Hyperthyroidism goiter
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Hyperthyroidism and Goiter: An Overview
Historical Context of Hyperthyroidism and Goiter
Hyperthyroidism, often associated with goiter and exophthalmos, has been recognized since antiquity. However, it wasn't until the early 19th century that detailed studies began to elucidate the nature of this disorder. Initially, the disease was misunderstood and attributed to cardiac or neurological origins. Treatments varied widely, including surgeries on the thyroid, orbit, and pituitary, as well as interventions targeting the autonomic nervous system. The discovery of long-acting thyroid stimulators eventually led to the understanding that Graves-Basedow's disease, a common cause of hyperthyroidism, is an autoimmune disorder 1.
Goiter in Children: Pathophysiology and Treatment
Goiter, an enlargement of the thyroid gland, is a prevalent condition in children with thyroid disorders. It can manifest in various forms, including diffuse or nodular, and can be toxic or non-toxic. The condition can present in euthyroid, hypothyroid, or hyperthyroid states. Clinicians must consider dietary intake, residence, and nutrient deficiencies when diagnosing and treating goiter in children. Treatment varies based on the thyroid state: iodine supplementation for euthyroid goiter, levothyroxine for hypothyroidism, and antithyroid drugs, iodine therapy, or surgery for hyperthyroidism 2.
Intrathoracic and Multinodular Goiters
Hyperthyroidism can sometimes be caused by an intrathoracic goiter, which may not present with an enlarged cervical thyroid gland. Such cases require thorough diagnostic imaging, including chest roentgenograms and radioisotope scans, to identify the intrathoracic goiter 3. Additionally, toxic multinodular goiter, a variant of autoimmune hyperthyroidism, can present with different scintiscan patterns. Type A patterns, characterized by diffuse but uneven technetium uptake, are often associated with autoimmune features similar to Graves' disease, while Type B patterns, with multiple discrete nodules, are not 4.
Subclinical Hyperthyroidism and Endothelial Function
Subclinical hyperthyroidism, often induced by levothyroxine (LT4) suppression therapy in euthyroid nodular goiter patients, can impair endothelial function and insulin sensitivity. Studies have shown that LT4 treatment significantly reduces TSH levels, leading to decreased flow-mediated vasodilatation (FMD) and insulin sensitivity index (ISI), while increasing oxidative stress markers and high-sensitivity C-reactive protein (hsCRP) levels 5.
Adenomatous Goiter and Hyperthyroidism
Adenomatous goiter with hyperthyroidism is a rare condition, distinct from Graves' disease. Patients often present with uneven cold areas on thyroid scintigrams and may require near-total thyroidectomy as the treatment of choice. Post-surgery, patients may develop hypothyroidism, hyperthyroidism, or euthyroidism, indicating the complex nature of this condition 6.
Complex Presentations and Genetic Mutations
Intrathoracic goiters can also present with severe complications such as tracheal compression, superior vena cava syndrome, and Horner's syndrome, highlighting the need for comprehensive management strategies 7. Additionally, hyperfunctioning thyroid nodules in toxic multinodular goiters share activating thyrotropin receptor mutations with solitary toxic adenomas, suggesting a common pathogenetic mechanism. These mutations lead to constitutive activity, driving the hyperfunction of the thyroid nodules 10.
Conclusion
Hyperthyroidism and goiter encompass a range of conditions with diverse etiologies and presentations. From historical misunderstandings to modern genetic insights, the management of these thyroid disorders requires a nuanced approach tailored to the specific type and underlying cause. Advances in diagnostic imaging and molecular biology continue to enhance our understanding and treatment of these complex endocrine disorders.
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Most relevant research papers on this topic
Hyperthyroidism, exophthalmos, and goiter: historical notes on the orbitopathy.
Exophthalmos associated with hyperthyroidism has been known since antiquity, but its nature and treatment remain unclear.
Total Insights on Goiter in Children: A Mini-review
Goiter in children can be managed with different treatments depending on the type of thyroid disorder, and addressing food intake, vitamin deficiency, and iodine status is crucial for effective management.
Systematic ReviewHyperthyroidism caused by a toxic intrathoracic goiter with a normal-sized cervical thyroid gland.
Toxic intrathoracic goiter can cause hyperthyroidism with a normal-sized cervical thyroid gland, highlighting the need for chest roentgenogram and radioisotope scan in cases of no cervical thyroid enlargement.
Case ReportToxic multinodular goiter: a variant of autoimmune hyperthyroidism.
A subgroup of patients with toxic multinodular goiter (type A) may have autoimmune hyperthyroidism, while in another subgroup (type B), hyperthyroidism is not related to an autoimmune etiology.
Observational StudyExogenous subclinical hyperthyroidism impairs endothelial function in nodular goiter patients.
TSH suppression therapy with levothyroxine may cause impaired endothelial function, increased oxidative stress, and decreased insulin sensitivity in euthyroid nodular goiter patients.
Adenomatous goiter with hyperthyroidism
Adenomatous goiter with hyperthyroidism has a different pathogenesis and clinical features from Graves' disease, and near-total thyroidectomy may be the preferred treatment.
Case ReportIntrathoracic goiter with hyperthyroidism, tracheal compression, superior vena cava syndrome, and Horner's syndrome.
Intrathoracic goiter can cause hyperthyroidism, tracheal compression, superior vena cava syndrome, and Horner's syndrome, causing mediastinal masses.
Case ReportAnimal models of disease: feline hyperthyroidism: an animal model for toxic nodular goiter.
Feline hyperthyroidism is a common disorder in middle-aged to senior domestic cats, similar to toxic nodular goiter in humans, with iodine deficiency, nutritional goitrogens, and environmental disruptors potentially playing a role in its pathogenesis.
Rigorous JournalRecurrent goiter, hyperthyroidism, galactorrhea and amenorrhea due to a thyrotropin and prolactin-producing pituitary tumor.
A pituitary tumor with overproduction of thyrotropin and prolactin caused recurrent goiter, hyperthyroidism, galactorrhea, and amenorrhea in a 22-year-old woman.
Case Report
Highly CitedHyperfunctioning thyroid nodules in toxic multinodular goiter share activating thyrotropin receptor mutations with solitary toxic adenoma.
Hyperfunctioning thyroid nodules in toxic multinodular goiter share the same pathogenetic event (TSH receptor mutation) as toxic adenoma, while nonfunctioning thyroid nodules in the same gland do not have this mutation.
Observational StudyHighly Cited