Abstract
BackgroundThe mechanisms of cerebellar degeneration attributed to prolonged and excessive alcohol intake remain unclear. Additional or even alternative causes of cerebellar degeneration are often overlooked in suspected cases of alcohol-related ataxia. The objectives of this study were two fold: (1) to investigate the prevalence of gluten-related serological markers in patients with alcohol-related ataxia and; (2) to compare the pattern of brain involvement on magnetic resonance imaging between patients with alcohol and gluten ataxias.Materials & MethodsPatients diagnosed with alcohol and gluten ataxias were identified from a retrospective review of patients attending a tertiary clinic. HLA genotype and serological markers of gluten-related disorders were recorded. Cerebellar volumetry, MR spectroscopy and voxel-based morphometric analyses were performed on patients and compared with matched control data.ResultsOf 904 registered patients, 104 had alcohol ataxia and 159 had gluten ataxia. 61% of the alcohol ataxia group and 70% of the gluten ataxia group had HLA DQ2/DQ8 genotype compared to 30% in healthy local blood donors. 44% of patients with alcohol ataxia had antigliadin antibodies compared to 12% in the healthy local population and 10% in patients with genetically confirmed ataxias. None of the patients with alcohol ataxia and antigliadin antibodies had celiac disease compared to 40% in patients with gluten ataxia. The pattern of structural brain abnormality in patients with alcohol ataxia who had antigliadin antibodies differed from gluten ataxia and was identical to that of alcohol ataxia.ConclusionsAlcohol related cerebellar degeneration may, in genetically susceptible individuals, induce sensitization to gluten. Such sensitization may result from a primary cerebellar insult, but a more systemic effect is also possible. The duration and amount of exposure to alcohol may not be the only factors responsible for the cerebellar insult.
Highlights
Previous studies have shown that patients with chronic alcohol abuse often have elevated serological levels of antibodies directed towards self-antigens as well as elevated IgA immunoglobulins and T-cells[1]
The primary aim of this study was to investigate the prevalence of serological evidence of sensitivity to gluten and HLA-status in patients with ataxia presumed to be due to chronic alcohol abuse (ACAA)
The secondary aim was to compare the pattern of cerebellar involvement using magnetic resonance (MR) imaging between patients with GA and patients with ACAA
Summary
Previous studies have shown that patients with chronic alcohol abuse often have elevated serological levels of antibodies directed towards self-antigens as well as elevated IgA immunoglobulins and T-cells[1]. Individuals with GA (and other gluten-related disorders) show genetic susceptibility, with almost all patients demonstrating the HLA-DQ2/DQ8 genotype[8,9]. 61% of the alcohol ataxia group and 70% of the gluten ataxia group had HLA DQ2/DQ8 genotype compared to 30% in healthy local blood donors. 44% of patients with alcohol ataxia had antigliadin antibodies compared to 12% in the healthy local population and 10% in patients with genetically confirmed ataxias. None of the patients with alcohol ataxia and antigliadin antibodies had celiac disease compared to 40% in patients with gluten ataxia. Conclusions: Alcohol related cerebellar degeneration may, in genetically susceptible individuals, induce sensitization to gluten. Such sensitization may result from a primary cerebellar insult, but a more systemic effect is possible. The duration and amount of exposure to alcohol may not be the only factors responsible for the cerebellar insult
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