Post-ganglionic autonomic neuropathy associated with anti-glutamic acid decarboxylase antibodies
| Autor: | Vincenzo Donadio, Roberto D'Angelo, Rocco Liguori, Maria Pia Giannoccaro, Alex Incensi, Rita Rinaldi, E. Fileccia |
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| Přispěvatelé: | Fileccia, E, Rinaldi, R., Liguori, R., Incensi, A., D’Angelo, R., Giannoccaro, Mp., Donadio, V. |
| Rok vydání: | 2016 |
| Předmět: |
Male
medicine.medical_specialty Neurology Anti-GAD antibodie Glutamate decarboxylase Neural Conduction Gastroenterology Endocrine and Autonomic System Autonomic neuropathy 03 medical and health sciences 0302 clinical medicine Internal medicine Diabetes mellitus Skin biopsy Humans Medicine Autoantibodies medicine.diagnostic_test Glutamate Decarboxylase Endocrine and Autonomic Systems business.industry Middle Aged Anti-glutamic acid decarboxylase antibodie medicine.disease Pathophysiology Post-ganglionic autonomic neuropathy Autonomic nervous system Endocrinology Peripheral neuropathy Autonomic Nervous System Diseases 030220 oncology & carcinogenesis Autonomic Fibers Postganglionic Cholinergic Neurology (clinical) business 030217 neurology & neurosurgery |
| Zdroj: | Clinical Autonomic Research. 27:51-55 |
| ISSN: | 1619-1560 0959-9851 |
| Popis: | Purpose: Antibodies to glutamic acid decarboxylase (GAD-Abs) have been associated with several conditions, rarely involving the autonomic nervous system. Here, we describe two patients complaining of autonomic symptoms in whom a post-ganglionic autonomic neuropathy has been demonstrated in association with significantly elevated serum and CSF GAD-Abs levels. Methods: Patients underwent nerve conduction studies, sympathetic skin response testing, evaluation of autonomic control of the cardiovascular system and skin biopsy. Also, serum screening to exclude predisposing causes of peripheral neuropathy was performed. Anti-GAD65 antibodies were evaluated in serum and CSF. Results: GAD-Abs titer was increased in both serum and CSF in both patients. Sympathetic skin response was absent and skin biopsy revealed a non-length-dependent small-fiber neuropathy with sympathetic cholinergic and adrenergic post-ganglionic damage in both patients. Nerve conduction studies and evaluation of autonomic control of the cardiovascular system were normal in both patients. Both patients were treated with steroids with good, but partial, (patient 2) recovery of the autonomic dysfunctions. Conclusions: Although the pathophysiological mechanisms involved are not fully defined, GAD-abs positivity in serum and CSF should be searched in patients with autonomic neuropathy when no other acquired causes are evident. This positivity may help to clarify autoimmune etiology and, subsequently, to consider immunomodulatory treatment. |
| Databáze: | OpenAIRE |
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