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Background: A prior small-scale single center study suggested an association between celiac disease (CD)-type immunity and refractory temporal lobe epilepsy (TLE) with hippocampal sclerosis (HS). The present study addresses this putative association in a large, well-characterized group of drug-resistant epilepsy (DRE) patients. These patients were grouped based on the spectrum of CD and gluten sensitivity-associated antibodies. Methods: In this cross-sectional study, 253 consecutive adult epilepsy patients (135 females, 118 males; age 16–76 years) were categorized into three groups: (i) CD-positive group with either prior diagnosis of CD or CD-specific TG2/EmA antibodies, (ii) AGA-positive group with antigliadin antibodies (AGA) but without CD, and (iii) CD/AGA-negative group without any gluten sensitivity-associated antibodies or CD. Clinical and immunological findings were then compared among the groups. Results: TLE with HS was more common in the CD-positive group compared to CD/AGA-negative group (31.8% versus 11.9%, P = 0.019). Autoimmune disorders were more common in the AGA-positive group than in the CD/AGA-negative group (P = 0.025). Considering HS lateralization; left lateralization was more common in CD-positive group compared to CD/AGA-negative group (71.4% versus 25%, P = 0.030). TG6 seropositivity did not differ among the groups (P > 0.05). Conclusions: This study provides further evidence linking TLE with HS and CD-type autoimmunity suggesting that CD-type immune response to gluten can be one potential mechanism as a disease modifier leading to DRE and HS. Understanding these immunological factors is imperative for developing immunomodulatory or dietary treatments for DRE potentially preventing HS progression. [ABSTRACT FROM AUTHOR]

Objective: Gluten neuropathy (GN) is the term used to describe peripheral neuropathy that occurs in patients with gluten sensitivity (GS) or coeliac disease (CD) in the absence of other risk factors. We aimed to describe the neurophysiological progression rate of GN across time and look into the potential role of genetic susceptibility in its development. Methods: This is a cohort study of 45 patients with GN with a mean follow-up period of 8 ± 5 years. The assessments included clinical and neurophysiological data and HLA-DQ genotyping. Results: The mean age at diagnosis was 60 ± 12 years. The majority of patients had a length-dependent neuropathy (75.6%), whereas the rest were diagnosed with sensory ganglionopathy (SG). DQA1*02-positive patients were more likely to suffer with SG compared to the DQA1*02 negative patients (60% versus 13.8%, p = 0.009). There was also a trend for statistical significance regarding the DQB1*06 allele and the DQA1*01/DQB1*06 haplotype were found more frequently in patients with GN than in healthy controls (p = 0.026 and p = 0.047, respectively). A linear effect of time on the neurophysiological findings was found in radial sensory nerve action potential (1.9% mean annual decrement, p = 0.036), sural sensory nerve action potential (3.3% mean annual decrement, p = 0.013) and tibial nerve motor compound action potential (6.5% mean annual decrement, p < 0.001) amplitudes, independently from age or gender. Conclusions: GN is a late manifestation of GS and CD. The majority of patients have the length-dependent neuropathy with a linear deterioration over time. HLA genotyping of GS and CD patients who suffer from neuropathic symptoms is recommended as it can help identifying patients at risk for developing SG. [ABSTRACT FROM AUTHOR]