Can head trauma trigger celiac disease? Nation-wide case–control study

Jonas F Ludvigsson,Marios Hadjivassiliou

doi:10.1186/1471-2377-13-105

Abstract

BackgroundTG6, a brain expressed transglutaminase, is implicated in the neurological manifestations of celiac disease (CD). We hypothesized that earlier brain injury due to head trauma may be more common in patients with CD, potentially through trauma-induced TG6 leading to interaction with TG2.MethodsThrough biopsy reports from all 28 pathology departments in Sweden we identified 29,096 individuals with CD (in this study defined as villous atrophy). We then examined the risk of earlier head trauma in CD compared to the risk in 144,522 controls matched for age, sex, county and calendar year. Odds ratios (ORs) were calculated using conditional logistic regression.Results981 (3.4%) individuals with CD and 4,449 (3.1%) controls had a record of earlier head trauma. Individuals with head trauma were hence at a 1.10-fold increased risk of future CD (95% CI = 1.02-1.17). ORs were independent of sex or age at CD. The highest risk of future CD was seen during the first year after trauma. There was no association between severity of trauma and risk of developing CD.ConclusionsThis study found a very small excess risk for future CD in individuals with an earlier head trauma.

Highlights

transglutaminase 6 (TG6), a brain expressed transglutaminase, is implicated in the neurological manifestations of celiac disease (CD)
Our research has shown that a large proportion of individuals with gluten ataxia show increased levels of tissue transglutaminase 6 (TG6) [8,9]
Restricting our analysis to head traumas occurring in adults we found a small excess risk of later CD (OR = 1.10; 95% Confidence interval (CI) = 1.03-1.18)

Summary

Introduction

TG6, a brain expressed transglutaminase, is implicated in the neurological manifestations of celiac disease (CD). Celiac disease (CD) occurs in about 1% of the population in Western Europe [1]. It is a multi-faceted disorder sometimes characterized by neurological manifestations such as gluten ataxia, [2] peripheral neuropathy [3,4], headache with white matter abnormalities, [5] and possibly epilepsy [6,7]. TG6 originates in the brain, it has been detected in the small intestinal mucosa, and can interact with TG2. It is capable of deamidating gliadin and it is gluten dependant [10]

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