Panagiotis Zis1,2,3, Ptolemaios Sarrigiannis4, Artemios Artemiadis5, David S Sanders6, Marios Hadjivassiliou4. 1. Academic Directorate of Neurosciences, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK. takiszis@gmail.com. 2. Medical School, University of Cyprus, Nicosia, Cyprus. takiszis@gmail.com. 3. Academic Unit of Gastroenterology, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK. takiszis@gmail.com. 4. Academic Directorate of Neurosciences, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK. 5. Medical School, University of Cyprus, Nicosia, Cyprus. 6. Academic Unit of Gastroenterology, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK.
Abstract
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.
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.
Authors: Panagiotis Zis; Marios Hadjivassiliou; Ptolemaios Georgios Sarrigiannis; Alexander St John Edward Barker; Dasappaiah Ganesh Rao Journal: Brain Behav Date: 2017-11-24 Impact factor: 2.708
Authors: Marios Hadjivassiliou; Iain D Croall; Richard A Grünewald; Nick Trott; David S Sanders; Nigel Hoggard Journal: Nutrients Date: 2021-05-28 Impact factor: 5.717