for identifying celiac disease, it is well known that a small minority of celiacs are seronegative, and show no blood markers for celiac disease. A team of researchers wanted to define the prevalence and features of seronegative compared to seropositive celiac disease, and to establish whether celiac disease is a common cause of seronegative villous atrophy.
Many doctors hear from celiac patients who suffer from persistent symptoms despite a long-term gluten-free diet. A research team recently set out to investigate the prevalence and severity of these symptoms in patients with variable duration of a gluten-free diet.
Study shows previously unappreciated diversity and plasticity of innate IEL compartment, along with loss of differentiation potential in patients with RCDII.
Some researchers have suggested that gluten may not be the actual trigger of symptoms in non-celiac gluten sensitivity. Others feel that gluten is definitely the trigger, especially in certain cases.
Metagenomics shows dysbiosis and a potentially pathogenic N. flavescens strain in adults with celiac disease.
Symptoms and damage in celiac disease is caused by partially-degraded gluten peptides from wheat, barley and rye. Susceptibility genes are necessary to trigger celiac disease, but they can't do it alone. Some researchers suspect that these susceptibility genes might get help from conditions resulting from unfavorable changes in the microbiota.
Study shows gliadin peptide p31-43 activates celiac-related innate immune pathways in vivo, also hints at a common mechanism for interaction between dietary gluten and viral infections in triggering celiac disease.