Hypothyroidism

Alejandro Diaz1, Elizabeth G Lipman Diaz2

  • 1Miami Children's Hospital, Miami, FL The Herbert Wertheim College of Medicine, Florida International University, Miami, FL.

Pediatrics in Review
|August 3, 2014
PubMed

Insights

Early identification and treatment of congenital hypothyroidism are crucial to prevent cognitive deficits. Levothyroxine dosage adjusts with age, and treatment withdrawal at age 3 is recommended for children with a eutopic thyroid to assess transient hypothyroidism.

Area of Science:

  • Pediatrics
  • Endocrinology
  • Neonatal care

Background:

  • Congenital hypothyroidism requires prompt diagnosis and management to prevent severe cognitive impairment.
  • Levothyroxine dosage needs careful titration, being higher in early life and decreasing with age.
  • Transient hypothyroidism can occur, necessitating periodic reassessment of treatment needs.

Purpose of the Study:

  • To summarize key clinical evidence and consensus regarding the management of congenital hypothyroidism.
  • To outline diagnostic and therapeutic strategies for various forms of pediatric hypothyroidism.
  • To provide guidance on levothyroxine dosing and treatment discontinuation protocols.

Main Methods:

  • Review of strong clinical evidence for early identification and treatment of congenital hypothyroidism.
  • Analysis of observational studies and expert consensus on levothyroxine dosing adjustments.
  • Evaluation of protocols for discontinuing levothyroxine in children with congenital hypothyroidism and eutopic thyroid glands.
  • Assessment of clinical presentations of Hashimoto thyroiditis and subclinical hypothyroidism in children.

Main Results:

  • Early treatment of congenital hypothyroidism prevents cognitive deficits.
  • Levothyroxine dosage is age-dependent, decreasing from infancy to adulthood.
  • Discontinuation of levothyroxine at age 3 is advised for children with congenital hypothyroidism and a eutopic thyroid to check for transient cases.
  • Hashimoto thyroiditis often presents with goiter but without hypothyroidism.
  • Subclinical hypothyroidism is more prevalent in obese children.
  • Central hypothyroidism warrants investigation for other pituitary hormone deficiencies.

Conclusions:

  • Timely intervention for congenital hypothyroidism is essential for neurodevelopmental outcomes.
  • Levothyroxine management requires age-specific dosing adjustments.
  • A structured approach to assess transient hypothyroidism is recommended.
  • Recognition of distinct clinical patterns in Hashimoto thyroiditis and subclinical hypothyroidism aids diagnosis.

Related Concept Videos

Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
15
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

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...
23
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

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...
18
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

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,...
15
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

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...
15
Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The...
7.0K