Does cryptic gluten sensitivity play a part in neurological illness?

Hadjivassiliou, Marios; Gibson, A. A. M.; Davies‐Jones, G.A.B.; Lobo, Alan; Stephenson, T.J.; Milford-Ward, A

doi:10.1016/s0140-6736(96)90540-1

Cited by 387 publications

(265 citation statements)

References 6 publications

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“…One hypothesis suggests an overt or even subclinical malabsorption causing deficiencies of nutrients known to exert neurotrophic and neuroprotective effects (folic acid and vitamin B 12 ) [8]. Selective vitamin E deficiency has been suggested as a potential cause of neurological complications in CD [27]; in addition, neurological involvement in CD may arise as a consequence of an autoimmune mechanism mediated by antigliadin antibodies [4,7]. Also, the significance of autoreactivity to gangliosides in CD is unclear, but it is probable that it may play a direct role in peripheral neuropathy [12].…”

Section: Discussionmentioning

confidence: 99%

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Peripheral Neurological Disturbances, Autonomic Dysfunction, and Antineuronal Antibodies in Adult Celiac Disease Before and After a Gluten-Free Diet

et al. 2006

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Thirty-two consecutive adult celiac disease (CD) patients (pts), complaining of peripheral neuropathy (12 pts), autonomic dysfunction (17 pts), or both (3 pts), were evaluated to assess the presence of neurological damage (by clinical neurological evaluation and electrophysiological study) and antineuronal antibodies and to assess the effect of a gluten-free diet (GFD) on the course of the neurological symptoms and on antineuronal antibodies. At entry, 12 of 32 (38%) pts showed signs and symptoms of neurological damage: 7 of 12 (58%), peripheral neurological damage; 3 of 12 (25%), autonomic dysfunction; and 2 (17%), both peripheral neurological damage and autonomic dysfunction. The overall TNS score was 105 at entry. Anti-GM1 antibodies were present in 5 of 12 (42%) pts: 3 showed peripheral neurological damage and 2 showed both peripheral neurological damage and autonomic dysfunction. One year after the GFD was started, histological lesions were still present in only 10 of 12 (83%) pts. TNS score was 99, 98, 98, and 101 at the 3rd, 6th, 9th, and 12th month after the GFD was started, so it did not improve throughout the follow-up. None of the pts showed disappearance of antineuronal antibodies throughout the follow-up. We conclude that adult CD patients may show neurological damage and presence of antineuronal antibodies. Unfortunately, these findings do not disappear with a GFD.

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Section: Discussionmentioning

confidence: 99%

“…Untreated CD may show various neurological manifestations such as cerebellar ataxia, epilepsy, and brain atrophy [3][4][5][6][7]. Moreover, associations among CD, peripheral neuropathy, and neuromuscular disorders have been described [8][9][10].…”

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confidence: 99%

Peripheral Neurological Disturbances, Autonomic Dysfunction, and Antineuronal Antibodies in Adult Celiac Disease Before and After a Gluten-Free Diet

et al. 2006

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“…In fact, Klee et al [9] have shown that gluten-derived polypeptides have endorphin and opioid-antagonist properties; such compounds could be adsorbed from an inflamed or altered gastrointestinal tract and possibly cause psychotic symptoms [10]. Hadjivassiliou et al [11], in 53 patients with neurological dysfunction of unknown origin, found 57% positive subjects for antigliadin antibodies, nine with histological evidence of coeliac diseases, ten with nonspecific duodenitis and seven with no lesion. They proposed that antigliadin antibodies are more directly involved in the neuropathological process, or are markers of autoimmune activity with an unidentified neurotoxic antibody [11], according to some epidemiological, genetic and clinical data supporting the hypothesis of an autoimmune process in schizophrenia [12᎐15].…”

Section: Discussionmentioning

confidence: 99%

Schizophrenic symptoms and SPECT abnormalities in a coeliac patient: regression after a gluten‐free diet

Santis¹,

Addolorato²,

Romito³

et al. 1997

Journal of Internal Medicine

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A 33-year-old patient, with pre-existing diagnosis of 'schizophrenic' disorder, came to our observation for severe diarrhoea and weight loss. Use of single photon emission computed tomography, ( 99m Tc)HMPAO SPECT, demonstrated hypoperfusion of the left frontal brain area, without evidence of structural cerebral abnormalities. Jejunal biopsy showed villous atrophy. Antiendomysial antibodies were present. A gluten-free diet was started, resulting in a disappearence of psychiatric symptoms, and normalization of histological duodenal findings and of ( 99m Tc)HMPAO SPECT pattern. This is the first case in which, in an undiagnosed and untreated coeliac patient with psychiatric manifestations, the ( 99m Tc)HMPAO SPECT demonstrated a dysfunction of frontal cortex disappearing after a gluten-free diet.

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“…In the former group, depression and anxiety have been reported, 41 whereas in the latter there are a number of idiopathic neurological disorders, such as epilepsy with and without parieto-occipital calcifications, cerebellar ataxia, intellectual deterioration with attention/memory impairment, brain atrophy, peripheral neuropathy, multiplex myoclonus (Friedreich's disease) and multiple sclerosis. [42][43][44][45][46] Reproductive system dysfunction may be a sign of CD in both sexes. In females, there is a trend to late menarche, amenorrhea, early menopause and infertility, which respond positively to gluten withdrawal.…”

Section: Introductionmentioning

confidence: 99%

Celiac disease: diagnostic criteria in progress

2011

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Until a few years ago, celiac disease (CD) was thought to be a rare food intolerance that was confined to childhood and characterized by severe malabsorption and flat intestinal mucosa. Currently, CD is regarded as an autoimmune disorder that is common in the general population (affecting 1 in 100 individuals), with possible onset at any age and with many possible presentations. The identification of CD is challenging because it can begin not only with diarrhea and weight loss but also with atypical gastrointestinal (constipation and recurrent abdominal pain) and extra-intestinal symptoms (anemia, raised transaminases, osteoporosis, recurrent miscarriages, aphthous stomatitis and associated autoimmune disorders), or it could be completely symptomless. Over the last 20 years, the diagnostic accuracy of serology for CD has progressively increased with the development of highly reliable tests, such as the detection of IgA tissue transglutaminase and antiendomysial and IgG antideamidated gliadin peptide antibodies. The routine use of antibody markers has allowed researchers to discover a very high number of 'borderline' cases, characterized by positive serology and mild intestinal lesions or normal small intestine architecture, which can be classified as potential CD. Therefore, it is evident that the 'old celiac disease' with flat mucosa is only a part of the spectrum of CD. It is possible that serology could identify CD in its early stages, before the appearance of severe intestinal damage. In cases with a positive serology but with mild or absent intestinal lesions, the detection of HLA-DQ2 and HLA-DQ8 can help reinforce or exclude the diagnosis of gluten sensitivity.

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Does cryptic gluten sensitivity play a part in neurological illness?

Cited by 387 publications

References 6 publications

Peripheral Neurological Disturbances, Autonomic Dysfunction, and Antineuronal Antibodies in Adult Celiac Disease Before and After a Gluten-Free Diet

Peripheral Neurological Disturbances, Autonomic Dysfunction, and Antineuronal Antibodies in Adult Celiac Disease Before and After a Gluten-Free Diet

Schizophrenic symptoms and SPECT abnormalities in a coeliac patient: regression after a gluten‐free diet

Celiac disease: diagnostic criteria in progress

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