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Coeliac Disease (CD) affects at least 1% of the population. "Classical" CD refers to gastrointestinal presentations with anaemia and gastrointestinal symptoms. CD can, however, present with extraintestinal manifestations, the commonest of which are dermatitis herpetiformis and neurological presentations (e.g., ataxia, neuropathy, encephalopathy). Recognition and research into the pathophysiology of such manifestations is likely to enhance our understanding of this complex autoimmune disorder.
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Coeliac Disease (CD) affects at least 1% of the population. "Classical" CD refers to gastrointestinal presentations with anaemia and gastrointestinal symptoms. CD can, however, present with extraintestinal manifestations, the commonest of which are dermatitis herpetiformis and neurological presentations (e.g., ataxia, neuropathy, encephalopathy). Recognition and research into the pathophysiology of such manifestations is likely to enhance our understanding of this complex autoimmune disorder.
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Coeliac Disease (CD) affects at least 1% of the population. "Classical" CD refers to gastrointestinal presentations with anaemia and gastrointestinal symptoms. CD can, however, present with extraintestinal manifestations, the commonest of which are dermatitis herpetiformis and neurological presentations (e.g., ataxia, neuropathy, encephalopathy). Recognition and research into the pathophysiology of such manifestations is likely to enhance our understanding of this complex autoimmune disorder.
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The extraintestinal manifestations of coeliac disease (CD) are now well recognised. We have previously edited a special issue for Nutrients covering all aspects of the extraintestinal manifestations in the context of CD. In this issue we wish to concentrate just on the neurological manifestations. The identification of TG6 autoantibodies in patients with neurological manifestations and its use in the diagnosis of such patients seems to be a good opportunity to focus on the neurological aspect of CD. In addition it is now clear that such manifestations can occur even in the absence of enteropathy but in the presence of antigliadin antibodies and/or TG6 antibodies. Given that such antigliadin antibodies can be found in up to 10% of the “healthy” population we anticipate that the neurological manifestations are likely to be very common and thus merit early recognition and treatment.
Research & information: general --- Biology, life sciences --- Food & society --- coeliac disease --- gluten free diet --- psychiatric manifestations --- autistic spectrum disorder --- attention deficit hyperactivity disorder --- depression --- anxiety --- bipolar disorder --- schizophrenia --- eating disorders --- gluten --- neurological disorders --- gliadin --- ataxia --- neuropathy --- myopathy --- encephalopathy --- food intolerance --- celiac disease --- gluten sensitivity --- gluten-free diet --- cognition --- neurology --- disease duration --- autoimmunity --- multiple sclerosis --- psoriasis --- autoimmune thyroid disease --- type 1 diabetes --- transglutaminase antibodies --- TG2 --- TG3 --- TG6 --- dermatitis herpetiformis --- gluten ataxia --- gluten encephalopathy --- gluten neuropathy --- autism spectrum disorder --- review --- stiff person syndrome --- anti-GAD antibodies --- cerebellar ataxia --- gluten-related pathology --- cortical excitability --- transcallosal inhibition --- transcranial magnetic stimulation --- executive dysfunction --- gamma-amino-butyric acid --- neurological dysfunction --- headaches --- anti-gliadin antibodies --- MR imaging --- TG6 antibodies --- non-celiac wheat sensitivity --- irritable bowel syndrome --- multiple food hypersensitivity --- neuropsychiatric symptoms --- HLA --- duodenal lymphocytosis
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