Quote:
Originally Posted by Redda
Celiac disease is an autoimmune reaction with damage to the villae of the small intestine.
Does anyone know, with the DQ1 genes and neurological symptoms, is there an autoimmue reaction? Or another kind of physiological action or reaction? In the brain, or in the nervous system?
Thanks, Redda in Ohio
two DQ1 genes
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My dear 13 year old nephew is double dq1 and has had fairly severe neurological damage that is most likely permanent.
Be sure to read the articles by Dr. Hadjii that Anne mentions. They are all on the gluten file site listed in Judys post.
http://jnnp.bmjjournals.com/cgi/content/full/72/5/560
I found this paragraph to be most interesting.
"Isn't the neurological damage nutritional?"
Nutrient deficiencies (B12, folate, vitamin D, vitamin E) are rare in this neurological population. Given that two thirds of these patients have no enteropathy this is hardly surprising. The concept of the neurological manifestations being nutritional in origin is now outmoded. Intestinal mucosal damage in coeliac disease is the result of both humoral and T cell mediated inflammation. Such inflammation is not, however, confined to the gut, as activated HLA restricted gliadin specific T cells25 and antigliadin antibodies are found systemically. Antigliadin antibodies are also found in the CSF.26 Postmortem findings from two of our patients with gluten ataxia has shown perivascular cuffing with both CD4 and CD8 cells. This inflammation was primarily seen in the white matter of the cerebellum. There was also marked but patchy Purkinje cell loss. We have also found antibodies against Purkinje cells in patients with gluten ataxia. Our research suggests that IgG antigliadin antibodies cross react with epitopes on Purkinje cells from human cerebellum.27 Characterisation of the anti-Purkinje cell antibodies by immunoblotting may provide a useful marker for the diagnosis of gluten ataxia in a manner analogous to the use of antiendomysium antibodies as a marker for coeliac disease or the anti-Yo antibody in paraneoplastic cerebellar degeneration.