Rheumatoid Arthritis Support

Idiopathic diseases are proposed as an expansion of the gluten-sensitivity. By the definition of idiopathic disease the cause is not well defined. One hundred years ago, before gluten was discovered as the cause of coeliac disease, coeliac disease in adults was called adult idiopathic steatorrhoea, non-tropical sprue, and many other names. The debate over this subset stems from the fact that identification of all grades of GSE and allergies is not uniformly approached. Most cases of early GSE go undetected, particularly before 2005. There appears to be a small fraction of non-GSE gluten-sensitive individuals that show neither gluten-allergies but do have elevated anti-gliadin IgA or IgG. Common symptoms are peripheral neuropathies and cerebral ataxia. Within the GSE set these may be explained by calcification of brain channels and avitaminosis. Within the remaining 'DQ2 and DQ8'less cohort. Given that this cohort of GS is idiopathic, the role of allergies, other sensitivities, or other factors in IGS is also unresolved.

Silent Disease. Depending on testing somewhere between 3 and 15% of the normal population have anti-gliadin antibodies (AGA). Studies using anti-gliadin antibodies (AGA) reveal that in undiagnosed or untreated individuals with AGA, with increasing risk for lymphoid cancers and decreased risk for other associated with affluence. Though it is unknown in these studies the percentage that are early stage GSE.

Neuropathies

Other conditions

Antibodies to α-gliadin have been significantly increased non-coeliacs individuals with oral ulceration. Anti-α-gliadin antibodies are frequently found in coeliac disease(CD), to a lesser degree subclinical CD, but are also found in a subset who do not have the disease. The 1991 reference comes from a period when testing for subclinical CD was undeveloped. Of people with pseudo-exfoliation syndrome, 25% showed increased levels of anti-gliadin IgA. One forth of people with Sjögren's syndrome had responses to gluten, of 5 that had positive response to gluten, only one could be confirmed as CD and another was potentially GSE, the remaining 3 appear to be gluten-sensitive. All were HLA-DQ2 and/or DQ8-positive. Treatment to produce remission of Crohns disease(CrD) symptoms on elimination diet indicated the most important foods provoking symptoms were wheat and dairy. A later paper showed little IgE mediated response except to the dairy, while another paper showed no significant anti-food IgE association. Crohn's disease (CrD) may have a link to wheat that is independent of gluten. CrD appears to be associated with high anti-yeast antibodies (ASCA - yeast antigens that are found in bread and other cereal derived products) and affected individuals lack lectin binding proteins such that the mannins in yeast, the antibodies that bind them and aggravate inflammatory colitis. One concern of the above studies is the high prevalence of markers for gluten-sensitive enteropathy, one has to question how idiopathic these conditions are if close examination for GSE has not been undertaken.


Adapted from the Wikipedia article Gluten sensitivity, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki