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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 iodine is then...
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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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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 receptors...
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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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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, and heat...
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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 in...

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In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse
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Thyroid function and exposure to styrene.

Ferruccio Santini1, Alberto Mantovani, Alfonso Cristaudo

  • 1Department of Endocrinology and Kidney, University Hospital of Pisa, Pisa, Italy. fsantini@endoc.med.unipi.it

Thyroid : Official Journal of the American Thyroid Association
|September 26, 2008
PubMed
Summary

Occupational styrene exposure did not increase thyroid disease but may alter thyroid hormone metabolism. Further research is needed to confirm styrene

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Area of Science:

  • Occupational health
  • Endocrinology
  • Environmental toxicology

Background:

  • Environmental pollutants, including pesticides and industrial compounds, are increasingly recognized for their potential to disrupt thyroid function.
  • Previous research indicates that various substances can induce goiter or thyroid dysfunction.

Purpose of the Study:

  • To investigate the impact of occupational styrene exposure on the thyroid axis in male workers.
  • To assess potential correlations between styrene exposure levels and thyroid function parameters.

Main Methods:

  • Compared 38 styrene-exposed (E) workers with 123 non-exposed (NE) controls.
  • Measured serum thyroid hormones (TSH, FT4, FT3), thyroid antibodies, and calcitonin; performed thyroid ultrasound.
  • Assessed urinary styrene metabolites (mandelic acid and phenylglyoxylic acid) in exposed workers.

Main Results:

  • No significant differences in thyroid volume, nodularity, or autoimmune markers between E and NE groups.
  • Positive correlation observed between duration of exposure and thyroid volume in E workers.
  • In E workers, urinary styrene metabolites correlated positively with FT4 and the FT4/FT3 ratio, but not with TSH levels.

Conclusions:

  • Chronic styrene exposure is not linked to increased thyroid nodularity or autoimmune thyroid diseases.
  • Styrene may interfere with peripheral thyroid hormone metabolism, specifically T4 to T3 conversion.
  • Further investigation in larger populations is required to validate these findings and elucidate the mechanism of action.