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Epilepsy is one of the most frequent neurological disorders affecting between 0.5% and 1% of the population, but in many the aetiology is unknown. A recent population-based study reported a fivefold increase in patients with type 1 diabetes mellitus (T1DM).1 Autoantibodies that recognise neuronal proteins have been identified in a number of immunotherapy-responsive seizure-related neurological disorders.2 High-titre autoantibodies to glutamic acid decarboxylase (GAD), an intracellular enzyme that catalyses the synthesis of gamma-aminobutyric acid (GABA) have been detected in neurological diseases including epilepsy although these patients show a less clear response to immunotherapies.3 ,4 GAD is also expressed by pancreatic β cells and is a major autoantigen in T1DM. Antibodies to GAD (GAD Abs) are present in up to 80% of patients with newly diagnosed T1DM, although not considered causative. There have been studies examining the incidence of GAD Abs in patients with epilepsy;5 however, we compare GAD and other Abs in patients with T1DM, with and without epilepsy.
Study design and participants
We recruited patients with T1DM (n=25) and coexistent epilepsy (T1DM/Ep) and sex-matched/age-matched patients with T1DM (n=36) from Nottingham and Sheffield Teaching Hospitals NHS Trust; the diagnoses of epilepsy and T1DM were established by specialist neurology (PM and SH) and diabetology (II) teams. Ethics approval was obtained, and written informed consent was obtained from all patients involved.
Voltage-gated potassium channel (VGKC)-complex antibodies were determined by immunoprecipitation of 125I-α-dendrotoxin-labelled VGKC complexes from rabbit brain extract (positive >100 pmoles/L).5 GAD65 Abs were measured using …
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