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Patients with celiac disease, nonceliac gluten sensitivity show similar neurological dysfunction
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Celiac disease and non-celiac gluten sensitivity may share common pathophysiological mechanisms, as patients with these conditions showed similar neurological manifestations that responded equally to a gluten-free diet, according to recent study data.
“This retrospective review of probably the largest cohort of patients presenting with neurological manifestations of [gluten-related disorders] suggests that there are no clear distinguishing neurological features between those patients with [celiac disease] and those with [non-celiac gluten sensitivity],” the researchers wrote.
Clinical, neurophysiological and imaging data were compared for patients with CD and non-celiac gluten sensitivity (NCGS). All 562 patients presented with neurological dysfunction related to gluten sensitivity when first assessed and all patients had circulating anti-gliadin antibodies. Patients were consecutively seen at the neuroscience department, Royal Hallamshire Hospital, Sheffield, UK, between 1994 and 2014, and remained on an active follow-up schedule.
Patients with evidence of enteropathy were designated to Group 1 (CD; 41%) and patients without evidence of enteropathy were designated to Group 2 (NCGS; 59%).
Cerebellar ataxia, peripheral neuropathy and encephalopathy were found to be the most common neurological manifestations among all of the patients. A larger percentage of patients in Group 1 had encephalopathy, and a greater percentage of patients in Group 2 had neuropathy; however, the neuropathy was more severe in Group 1. The two groups had similar severity of ataxia, and all patients responded to a gluten-free diet.
A greater percentage of patients had TG2 antibodies in Group 1 (91%), compared with 29% of the patients in Group 2. Similar prevalence of TG6 antibodies were found in both groups (67% vs. 60%).
“An important finding in this study is that patients with NCGS can present with neurological dysfunction in an identical manner to those patients with CD, suggesting similar immunological processes being responsible at least for the neural damage,” the researchers wrote. “This is also supported by the similar prevalence of TG6 antibodies in the two groups.” – by Suzanne Reist
Disclosures: The researchers report no relevant financial disclosures.
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