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The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
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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.
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The thyroid gland is a small, butterfly-shaped gland located in the neck and covers the anterior surface of the trachea. The gland has two lateral lobes connected by a thin tissue mass called the isthmus. Internally, each lobe comprises many small spherical structures known as thyroid follicles, surrounded by a network of blood vessels.
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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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Hyperthyroidism II: Pathophysiology01:27

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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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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...
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An Ex vivo Culture System to Study Thyroid Development
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Human fetal thyroid function.

Michel Polak1

  • 1Pediatric Endocrinology, Gynecology and Diabetology, Necker Enfants-Malades University Hospital, Assistance Publique-Hôpitaux de Paris, INSERM U1016, IMAGINE Institute, Université Paris Descartes, Sorbonne Paris Cité, Paris, France.

Endocrine Development
|September 19, 2014
PubMed
Summary
This summary is machine-generated.

Maternal thyroxine (T4) transfer is vital for fetal thyroid development and function. Fetal thyroid hormone production begins early, with significant T4 secretion occurring later in pregnancy, crucial for development.

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Area of Science:

  • Endocrinology
  • Developmental Biology
  • Maternal-Fetal Medicine

Background:

  • Thyroid development is essential for fetal well-being and maturation.
  • Maternal thyroid hormone transfer significantly impacts fetal thyroid function throughout pregnancy.

Purpose of the Study:

  • To review the early stages of human fetal thyroid development and maturation.
  • To highlight the critical role of maternal thyroxine transfer and the sodium/iodine symporter in fetal thyroid function.
  • To discuss the hormonal patterns and mechanisms governing fetal thyroid maturation.

Main Methods:

  • Review of existing literature on human fetal thyroid development.
  • Analysis of temporal and structural correlations in early pregnancy.
  • Examination of fetal blood sampling data for thyroid hormone and TSH levels.

Main Results:

  • Thyroid hormone synthesis and folliculogenesis are closely linked in the first trimester.
  • The sodium/iodine symporter is crucial for initiating fetal thyroid function.
  • Fetal thyroxine (T4) is detectable by week 11 and increases progressively; thyroid-stimulating hormone (TSH) patterns are detailed.

Conclusions:

  • Human thyroid terminal differentiation follows a precise gene expression program.
  • Understanding fetal thyroid physiology is fundamental for fetal medicine and thyroidology.
  • Fetal thyroid dysfunction, as seen in Down syndrome, underscores the importance of normal development.