Epilepsy, cerebral calcifications, and gluten-related disorders: Are anti-transglutaminase 6 antibodies the missing link?. (December 2019)

• Record Type: Journal Article
• Authors: Ferlazzo, Edoardo; Polidoro, Serena; Gobbi, Giuseppe; Gasparini, Sara; Sueri, Chiara; Cianci, Vittoria; Sofia, Vito; Giuliano, Loretta; Giallonardo, Anna Teresa; Di Bonaventura, Carlo; Casciato, Sara; Messana, Tullio; Coppola, Antonietta; Striano, Salvatore; Bilo, Leonilda; Monoriti, Marika; Genovese, Giuseppe; Sarica, Paola; Arcudi, Luciano; Aguglia, Umberto
• Is Part Of: Seizure. Volume 73(2019)
• Page Start: 17
• Page End: 20
• Publication Date: 2019-12
• Subjects: Coeliac disease -- Seizures -- Transglutaminases -- Gluten -- Diet; Epilepsy -- Periodicals; Epilepsy -- Periodicals; Seizures -- Periodicals; Épilepsie -- Périodiques; Electronic journals; Electronic journals; 616.853
• DOI: 10.1016/j.seizure.2019.10.012
• Languages: English
• ISSNs: 1059-1311

Abstract

Highlights: Transglutaminase 6 antibodies (anti-TG6) are considered a biomarker for gluten-related ataxia and neuropathy. We evaluated anti-TG6 prevalence in patients with epilepsies with cerebral calcifications. Anti-TG6 do not seem to be associated to epilepsies with cerebral calcifications. Abstract: Purpose: Gluten-related disorders (GRDs) are a group of immune-mediated diseases often associated to neurologic manifestations. Epilepsies with cerebral calcifications, with or without coeliac disease (CD), are rare neurological disorders characterized by childhood-onset focal seizures, often refractory to antiepileptic drugs. Transglutaminase 6 antibodies (anti-TG6) have been considered a biomarker for gluten-related ataxia and neuropathy, but their prevalence in epilepsies with cerebral calcifications is unknown. The aim of this study is to evaluate anti-TG6 prevalence in patients with epilepsies and cerebral calcifications. Method: this was a cross-sectional study conducted at five Italian epilepsy centres. The following groups were included. Group 1: nine patients with CD, posterior cerebral calcifications and epilepsy (CEC); group 2: nine patients with epilepsy and posterior cerebral calcifications, without CD; group 3: twenty patients with focal epilepsy of unknown etiology; group 4: twenty-two healthy controls (HC). All subjects were tested for serological evidence of anti-TG6 IgA and IgG. Differences among groups were analysed using χ ² test. Results: anti-TG6 were present in 1/9 subjects (11%) of group 1, 2/9 subjects (22%) of group 2, 0/20 subjects in group 3, 3/22 (13.6%) of HC. No significant difference was found among the 4 groups. Conclusions: Anti-TG6 do not seem to be associated to epilepsies with cerebral calcifications.