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Gland Surgery Feb 2020Hyperthyroidism is a condition where the thyroid gland produces and secretes inappropriately high amounts of thyroid hormone which can lead to thyrotoxicosis. The... (Review)
Review
Hyperthyroidism is a condition where the thyroid gland produces and secretes inappropriately high amounts of thyroid hormone which can lead to thyrotoxicosis. The prevalence of hyperthyroidism in the United States is approximately 1.2%. There are many different causes of hyperthyroidism, and the most common causes include Graves' disease (GD), toxic multinodular goiter and toxic adenoma. The diagnosis can be made based on clinical findings and confirmed with biochemical tests and imaging techniques including ultrasound and radioactive iodine uptake scans. This condition impacts many different systems of the body including the integument, musculoskeletal, immune, ophthalmic, reproductive, gastrointestinal and cardiovascular systems. It is important to recognize common cardiovascular manifestations such as hypertension and tachycardia and to treat these patients with beta blockers. Early treatment of cardiovascular manifestations along with treatment of the hyperthyroidism can prevent significant cardiovascular events. Management options for hyperthyroidism include anti-thyroid medications, radioactive iodine, and surgery. Anti-thyroid medications are often used temporarily to treat thyrotoxicosis in preparation for more definitive treatment with radioactive iodine or surgery, but in select cases, patients can remain on antithyroid medications long-term. Radioactive iodine is a successful treatment for hyperthyroidism but should not be used in GD with ophthalmic manifestations. Recent studies have shown an increased concern for the development of secondary cancers as a result of radioactive iodine treatment. In the small percentage of patients who are not successfully treated with radioactive iodine, they can undergo re-treatment or surgery. Surgery includes a total thyroidectomy for GD and toxic multinodular goiters and a thyroid lobectomy for toxic adenomas. Surgery should be considered for those who have a concurrent cancer, in pregnancy, for compressive symptoms and in GD with ophthalmic manifestations. Surgery is cost effective with a high-volume surgeon. Preoperatively, patients should be on anti-thyroid medications to establish a euthyroid state and on beta blockers for any cardiovascular manifestations. Thyroid storm is a rare but life-threatening condition that can occur with thyrotoxicosis that must be treated with a multidisciplinary approach and ultimately, definitive treatment of the hyperthyroidism.
PubMed: 32206604
DOI: 10.21037/gs.2019.11.01 -
Frontiers in Endocrinology 2021Resistance to thyroid hormone (RTH) is a clinical syndrome defined by impaired sensitivity to thyroid hormone (TH) and its more common form is caused by mutations in the... (Review)
Review
Resistance to thyroid hormone (RTH) is a clinical syndrome defined by impaired sensitivity to thyroid hormone (TH) and its more common form is caused by mutations in the gene, termed RTHβ. The characteristic biochemical profile is that of elevated serum TH levels in absence of thyrotropin suppression. Although most individuals are considered clinically euthyroid, there is variability in phenotypic manifestation among individuals harboring different mutations and among tissue types in the same individual due in part to differential expression of the mutant TRβ protein. As a result, management is tailored to the specific symptoms of TH excess or deprivation encountered in the affected individual as currently there is no available therapy to fully correct the TRβ defect. This focused review aims to provide a concise update on RTHβ, discuss less well recognized associations with other thyroid disorders, such as thyroid dysgenesis and autoimmune thyroid disease, and summarize existing evidence and controversies regarding the phenotypic variability of the syndrome. Review of management addresses goiter, attention deficit disorder and "foggy brain". Lastly, this work covers emerging areas of interest, such as the relevance of variants of unknown significance and novel data on the epigenetic effect resulting from intrauterine exposure to high TH levels and its transgenerational inheritance.
Topics: Humans; Inheritance Patterns; Mutation; Thyroid Hormone Receptors beta; Thyroid Hormone Resistance Syndrome
PubMed: 33868182
DOI: 10.3389/fendo.2021.656551 -
Journal of Nuclear Medicine : Official... Mar 2021Benign thyroid disorders, especially hyper- and hypothyroidism, are the most prevalent endocrine disorders. The most common etiologies of hyperthyroidism are autoimmune... (Review)
Review
Benign thyroid disorders, especially hyper- and hypothyroidism, are the most prevalent endocrine disorders. The most common etiologies of hyperthyroidism are autoimmune hyperthyroidism (Graves disease, GD), toxic multinodular goiter (TMNG), and toxic thyroid adenoma (TA). Less common etiologies include destructive thyroiditis (e.g., amiodarone-induced thyroid dysfunction) and factitious hyperthyroidism. GD is caused by autoantibodies against the thyroid-stimulating hormone (TSH) receptor. TMNG and TA are caused by a somatic activating gain-of-function mutation. Typical laboratory findings in patients with hyperthyroidism are low TSH, elevated free-thyroxine and free-triiodothyronine levels, and TSH-receptor autoantibodies in patients with GD. Ultrasound imaging is used to determine the size and vascularity of the thyroid gland and the location, size, number, and characteristics of thyroid nodules. Combined with lab tests, these features constitute the first-line diagnostic approach to distinguishing different forms of hyperthyroidism. Thyroid scintigraphy with either radioiodine or Tc-pertechnetate is useful to characterize different forms of hyperthyroidism and provides information for planning radioiodine therapy. There are specific scintigraphic patterns for GD, TMNG, TA, and destructive thyroiditis. Scintigraphy with Tc-sestamibi allows differentiation of type 1 from type 2 amiodarone-induced hyperthyroidism. The radioiodine uptake test provides information for planning radioiodine therapy of hyperthyroidism. Hyperthyroidism can be treated with oral antithyroid drugs, surgical thyroidectomy, or I-iodide. Radioiodine therapy is generally considered after failure of treatment with antithyroid drugs, or when surgery is contraindicated or refused by the patient. In patients with TA or TMNG, the goal of radioiodine therapy is to achieve euthyroid status. In GD, the goal of radioiodine therapy is to induce hypothyroidism, a status that is readily treatable with oral thyroid hormone replacement therapy. Dosimetric estimates based on the thyroid volume to be treated and on radioiodine uptake should guide selection of the I-activity to be administered. Early side effects of radioiodine therapy (typically mild pain in the thyroid) can be handled by nonsteroidal antiinflammatory drugs. Delayed side effects after radioiodine therapy for hyperthyroidism are hypothyroidism and a minimal risk of radiation-induced malignancies.
Topics: Clinical Laboratory Techniques; Humans; Hyperthyroidism; Nuclear Medicine
PubMed: 33008929
DOI: 10.2967/jnumed.120.243170 -
Hormone Research in Paediatrics 2022The history of the thyroid dates from 2697 BCE when the "Yellow Emperor" Hung Ti described the use of seaweed to treat goiter. The English name "thyroid" was coined by... (Review)
Review
The history of the thyroid dates from 2697 BCE when the "Yellow Emperor" Hung Ti described the use of seaweed to treat goiter. The English name "thyroid" was coined by Thomas Wharton in 1656 from the Greek word for a shield. Bernard Courtois discovered iodine in 1811 when he noted a residual purplish ash while burning seaweed. Robert Graves is known for his classic 1835 report of "palpitations, goiter, and exophthalmos" in three women, but Caleb Parry observed the same clinical features in 1786. The clinical syndrome we now recognize as hypothyroidism was characterized as "myxoedema" in 1878 by William Ord at St. Thomas Hospital. In 1891, George Murray reported that injection of thyroid extract from sheep led to improvement in symptoms in a woman with myxedema. Thomas Kocher, who reported that patients with goiter who underwent complete thyroidectomy developed cachexia strumipriva, was awarded the Nobel Prize in Physiology and Medicine in 1909. Edward Kendall discovered "thyroxin" on Christmas day in 1914. Studies by David Marine that iodine treatment prevented endemic goiter led to salt iodination, which has largely eradicated endemic cretinism. In 1973, Jean Dussault reported detection of congenital hypothyroidism by screening newborn populations.
Topics: Female; Male; Animals; Humans; Sheep; Goiter; Thyroidectomy; Hypothyroidism; Myxedema; Iodine
PubMed: 36446327
DOI: 10.1159/000526621 -
Journal of Rural Medicine : JRM Oct 2020Pendred syndrome is an autosomal recessive disorder characterized by the combination of sensorineural deafness and goiter and is caused by biallelic mutations in the...
Pendred syndrome is an autosomal recessive disorder characterized by the combination of sensorineural deafness and goiter and is caused by biallelic mutations in the gene. Thyroid function is generally reported as euthyroid or hypothyroid in this condition. We present a case of Pendred syndrome with hyperthyroidism. An 83-year-old woman with congenital deaf-mutism presented with complaints of nausea. She developed a large goiter and had hearing impairment. Her hearing level was 105 dB in both ears. She presented with hyperthyroidism and was treated with thiamazole. She had a homozygous mutation in c.1579A>C:p.T527P of the gene, confirming a diagnosis of Pendred syndrome. Pendred syndrome may develop into hyperthyroidism if the size of the goiter increases. Moreover, a homozygous mutation in c.1579A>C:p.T527P of the gene, which was previously reported to be associated with nonsyndromic hearing loss with enlarged vestibular aqueduct, may also cause Pendred syndrome.
PubMed: 33033545
DOI: 10.2185/jrm.2020-011 -
Immunologic Research Apr 2021Adequate iodine intake is necessary for normal thyroid function. Iodine deficiency is associated with serious complications, but also iodine excess can lead to thyroid... (Review)
Review
Adequate iodine intake is necessary for normal thyroid function. Iodine deficiency is associated with serious complications, but also iodine excess can lead to thyroid dysfunction, and iodine supplementation aimed to prevent iodine deficiency disorders has been associated with development of thyroid autoimmunity. The epidemiology of thyroid diseases has undergone profound changes since the implementation of iodoprophylaxis, notably by means of iodine-enriched salt, specifically resulting in decreased prevalence of goiter and neonatal hypothyroidism, improved cognitive function development in infancy, and reduced incidence of more aggressive forms of thyroid cancer. The main question we address with this review is the clinical relevance of the possible effect on autoimmunity exerted by the use of iodine-enriched salt to correct iodine deficiency. In animal models, exogenous iodine is able to trigger or exacerbate thyroid autoimmunity, but it is still not clear whether the observed immunological changes are due to a direct effect of iodine on immune response, or whether they represent a secondary response to a toxic effect of iodine on thyroid tissue. Previous iodine status of a population seems to influence the functional thyroid response to increased iodine intake and possibly the development of thyroid autoimmunity. Moreover, the prevalence of thyroid antibodies, regarded as hallmark of autoimmune thyroid disease, varies between populations under the influence of genetic and environmental factors, and the presence of thyroid antibodies does not always coincide with the presence of thyroid disease or its future development. In addition, the incidence of autoimmune diseases shows a general increasing trend in the last decades. For all these reasons, available data are quite heterogeneous and difficult to analyze and compare. In conclusion, available data from long-term population surveys show that a higher than adequate population iodine intake due to a poorly controlled program of iodine prophylaxis could induce thyroid dysfunction, including thyroid autoimmunity mostly represented by euthyroid or subclinical hypothyroid autoimmune thyroiditis. Close monitoring iodine prophylaxis is therefore advised to ensure that effects of both iodine deficiency and iodine excess are avoided.
Topics: Animals; Autoimmune Diseases; Autoimmunity; Humans; Iodine; Sodium Chloride, Dietary; Thyroid Diseases; Thyroid Gland
PubMed: 33914231
DOI: 10.1007/s12026-021-09192-6