ECE2016 Eposter Presentations Clinical case reports - Thyroid/Others (71 abstracts)
Diabetes mellitus and ataxia with anti-glutamic acid decarboxylase antibodies
Diana Oliveira 1 , Rui Araújo 2 , Carolina Moreno 1 , Dírcea Rodrigues 1 , Daniela Guelho 1 , Nuno Vicente 1 , Luís Cardoso 1 , Diana Martins 1 , Adriana Lages 1 , Mara Ventura 1 , Sandra Paiva 1 & Francisco Carrilho 1
1Endocrinology, Diabetes and Metabolism Department, Coimbra University and Hospital Center, Coimbra, Portugal; 2Neurology Department, Coimbra University and Hospital Center, Coimbra, Portugal.
Introduction: Glutamic acid decarboxylase (GAD65) is expressed by pancreatic beta cells and also by GABA (gamma-aminobutyric acid)-secreting neurons. Cerebellar ataxia associated with anti-GAD65 antibodies (antiGAD Ab) is a rare neurological disorder that frequently coexists with other autoimmune conditions, namely Diabetes Mellitus (DM).
Case reports: We describe two cases of ataxia associated with antiGAD Ab. The first case is a 69-year-old obese man with DM known for 5 years, initially medicated with oral antidiabetic agents and with premature need for insulin therapy, 4 years after diagnosis, for chronic inadequate metabolic control. At age 65, he developed dysarthria and ataxic gait and after extensive investigation was diagnosed with antiGAD Ab ataxia, and underwent treatment with intravenous immunoglobulin. Levels of antiGAD Ab were 13.3 U/ml (<1.0), ICA (Islet-cell cytoplasmic antibodies) and anti-insulin Ab negative, anti-IA2 Ab (insulinoma 2-associated) 1.30 U/ml (<1), C-peptide 6.7 ng/ml (1.0–7.6). The glycemic control was improved after intensification of insulin therapy. The second case is a 68-year-old woman, paraplegic after vertebromedullary traumatism, with DM since she was 60. The metabolic control was difficult with oral antidiabetic medication for 5 years, so insulin was added in 2012, but she mantained significant glycemic lability. In 2015 she was diagnosed with antiGAD Ab ataxia after presenting with progressive positional vertigo, dysarthria and diplopia. AntiGAD Ab 239.07 U/ml (<1.0), ICA (Islet-cell cytoplasmic antibodies) positive, anti-insulin Ab negative. Considering the analytical results and glycemic lability, oral antidiabetic agents were suspended and she initiated multiple daily injections of insulin.
Conclusion: The autoimmune etiology of DM can be considered in any age group, especially when other autoimmune conditions are present. An accurate DM classification allows therapeutic adjustment and metabolic control optimization. In patients with DM and positive autoimmunity, with neurologic disorders not explained by diabetic neuropathy and after exclusion of other causes, ataxia associated with antiGAD Ab can be considered.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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