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There are indications that patients with non-coeliac gluten sensitivity show a reappearance of symptoms in far shorter time than is the case for coeliac disease: in non-coeliac gluten sensitivity, symptoms usually relapse in a few hours or days of gluten challenge. [13] [14]
This condition is known as refractory coeliac disease (RCD), defined as malabsorption due to gluten-related enteropathy (villous atrophy or elevated intraepitheal lymphocytes) after initial or subsequent failure of a strict gluten-free diet (usually 1 year) and after exclusion of any disorder mimicking coeliac disease. [106] [107]
Coeliac disease (British English) or celiac disease (American English) is a long-term autoimmune disorder, primarily affecting the small intestine, where individuals develop intolerance to gluten, present in foods such as wheat, rye, spelt and barley. [10]
Non-celiac gluten sensitivity (NCGS) or gluten sensitivity [14] is a controversial disorder which can cause both gastrointestinal and other problems. NCGS is included in the spectrum of gluten-related disorders. [3] [4] The definition and diagnostic criteria of non-celiac gluten sensitivity were debated and established by three consensus ...
The degree of gluten cross contamination tolerated by people with non-celiac gluten sensitivity is not clear but there is some evidence that they can present with symptoms even after consumption of small amounts. [37] Sporadic accidental contaminations with gluten can reactivate movement disorders associated with non-celiac gluten sensitivity. [72]
The effectiveness of the treatment depends on the elapsed time from the onset of the ataxia until diagnosis, because the death of neurons in the cerebellum as a result of gluten exposure is irreversible. [57] [58] Gluten ataxia accounts for 40% of ataxias of unknown origin and 15% of all ataxias.
There is a growing body of evidence that the gluten-sensitive intestine differs from the normal gut, several gluten peptides can enter behind the brush border membrane cells. For example, a "33mer" of α-2 gliadin is a magnitude larger than the size exclusion of the tight junction, ω-5 gliadin peptides have been found in the blood stream of ...
The effectiveness of the treatment depends on the elapsed time from the onset of the ataxia until diagnosis, because the death of neurons in the cerebellum as a result of gluten exposure is irreversible. [80] [81] Gluten ataxia accounts for 40% of ataxias of unknown origin and 15% of all ataxias.