{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,5,14]],"date-time":"2025-05-14T04:50:36Z","timestamp":1747198236859,"version":"3.40.5"},"reference-count":10,"publisher":"Walter de Gruyter GmbH","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,10,26]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec id=\"j_jpem-2020-0697_abs_001\">\n                  <jats:title>Objectives<\/jats:title>\n                  <jats:p>Hashimoto\u2019s thyroiditis (HT) is characterized by lymphocytic thyroid infiltration. Gradual thyroid failure can occur due to thyroid cell apoptosis. Rarely neurological autoimmunity due to glutamic acid decarboxylase (GAD) antigen can co exist with HT.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec id=\"j_jpem-2020-0697_abs_002\">\n                  <jats:title>Case presentation<\/jats:title>\n                  <jats:p>A seven-year-old male presented with tiredness, weight loss, frequent falls, tachycardia, firm thyromegaly, and abnormal gait. Biochemical markers and thyroid ultrasound (TUS) showed autoimmune hyperthyroidism. Methimazole (MMI) was started and continued for 2.2 years. MRI brain was normal and neurological symptoms resolved. At nine years, he became hypothyroid and levothyroxine (LT4) was started. Serial TUS showed progressive thyroid atrophy. At 14.8 years, he developed epilepsy and fourth cranial nerve palsy, and diagnosed with GAD-65 central nervous system disease. At 15.3 years, TUS showed complete atrophy of right lobe with involuting left lobe volume.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec id=\"j_jpem-2020-0697_abs_003\">\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>This is an unusual form of atrophic thyroiditis (AT) with coexisting neurological autoimmunity. GAD-65 CNS autoimmunity should be considered in children with AT presenting with neurological signs.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1515\/jpem-2020-0697","type":"journal-article","created":{"date-parts":[[2021,6,24]],"date-time":"2021-06-24T00:00:27Z","timestamp":1624492827000},"page":"1329-1333","source":"Crossref","is-referenced-by-count":0,"title":["Auto-destruction of the thyroid gland and coexisting glutamic acid decarboxylase mediated neurological disease in an adolescent: an unusual presentation of autoimmunity"],"prefix":"10.1515","volume":"34","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7290-1471","authenticated-orcid":false,"given":"Deepa","family":"Badrinath Murthy","sequence":"first","affiliation":[{"name":"Pediatric Endocrinology , NYU Langone Medical Center , New York , USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ana","family":"Gutierrez Alvarez","sequence":"additional","affiliation":[{"name":"Pediatric Endocrinology , NYU Langone Health , New York , USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wendy","family":"Vargas","sequence":"additional","affiliation":[{"name":"Columbia University Medical Center , New York , USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Melissa Kaori Silva","family":"Litao","sequence":"additional","affiliation":[{"name":"Pediatric Endocrinology , NYU Langone Health , New York , USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bina","family":"Shah","sequence":"additional","affiliation":[{"name":"Pediatric Endocrinology , NYU Langone Medical Center , New York , USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"374","published-online":{"date-parts":[[2021,6,24]]},"reference":[{"key":"2023040101125225537_j_jpem-2020-0697_ref_001","doi-asserted-by":"crossref","unstructured":"Carl\u00e9, A, Pedersen, IB, Knudsen, N, Perrild, H, Ovesen, L, J\u00f8rgensen, T, et al.. Thyroid volume in hypothyroidism due to autoimmune disease follows a unimodal distribution: evidence against primary thyroid atrophy and autoimmune thyroiditis being distinct diseases. J Clin Endocrinol Metab 2009;94:833\u20139. https:\/\/doi.org\/10.1210\/jc.2008-1370.","DOI":"10.1210\/jc.2008-1370"},{"key":"2023040101125225537_j_jpem-2020-0697_ref_002","doi-asserted-by":"crossref","unstructured":"BakerJr.JR. Dying (apoptosing?) for a consensus on the Fas death pathway in the thyroid. J Clin Endocrinol Metab 1999;84:2593\u20135. https:\/\/doi.org\/10.1210\/jcem.84.8.5993.","DOI":"10.1210\/jcem.84.8.5993"},{"key":"2023040101125225537_j_jpem-2020-0697_ref_003","doi-asserted-by":"crossref","unstructured":"Graus, F, Saiz, A, Dalmau, J. GAD antibodies in neurological disorders\u00a0\u2013 insights and challenges. 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