Encephalopathy associated with autoimmune thyroid disease in patients with Graves' disease: clinical manifestations, follow-up, and outcomes.
Authors
Tamagno, GianlucaCelik, Yahya
Simo, Rafael
Dihne, Marcel
Kimura, Kazumi
Gelosa, Giorgio
Lee, Byung I
Hommet, Caroline
Murialdo, Giovanni
Affiliation
Department of Endocrinology and Diabetes Mellitus, St Vincent's University, Hospital, University College Dublin, Dublin, Ireland. gianluca.tamagno@ucd.ieIssue Date
2012-02-01T10:34:59ZMeSH
AdolescentAdrenal Cortex Hormones/therapeutic use
Adult
Aged
Autoantibodies/blood/immunology
Child
Electroencephalography/methods
Encephalitis/blood/*complications/drug therapy
Female
Follow-Up Studies
Graves Disease/*complications/drug therapy
Humans
Male
Middle Aged
Thyroiditis, Autoimmune/*complications/drug therapy
Treatment Outcome
Young Adult
Metadata
Show full item recordCitation
BMC Neurol. 2010 Apr 28;10:27.Journal
BMC neurologyDOI
10.1186/1471-2377-10-27PubMed ID
20426819Abstract
BACKGROUND: The encephalopathy associated with autoimmune thyroid disease (EAATD) is characterized by neurological/psychiatric symptoms, high levels of anti-thyroid antibodies, increased cerebrospinal fluid protein concentration, non-specific electroencephalogram abnormalities, and responsiveness to the corticosteroid treatment in patients with an autoimmune thyroid disease. Almost all EAATD patients are affected by Hashimoto's thyroiditis (HT), although fourteen EAATD patients with Graves' disease (GD) have been also reported. METHODS: We have recorded and analyzed the clinical, biological, radiological, and electrophysiological findings and the data on the therapeutic management of all GD patients with EAATD reported so far as well as the clinical outcomes in those followed-up in the long term. RESULTS: Twelve of the fourteen patients with EAATD and GD were women. The majority of GD patients with EAATD presented with mild hyperthyroidism at EAATD onset or shortly before it. Active anti-thyroid autoimmunity was detected in all cases. Most of the patients dramatically responded to corticosteroids. The long term clinical outcome was benign but EAATD can relapse, especially at the time of corticosteroid dose tapering or withdrawal. GD and HT patients with EAATD present with a similar clinical, biological, radiological, and electrophysiological picture and require an unaffected EAATD management. CONCLUSIONS: GD and HT equally represent the possible background condition for the development of EAATD, which should be considered in the differential diagnosis of all patients with encephalopathy of unknown origin and an autoimmune thyroid disease, regardless of the nature of the underlying autoimmune thyroid disease.Language
engISSN
1471-2377 (Electronic)1471-2377 (Linking)
ae974a485f413a2113503eed53cd6c53
10.1186/1471-2377-10-27