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Auto-destruction of the thyroid gland and coexisting glutamic acid decarboxylase mediated neurological disease in an adolescent: an unusual presentation of autoimmunity

  • Deepa Badrinath Murthy ORCID logo EMAIL logo , Ana Gutierrez Alvarez , Wendy Vargas , Melissa Kaori Silva Litao and Bina Shah
Published/Copyright: June 24, 2021

Abstract

Objectives

Hashimoto’s 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.

Case presentation

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.

Conclusions

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.


Corresponding author: Deepa Badrinath Murthy, Pediatric Endocrinology, NYU Langone Medical Center, New York, USA, E-mail:

  1. Research funding: None declared.

  2. Author contributions: All authors have accepted responsibility for the entire content of this manuscript and approved its submission.

  3. Competing interests: Authors state no conflict of interest.

  4. Informed consent: Written informed consent was obtained.

  5. Ethical approval: The authors consciously assure that for this manuscript, the following are fulfilled: 1) This material is the authors’ own original work, which has not been previously published elsewhere. 2) The paper is not currently being considered for publication elsewhere. 3) The paper reflects the authors’ own research and analysis in a truthful and complete manner. 4) The paper properly credits the meaningful contributions of co-authors and co-researchers. 5) The results are appropriately placed in the context of prior and existing research. 6) All sources used are properly disclosed (correct citation). 7) All authors have been personally and actively involved in substantial work leading to the paper, and will take public responsibility for its content.

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Received: 2021-01-15
Accepted: 2021-03-31
Published Online: 2021-06-24
Published in Print: 2021-10-26

© 2021 Walter de Gruyter GmbH, Berlin/Boston

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