Glutamic acid decarboxylase (GAD) is the enzyme that catalyzes the conversion of L-glutamat into GABA, one of the classical neurotransmitters with neuroinhibitory function. GAD is present in GABAergic neurons and in pancreatic beta cells. It is remarkable that Anti-GAD antibody(Anti-GADab) can have different disease manifestations, i.e., Type 1 diabetes mellitus (T1DM), Stiff-Person Syndrome, limbic encephalitis (LE), epilepsy. Cooccurence of T1DM and LE is reported in the literature. There is no study in the literature about the presence of LE in patients with T1DM.
We aimed to investigate the presence of LE in patients with T1DM and its association with Anti-GADab levels.
Method: Anti-GADab high positive (> 100 IU/ml), Anti-GADab low positive (10-100 IU/ml) and Anti-GADab negative (≤10 IU/ml), 34 cases with T1DM were included in Gazi University Faculty of Medicine Pediatric Endocrinology Department. Anti-GADab levels of the patients were evaluated retrospectively. Physical examination and electroencephalography (EEG) were performed in the pediatric neurology department. Cranial Magnetic Resonance was planned for cases with positive findings in terms of neurological examination and / or LE in EEG. All EEGs were ordered with sleep deprivation.
Results: The general characteristics of the patients are given in the table. Anti-GAD levels were correlated with HbA1c averages (P <0.05). The mean HbA1c of the Anti-GADab negative cases was 8.2%, the mean HbA1c of the Anti-GADab low positive cases was 9.4%, and the mean HbA1c of the Anti-GADab high positive cases was 8.7%. A total of 34 EEG records were identified. Of the total number of records, 24(70.6%)were normal and 10 (29.4%) abnormal. There was no significant relationship between Anti-GADab levels and epileptic activity. In this summary, preliminary reports of the study were shared and study has been ongoing.
Conclusion: Our study shows that especially sleep deprived EEG may be used as an indicator of LE or autoimmune epilepsy in children with T1DM. These patients are going to be followed for long term for the development of LE in the future. Our hypothesis is the GAD autoimmunity, even after many years, can spread to the CNS. As early treatment of GAD antibody-associated CNS disorders has a better prognosis, vigilance for electroencephalographic findings indicating GAD antibody-associated CNS autoimmunity is mandatory in patients with T1DM.
|Age (on diagnosis)||6.8±2.9|
|Anti GAD Level||≤10|
19 - 21 Sep 2019
European Society for Paediatric Endocrinology