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Related Concept Videos

Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

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Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence...
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Goiter01:27

Goiter

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Goiter refers to an abnormal enlargement of the thyroid gland that may appear as a diffuse goiter (uniform enlargement) or nodular (single or multiple nodules). Functionally, it is classified as nontoxic (normal/low hormone levels) or toxic (excess hormone production).PathophysiologyDiffuse thyroid enlargement typically results from prolonged stimulation by thyroid-stimulating hormone (TSH) or TSH-like agents, commonly seen in hypothyroidism or iodine deficiency. In contrast, in hyperthyroid...
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Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

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Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor,...
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Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

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Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH...
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Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

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Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
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Myasthenia Gravis: Overview and Treatment01:20

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Myasthenia gravis is a neuromuscular transmission disorder characterized by weakness and increased fatigability of skeletal muscles. It is an autoimmune disease affecting approximately one in 2000 people, where antibodies against the α1 subunit of nicotinic acetylcholine receptors are produced.
These antibodies interfere with the function of the nicotinic receptors in three ways: by binding to the receptor and disrupting acetylcholine binding; by causing cross-linking of receptors which...
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Related Experiment Video

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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Nongoitrous autoimmune thyroiditis with facial palsy.

Hyung Jik Lee1, Jin Kyung Kim1

  • 1Department of Pediatrics, Catholic University of Daegu School of Medicine, Daegu, Korea.

Annals of Pediatric Endocrinology & Metabolism
|June 7, 2014
PubMed
Summary

Severe hypothyroidism in a 13-year-old boy caused facial palsy, which resolved with thyroxine treatment. Autoimmune thyroiditis and pituitary hyperplasia were diagnosed.

Keywords:
Autoimmune thyroiditisFacial palsyHypothyroidism

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Area of Science:

  • Endocrinology
  • Pediatric Medicine
  • Immunology

Background:

  • Autoimmune thyroiditis can present with varied clinical manifestations.
  • Facial palsy is an uncommon symptom associated with severe hypothyroidism.
  • Pituitary hyperplasia can occur secondary to prolonged hypothyroidism.

Purpose of the Study:

  • To report a rare case of severe hypothyroidism presenting with facial palsy and pituitary hyperplasia.
  • To highlight the diagnostic challenges and therapeutic response in such cases.
  • To emphasize the importance of thyroid hormone replacement in resolving neurological symptoms.

Main Methods:

  • Case report of a 13-year-old male with sudden onset left-sided facial palsy.
  • Endocrinological evaluation including thyroid function tests, antibody levels, and imaging.
  • Treatment with prednisolone and antiviral medication, followed by thyroxine replacement therapy.

Main Results:

  • Severe hypothyroidism confirmed by elevated TSH (>100 µIU/mL) and low free T4 (0.07 ng/dL).
  • High titers of antithyroid peroxidase and antithyroglobulin antibodies indicated autoimmune thyroiditis.
  • Facial palsy resolved completely after initiating thyroxine treatment; pituitary hyperplasia was noted on MRI.

Conclusions:

  • Severe hypothyroidism can manifest with neurological symptoms like facial palsy.
  • Prompt diagnosis and treatment with thyroxine are crucial for symptom resolution.
  • This case underscores the link between thyroid dysfunction, autoimmune processes, and pituitary abnormalities in adolescents.