Antithyroid Agents
Methimazole
Propylthiouracil
Carbimazole
Graves Disease
Hyperthyroidism
Thyrotoxicosis
Immunoglobulins, Thyroid-Stimulating
Thyroid Gland
Thyroxine
Hypothyroidism
Thyrotropin
Thiouracil
Receptors, Thyrotropin
Triiodothyronine
Thyroiditis, Autoimmune
Thyroid Hormones
Iodine Radioisotopes
Thyroiditis
Goiter
Autoantibodies
Thyroglobulin
Hashimoto Disease
Methylthiouracil
Iodide Peroxidase
Alternating antineutrophil cytoplasmic antibody specificity: drug-induced vasculitis in a patient with Wegener's granulomatosis. (1/466)
We describe a patient who presented with Wegener's granulomatosis associated with antineutrophil cytoplasmic antibodies (ANCA) directed against proteinase 3 (PR3) with a cytoplasmic immunofluorescence pattern (cANCA), whose ANCA type changed to antimyeloperoxidase antibodies with a perinuclear immunofluorescence pattern (pANCA) when treated with propylthiouracil, and changed back to anti-PR3 antibodies with cANCA after the medication was discontinued. The patient developed flares of vasculitis symptoms associated with rises in either type of ANCA. Tests for antimyeloperoxidase ANCA were repeatedly negative before the drug was started, strongly implicating the drug as the cause of the episode. This case demonstrates that patients with idiopathic ANCA-positive vasculitis may quickly develop a superimposed drug-associated ANCA-positive vasculitis. Iatrogenic vasculitis should be suspected when a patient with idiopathic vasculitis with one type of ANCA develops the other type of ANCA. (+info)Screening methods for thyroid hormone disruptors. (2/466)
The U.S. Congress has passed legislation requiring the EPA to implement screening tests for identifying endocrine-disrupting chemicals. A series of workshops was sponsored by the EPA, the Chemical Manufacturers Association, and the World Wildlife Fund; one workshop focused on screens for chemicals that alter thyroid hormone function and homeostasis. Participants at this meeting identified and examined methods to detect alterations in thyroid hormone synthesis, transport, and catabolism. In addition, some methods to detect chemicals that bind to the thyroid hormone receptors acting as either agonists or antagonists were also identified. Screening methods used in mammals as well as other vertebrate classes were examined. There was a general consensus that all known chemicals which interfere with thyroid hormone function and homeostasis act by either inhibiting synthesis, altering serum transport proteins, or by increasing catabolism of thyroid hormones. There are no direct data to support the assertion that certain environmental chemicals bind and activate the thyroid hormone receptors; further research is indicated. In light of this, screening methods should reflect known mechanisms of action. Most methods examined, albeit useful for mechanistic studies, were thought to be too specific and therefore would not be applicable for broad-based screening. Determination of serum thyroid hormone concentrations following chemical exposure in rodents was thought to be a reasonable initial screen. Concurrent histologic evaluation of the thyroid would strengthen this screen. Similar methods in teleosts may be useful as screens, but would require indicators of tissue production of thyroid hormones. The use of tadpole metamorphosis as a screen may also be useful; however, this method requires validation and standardization prior to use as a broad-based screen. (+info)Risk of iodine-induced thyrotoxicosis after coronary angiography: an investigation in 788 unselected subjects. (3/466)
In this study, the risk of iodine-induced thyrotoxicosis in unselected patients from an iodine-deficient area was investigated. The patients were consecutively enrolled. Thyroid hormone values and urinary iodine excretion were determined before, as well as 1, 4 and 12 weeks after iodine contamination by coronary angiography. Two of 788 unselected patients developed hyperthyroidism within 12 weeks. The two patients did not belong to a risk group for iodine-induced thyrotoxicosis (i.e. old people, patients with goiter or possible thyroid autonomy, low TSH). Both patients had normal TSH levels at baseline and ultrasound of the thyroid was without evidence of nodules. The study shows that in euthyroid unselected patients from an iodine-deficient area short-term iodine contamination by contrast media rarely leads to hyperthyroidism. On account of these facts, prophylactic therapy, e.g. by perchlorate or thiamazole, is not generally recommended, because the risk of side-effects is perhaps even greater than the risk of iodine-induced thyrotoxicosis. (+info)Identification of thyroid hormone residues on serum thyroglobulin: a clue to the source of circulating thyroglobulin in thyroid diseases. (4/466)
Thyroglobulin (Tg) present in the serum of normal individuals and patients with thyroid disorders could be partly newly synthesized non-iodinated Tg and partly Tg containing iodine and hormone residues originating from the lumen of thyroid follicles. With the aim of examining the contribution of the latter source of Tg to the elevation of serum Tg concentration in thyroid pathophysiological situations, we devised a procedure to identify thyroxine (T4) and tri-iodothyronine (T3) residues on Tg from unfractionated serum. A two-step method, basedon (i)adsorption of Tg on an immobilized anti-human Tg (hTg) monoclonal antibody (mAb) and (ii)recognition of hormone residues on adsorbed Tg by binding of radioiodinated anti-T4 mAb and anti-T3 mAb, was used to analyze serum Tg from patients with either Graves' disease (GD), subacute thyroiditis (ST) or metastatic differentiated thyroid cancer (DTC). Purified hTg preparations with different iodine and hormone contents were used as reference. Adsorption of purified Tg and serum Tg on immobilized anti-hTg mAb ranged between 85 and 90% over a wide concentration range. Labeled anti-T4 and anti-T3 mAbs bound to adsorbed purified Tg in amounts related to its iodine content. Tg adsorbed from six out of six sera from ST exhibited anti-T4 and anti-T3 mAb binding activities. In contrast, significant mAb binding was only observed in one out of eight sera from untreated GD patients and in 1 out of 13 sera from patients with DTC. The patient with DTC, whose serum Tg contained T4 and T3, represented a case of hyperthyroidism caused by a metastatic follicular carcinoma. In conclusion, we have identified, for the first time, T4 and T3 residues on circulating Tg. The presence of Tg with hormone residues in serum is occasional in GD and DTC but is a common and probably distinctive feature of ST. (+info)Improved suppression by dietary taurine of the fecal excretion of bile acids from hypothyroid rats. (5/466)
The effect of dietary taurine, 2-aminoethanesulfonic acid, on hypercholesterolemia caused by thiouracil-induced hypothyroidism was investigated in hypothyroid rats. Serum total- and HDL-cholesterol were significantly increased, and the excretion of fecal bile acids was significantly decreased. Taurine did not change the hypercholesterolemia, but significantly recovered the excretion of bile acids. (+info)Effects of oral propylthiouracil treatment on nitric oxide production in rat aorta. (6/466)
The effects of oral propylthiouracil (PTU) treatment on vascular nitric oxide (NO) production were studied in the rat aorta. Rats were fed a standard low fat diet with or without 0.1% PTU, for 2 or 4 weeks, or for 2 weeks with additional thyroxine injections. Concentration response curves were then constructed to phenylephrine (PE) in both endothelium-intact and denuded aortic rings from these animals and after incubation with 0.1 mM L-N(G)nitroarginine (L-NOARG). In addition, expression of nitric oxide synthase (NOS) was analysed in sections of aorta from PTU-treated and control rats using rabbit polyclonal antibodies to both inducible NOS (iNOS) and endothelial NOS (eNOS). Oral PTU treatment resulted in a significant reduction in both the maximum response (control, 0.53+/-0.02; 2 week PTU, 0.20+/-0.07; 4 week PTU, 0.07+/-0.02 g mg(-1)) and vessel sensitivity (EC50 values: control, 9.10x10(-8)+/-0.67; 2 week PTU, 7.45x10(-7)+/-1.15; 4 week PTU, 9.73x10(-7)+/-0.45 M) to PE in endothelium-intact vessel rings, as compared to controls (P<0.05). Both endothelial removal and incubation with L-NOARG restored the maximum response after 2, but not 4 weeks, although, in general, vessel sensitivity was not altered by either treatment. Vessels from PTU-treated rats given thyroxine injections showed no significant differences between any of the dose response curve parameters. Immunohistochemical analysis suggested that labelling for eNOS may be increased after PTU treatment as compared to control animals, whereas iNOS antibody immunoreactivity was not different between the two groups. These results suggest that the hyporesponsiveness to PE observed after oral PTU treatment is, in part, due to enhanced nitric oxide (NO) production by the endothelium, and demonstrate for the first time that thyroid hormones may play a role in the regulation of eNOS activity in the rat aorta. (+info)Remission of insulin autoimmune syndrome in a patient with Grave's disease by treatment with methimazole. (7/466)
The patient, a 24-year-old man, had suffered from hunger, sweating, tachycardia and palpitation for three years. He was diagnosed as having Graves' disease (GD) and treated with methimazole (MMI) for 3 months. He noted that palpitation and perspiration seemed to particularly occur when he was hungry, and thus he was examined to determine whether these symptoms were caused by hypoglycemia. As a markedly elevated immunoreactive insulin level and the presence of insulin antibody in serum were found, he was diagnosed as having insulin autoimmune syndrome (IAS). HLA typing revealed the patient to be positive for group Bw62/Cw4/DR4, which is reportedly a specific HLA type in MMI-treated euthyoroid GD patients with IAS. In spite of the continuation of MMI treatment, the % binding of IRI decreased and the hypoglycemic episode disappeared. In contrast to the previously reported MMI induced IAS in GD cases, MMI is unlikely to have exacerbated IAS in the present case, although his HLA combination is identical to that of the previous cases. (+info)Hypercalcemia accompanied by hypothalamic hypopituitarism, central diabetes inspidus and hyperthyroidism. (8/466)
We present here a case of prominent hypercalcemia accompanied by hypothalamic tumor and Graves' disease. A 24-year-old man with hypothalamic tumor showed hypopituitarism, central diabetes inspidus (DI) and hyperthyroidism. Nausea, loss of thirst and appetite, and general fatigue were found with the unveiling of hypercalcemia and hypernatremia. Parathyroid hormone (PTH) and 1alpha-dihydroxyvitamin D levels were suppressed with a normal range of PTH-related protein values. One-desamino-(8-D-arginine)-vasopressin (DDAVP) and half-saline administration normalized hypernatremia, while hypercalcemia was still sustained. Administration of cortisone acetate and thiamazole reduced the elevated serum Ca level. In the present case, concurrent hyperthyroidism was assumed to accelerate skeletal mobilization of calcium into the circulation. Hypocortisolism and central DI was also considered to contribute, to some extent, to the hypercalcemia through renal handling of Ca. (+info)Antithyroid agents are a class of medications that are used to treat hyperthyroidism, a condition in which the thyroid gland produces too much thyroid hormone. These medications work by inhibiting the production of thyroid hormones in the thyroid gland. There are several types of antithyroid agents available, including:
1. Propylthiouracil (PTU): This medication works by blocking the enzyme that is needed to produce thyroid hormones. It also reduces the conversion of thyroxine (T4) to triiodothyronine (T3), another thyroid hormone, in peripheral tissues.
2. Methimazole: This medication works similarly to propylthiouracil by blocking the enzyme that is needed to produce thyroid hormones. However, it does not affect the conversion of T4 to T3 in peripheral tissues.
3. Carbimazole: This medication is converted to methimazole in the body and works similarly to block the production of thyroid hormones.
Antithyroid agents are usually taken orally, and their effects on thyroid hormone production begin within a few hours after ingestion. However, it may take several weeks for patients to notice an improvement in their symptoms. These medications can have side effects, including rash, hives, and joint pain. In rare cases, they can cause liver damage or agranulocytosis, a condition in which the body does not produce enough white blood cells.
It is important to note that antithyroid agents do not cure hyperthyroidism; they only treat the symptoms by reducing thyroid hormone production. Therefore, patients may need to take these medications for several months or even years, depending on their individual circumstances. In some cases, surgery or radioactive iodine therapy may be recommended as alternative treatments for hyperthyroidism.
Methimazole is an anti-thyroid medication that is primarily used to treat hyperthyroidism, a condition in which the thyroid gland produces excessive amounts of thyroid hormones. It works by inhibiting the enzyme thyroperoxidase, which is essential for the production of thyroid hormones. By blocking this enzyme, methimazole reduces the amount of thyroid hormones produced by the thyroid gland, helping to restore normal thyroid function.
Methimazole is available in oral tablet form and is typically taken two to three times a day. Common side effects of methimazole include nausea, vomiting, skin rashes, and joint pain. In rare cases, it can cause more serious side effects such as liver damage or agranulocytosis (a severe decrease in white blood cell count).
It is important to note that methimazole should only be used under the close supervision of a healthcare provider, as regular monitoring of thyroid function and potential side effects is necessary. Additionally, it may take several weeks or months of treatment with methimazole before thyroid function returns to normal.
Propylthiouracil is a medication that is primarily used to treat hyperthyroidism, a condition characterized by an overactive thyroid gland that produces too much thyroid hormone. The medication works by inhibiting the production of thyroid hormones in the body. It belongs to a class of drugs called antithyroid agents or thionamides.
In medical terms, propylthiouracil is defined as an antithyroid medication used to manage hyperthyroidism due to Graves' disease or toxic adenoma. It acts by inhibiting the synthesis of thyroid hormones, triiodothyronine (T3) and thyroxine (T4), in the thyroid gland. Propylthiouracil also reduces the peripheral conversion of T4 to T3. The medication is available as a tablet for oral administration and is typically prescribed at a starting dose of 100-150 mg three times daily, with adjustments made based on the patient's response and thyroid function tests.
It's important to note that propylthiouracil should be used under the close supervision of a healthcare provider due to potential side effects and risks associated with its use. Regular monitoring of thyroid function tests is necessary during treatment, and patients should promptly report any signs or symptoms of adverse reactions to their healthcare provider.
Carbimazole is an antithyroid medication that is primarily used to manage hyperthyroidism, a condition characterized by an overactive thyroid gland that produces excessive amounts of thyroid hormones. The drug works by inhibiting the enzyme responsible for producing these hormones, thereby reducing their levels in the body and alleviating symptoms associated with the disorder.
Hyperthyroidism can manifest as various signs and symptoms, including rapid heartbeat, weight loss, heat intolerance, tremors, anxiety, and sleep disturbances. Common causes of hyperthyroidism include Graves' disease, toxic adenoma, and thyroiditis.
Carbimazole is a prodrug that gets converted to its active metabolite, methimazole, in the liver. Methimazole inhibits the activity of thyroperoxidase, an enzyme involved in the synthesis of thyroid hormones triiodothyronine (T3) and thyroxine (T4). By blocking this enzyme, carbimazole reduces the production of T3 and T4, ultimately helping to control hyperthyroidism.
The medication is typically administered orally in tablet form, with dosages varying depending on individual patient needs and response to treatment. Common side effects of carbimazole include gastrointestinal disturbances such as nausea, vomiting, and diarrhea. Rare but severe adverse reactions may include agranulocytosis (a severe decrease in white blood cells), aplastic anemia (a condition where the bone marrow fails to produce sufficient numbers of blood cells), and hepatotoxicity (liver damage).
Patients taking carbimazole should be closely monitored for signs of adverse reactions, and regular blood tests are necessary to assess thyroid hormone levels and potential side effects. Pregnant women should avoid using carbimazole due to the risk of birth defects in the developing fetus. In such cases, alternative antithyroid medications like propylthiouracil may be prescribed instead.
In summary, carbimazole is an antithyroid medication used primarily for managing hyperthyroidism by inhibiting thyroperoxidase and reducing the production of thyroid hormones T3 and T4. While effective, it carries potential risks and side effects that necessitate close monitoring during treatment.
Graves' disease is defined as an autoimmune disorder that leads to overactivity of the thyroid gland (hyperthyroidism). It results when the immune system produces antibodies that stimulate the thyroid gland, causing it to produce too much thyroid hormone. This can result in a variety of symptoms such as rapid heartbeat, weight loss, heat intolerance, and bulging eyes (Graves' ophthalmopathy). The exact cause of Graves' disease is unknown, but it is more common in women and people with a family history of the disorder. Treatment may include medications to control hyperthyroidism, radioactive iodine therapy to destroy thyroid tissue, or surgery to remove the thyroid gland.
Hyperthyroidism is a medical condition characterized by an excessive production and release of thyroid hormones from the thyroid gland, leading to an increased metabolic rate in various body systems. The thyroid gland, located in the front of the neck, produces two main thyroid hormones: triiodothyronine (T3) and thyroxine (T4). These hormones play crucial roles in regulating many bodily functions, including heart rate, digestion, energy levels, and mood.
In hyperthyroidism, the elevated levels of T3 and T4 can cause a wide range of symptoms, such as rapid heartbeat, weight loss, heat intolerance, increased appetite, tremors, anxiety, and sleep disturbances. Some common causes of hyperthyroidism include Graves' disease, toxic adenoma, Plummer's disease (toxic multinodular goiter), and thyroiditis. Proper diagnosis and treatment are essential to manage the symptoms and prevent potential complications associated with this condition.
Thyrotoxicosis is a medical condition that results from an excess of thyroid hormones in the body, leading to an overactive metabolic state. It can be caused by various factors such as Graves' disease, toxic adenoma, Plummer's disease, or excessive intake of thyroid hormone medication. Symptoms may include rapid heart rate, weight loss, heat intolerance, tremors, and increased sweating, among others. Thyrotoxicosis is not a diagnosis itself but a manifestation of various underlying thyroid disorders. Proper diagnosis and management are crucial to prevent complications and improve quality of life.
Immunoglobulins, Thyroid-Stimulating (TSI), are autoantibodies that bind to the thyroid-stimulating hormone receptor (TSHR) on the surface of thyroid cells. These antibodies mimic the action of TSH and stimulate the growth and function of the thyroid gland, leading to excessive production of thyroid hormones. This results in a condition known as Graves' disease, which is characterized by hyperthyroidism, goiter, and sometimes ophthalmopathy (eye problems). The presence and titer of TSIs are used in the diagnosis of Graves' disease.
The thyroid gland is a major endocrine gland located in the neck, anterior to the trachea and extends from the lower third of the Adams apple to the suprasternal notch. It has two lateral lobes, connected by an isthmus, and sometimes a pyramidal lobe. This gland plays a crucial role in the metabolism, growth, and development of the human body through the production of thyroid hormones (triiodothyronine/T3 and thyroxine/T4) and calcitonin. The thyroid hormones regulate body temperature, heart rate, and the production of protein, while calcitonin helps in controlling calcium levels in the blood. The function of the thyroid gland is controlled by the hypothalamus and pituitary gland through the thyroid-stimulating hormone (TSH).
Thyroxine (T4) is a type of hormone produced and released by the thyroid gland, a small butterfly-shaped endocrine gland located in the front of your neck. It is one of two major hormones produced by the thyroid gland, with the other being triiodothyronine (T3).
Thyroxine plays a crucial role in regulating various metabolic processes in the body, including growth, development, and energy expenditure. Specifically, T4 helps to control the rate at which your body burns calories for energy, regulates protein, fat, and carbohydrate metabolism, and influences the body's sensitivity to other hormones.
T4 is produced by combining iodine and tyrosine, an amino acid found in many foods. Once produced, T4 circulates in the bloodstream and gets converted into its active form, T3, in various tissues throughout the body. Thyroxine has a longer half-life than T3, which means it remains active in the body for a more extended period.
Abnormal levels of thyroxine can lead to various medical conditions, such as hypothyroidism (underactive thyroid) or hyperthyroidism (overactive thyroid). These conditions can cause a range of symptoms, including weight gain or loss, fatigue, mood changes, and changes in heart rate and blood pressure.
Thyroid function tests (TFTs) are a group of blood tests that assess the functioning of the thyroid gland, which is a small butterfly-shaped gland located in the front of the neck. The thyroid gland produces hormones that regulate metabolism, growth, and development in the body.
TFTs typically include the following tests:
1. Thyroid-stimulating hormone (TSH) test: This test measures the level of TSH, a hormone produced by the pituitary gland that regulates the production of thyroid hormones. High levels of TSH may indicate an underactive thyroid gland (hypothyroidism), while low levels may indicate an overactive thyroid gland (hyperthyroidism).
2. Thyroxine (T4) test: This test measures the level of T4, a hormone produced by the thyroid gland. High levels of T4 may indicate hyperthyroidism, while low levels may indicate hypothyroidism.
3. Triiodothyronine (T3) test: This test measures the level of T3, another hormone produced by the thyroid gland. High levels of T3 may indicate hyperthyroidism, while low levels may indicate hypothyroidism.
4. Thyroid peroxidase antibody (TPOAb) test: This test measures the level of TPOAb, an antibody that attacks the thyroid gland and can cause hypothyroidism.
5. Thyroglobulin (Tg) test: This test measures the level of Tg, a protein produced by the thyroid gland. It is used to monitor the treatment of thyroid cancer.
These tests help diagnose and manage various thyroid disorders, including hypothyroidism, hyperthyroidism, thyroiditis, and thyroid cancer.
Hypothyroidism is a medical condition where the thyroid gland, which is a small butterfly-shaped gland located in the front of your neck, does not produce enough thyroid hormones. This results in a slowing down of the body's metabolic processes, leading to various symptoms such as fatigue, weight gain, constipation, cold intolerance, dry skin, hair loss, muscle weakness, and depression.
The two main thyroid hormones produced by the thyroid gland are triiodothyronine (T3) and thyroxine (T4). These hormones play crucial roles in regulating various bodily functions, including heart rate, body temperature, and energy levels. In hypothyroidism, the production of these hormones is insufficient, leading to a range of symptoms that can affect multiple organ systems.
Hypothyroidism can be caused by several factors, including autoimmune disorders (such as Hashimoto's thyroiditis), surgical removal of the thyroid gland, radiation therapy for neck cancer, certain medications, and congenital defects. Hypothyroidism is typically diagnosed through blood tests that measure levels of TSH (thyroid-stimulating hormone), T3, and T4. Treatment usually involves taking synthetic thyroid hormones to replace the missing hormones and alleviate symptoms.
Thyrotropin, also known as thyroid-stimulating hormone (TSH), is a hormone secreted by the anterior pituitary gland. Its primary function is to regulate the production and release of thyroxine (T4) and triiodothyronine (T3) hormones from the thyroid gland. Thyrotropin binds to receptors on the surface of thyroid follicular cells, stimulating the uptake of iodide and the synthesis and release of T4 and T3. The secretion of thyrotropin is controlled by the hypothalamic-pituitary-thyroid axis: thyrotropin-releasing hormone (TRH) from the hypothalamus stimulates the release of thyrotropin, while T3 and T4 inhibit its release through a negative feedback mechanism.
Agranulocytosis is a medical condition characterized by an abnormally low concentration of granulocytes (a type of white blood cells) in the peripheral blood. Granulocytes, which include neutrophils, eosinophils, and basophils, play a crucial role in the body's defense against infections. A significant reduction in their numbers can make an individual highly susceptible to various bacterial and fungal infections.
The condition is typically defined as having fewer than 150 granulocytes per microliter of blood or less than 1% of the total white blood cell count. Symptoms of agranulocytosis may include fever, fatigue, sore throat, mouth ulcers, and susceptibility to infections. The condition can be caused by various factors, including certain medications, medical treatments (such as chemotherapy or radiation therapy), autoimmune disorders, and congenital conditions. Immediate medical attention is required for individuals diagnosed with agranulocytosis to prevent and treat potential infections and restore the normal granulocyte count.
Thyroid diseases are a group of conditions that affect the function and structure of the thyroid gland, a small butterfly-shaped endocrine gland located in the base of the neck. The thyroid gland produces hormones that regulate many vital functions in the body, including metabolism, growth, and development.
Thyroid diseases can be classified into two main categories: hypothyroidism and hyperthyroidism. Hypothyroidism occurs when the thyroid gland does not produce enough hormones, leading to symptoms such as fatigue, weight gain, cold intolerance, constipation, and depression. Hyperthyroidism, on the other hand, occurs when the thyroid gland produces too much hormone, resulting in symptoms such as weight loss, heat intolerance, rapid heart rate, tremors, and anxiety.
Other common thyroid diseases include:
1. Goiter: an enlargement of the thyroid gland that can be caused by iodine deficiency or autoimmune disorders.
2. Thyroid nodules: abnormal growths on the thyroid gland that can be benign or malignant.
3. Thyroid cancer: a malignant tumor of the thyroid gland that requires medical treatment.
4. Hashimoto's disease: an autoimmune disorder that causes chronic inflammation of the thyroid gland, leading to hypothyroidism.
5. Graves' disease: an autoimmune disorder that causes hyperthyroidism and can also lead to eye problems and skin changes.
Thyroid diseases are diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as ultrasound or CT scan. Treatment options depend on the specific type and severity of the disease and may include medication, surgery, or radioactive iodine therapy.
Thiouracil is not typically used as a medical treatment in current clinical practice. It is an anti-thyroid medication that was historically used to manage hyperthyroidism, particularly in cases of Graves' disease. However, due to its adverse effect profile and the availability of safer and more effective treatment options, thiouracil has largely been replaced by other medications such as methimazole and propylthiouracil.
Thiouracil works by inhibiting the enzyme thyroperoxidase, which is necessary for the production of thyroid hormones in the body. By blocking this enzyme, thiouracil reduces the amount of thyroid hormones produced and can help to control symptoms of hyperthyroidism such as rapid heart rate, tremors, and weight loss.
While thiouracil is still available for use in some cases, its use is generally reserved for patients who cannot tolerate or have failed other treatments. The medication can cause serious side effects, including liver damage, bone marrow suppression, and allergic reactions, and requires careful monitoring during treatment.
Thyrotropin receptors (TSHRs) are a type of G protein-coupled receptor found on the surface of cells in the thyroid gland. They bind to thyroid-stimulating hormone (TSH), which is produced and released by the pituitary gland. When TSH binds to the TSHR, it activates a series of intracellular signaling pathways that stimulate the production and release of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). These hormones are important for regulating metabolism, growth, and development in the body. Mutations in the TSHR gene can lead to various thyroid disorders, such as hyperthyroidism or hypothyroidism.
Triiodothyronine (T3) is a thyroid hormone, specifically the active form of thyroid hormone, that plays a critical role in the regulation of metabolism, growth, and development in the human body. It is produced by the thyroid gland through the iodination and coupling of the amino acid tyrosine with three atoms of iodine. T3 is more potent than its precursor, thyroxine (T4), which has four iodine atoms, as T3 binds more strongly to thyroid hormone receptors and accelerates metabolic processes at the cellular level.
In circulation, about 80% of T3 is bound to plasma proteins, while the remaining 20% is unbound or free, allowing it to enter cells and exert its biological effects. The primary functions of T3 include increasing the rate of metabolic reactions, promoting protein synthesis, enhancing sensitivity to catecholamines (e.g., adrenaline), and supporting normal brain development during fetal growth and early infancy. Imbalances in T3 levels can lead to various medical conditions, such as hypothyroidism or hyperthyroidism, which may require clinical intervention and management.
Autoimmune thyroiditis, also known as Hashimoto's disease, is a chronic inflammation of the thyroid gland caused by an autoimmune response. In this condition, the immune system produces antibodies that attack and damage the thyroid gland, leading to hypothyroidism (underactive thyroid). The thyroid gland may become enlarged (goiter), and symptoms can include fatigue, weight gain, cold intolerance, constipation, dry skin, and depression. Autoimmune thyroiditis is more common in women than men and tends to run in families. It is often associated with other autoimmune disorders such as rheumatoid arthritis, Addison's disease, and type 1 diabetes. The diagnosis is typically made through blood tests that measure levels of thyroid hormones and antibodies. Treatment usually involves thyroid hormone replacement therapy to manage the symptoms of hypothyroidism.
Thyroid hormones are hormones produced and released by the thyroid gland, a small endocrine gland located in the neck that helps regulate metabolism, growth, and development in the human body. The two main thyroid hormones are triiodothyronine (T3) and thyroxine (T4), which contain iodine atoms. These hormones play a crucial role in various bodily functions, including heart rate, body temperature, digestion, and brain development. They help regulate the rate at which your body uses energy, affects how sensitive your body is to other hormones, and plays a vital role in the development and differentiation of all cells of the human body. Thyroid hormone levels are regulated by the hypothalamus and pituitary gland through a feedback mechanism that helps maintain proper balance.
Iodine radioisotopes are radioactive isotopes of the element iodine, which decays and emits radiation in the form of gamma rays. Some commonly used iodine radioisotopes include I-123, I-125, I-131. These radioisotopes have various medical applications such as in diagnostic imaging, therapy for thyroid disorders, and cancer treatment.
For example, I-131 is commonly used to treat hyperthyroidism and differentiated thyroid cancer due to its ability to destroy thyroid tissue. On the other hand, I-123 is often used in nuclear medicine scans of the thyroid gland because it emits gamma rays that can be detected by a gamma camera, allowing for detailed images of the gland's structure and function.
It is important to note that handling and administering radioisotopes require specialized training and safety precautions due to their radiation-emitting properties.
Thyroiditis is a general term that refers to inflammation of the thyroid gland. It can be caused by various factors such as infections, autoimmune disorders, or medications. Depending on the cause and severity, thyroiditis may lead to overproduction (hyperthyroidism) or underproduction (hypothyroidism) of thyroid hormones, or it can result in a temporary or permanent loss of thyroid function.
There are several types of thyroiditis, including:
1. Hashimoto's thyroiditis - an autoimmune disorder where the body attacks and damages the thyroid gland, leading to hypothyroidism.
2. Subacute granulomatous thyroiditis (De Quervain's thyroiditis) - often follows a viral infection and results in painful inflammation of the thyroid gland, causing hyperthyroidism followed by hypothyroidism.
3. Silent thyroiditis - an autoimmune disorder similar to Hashimoto's thyroiditis but without symptoms like pain or tenderness; it can cause temporary hyperthyroidism and later hypothyroidism.
4. Postpartum thyroiditis - occurs in women after childbirth, causing inflammation of the thyroid gland leading to hyperthyroidism followed by hypothyroidism.
5. Acute suppurative thyroiditis - a rare bacterial infection that causes painful swelling and redness of the thyroid gland, usually requiring antibiotics for treatment.
Symptoms of thyroiditis depend on whether it leads to hyperthyroidism or hypothyroidism. Hyperthyroidism symptoms include rapid heartbeat, weight loss, heat intolerance, anxiety, and tremors. Hypothyroidism symptoms include fatigue, weight gain, cold intolerance, constipation, dry skin, and depression. Treatment varies depending on the type of thyroiditis and its severity.
Goiter is a medical term that refers to an enlarged thyroid gland. The thyroid gland is a small, butterfly-shaped gland located in the front of your neck below the larynx or voice box. It produces hormones that regulate your body's metabolism, growth, and development.
Goiter can vary in size and may be visible as a swelling at the base of the neck. It can be caused by several factors, including iodine deficiency, autoimmune disorders, thyroid cancer, pregnancy, or the use of certain medications. Depending on the underlying cause and the severity of the goiter, treatment options may include medication, surgery, or radioactive iodine therapy.
Autoantibodies are defined as antibodies that are produced by the immune system and target the body's own cells, tissues, or organs. These antibodies mistakenly identify certain proteins or molecules in the body as foreign invaders and attack them, leading to an autoimmune response. Autoantibodies can be found in various autoimmune diseases such as rheumatoid arthritis, lupus, and thyroiditis. The presence of autoantibodies can also be used as a diagnostic marker for certain conditions.
Thyroglobulin is a protein produced and used by the thyroid gland in the production of thyroid hormones, primarily thyroxine (T4) and triiodothyronine (T3). It is composed of two subunits, an alpha and a beta or gamma unit, which bind iodine atoms necessary for the synthesis of the thyroid hormones. Thyroglobulin is exclusively produced by the follicular cells of the thyroid gland.
In clinical practice, measuring thyroglobulin levels in the blood can be useful as a tumor marker for monitoring treatment and detecting recurrence of thyroid cancer, particularly in patients with differentiated thyroid cancer (papillary or follicular) who have had their thyroid gland removed. However, it is important to note that thyroglobulin is not specific to thyroid tissue and can be produced by some non-thyroidal cells under certain conditions, which may lead to false positive results in some cases.
Thyroidectomy is a surgical procedure where all or part of the thyroid gland is removed. The thyroid gland is a butterfly-shaped endocrine gland located in the neck, responsible for producing hormones that regulate metabolism, growth, and development.
There are different types of thyroidectomy procedures, including:
1. Total thyroidectomy: Removal of the entire thyroid gland.
2. Partial (or subtotal) thyroidectomy: Removal of a portion of the thyroid gland.
3. Hemithyroidectomy: Removal of one lobe of the thyroid gland, often performed to treat benign solitary nodules or differentiated thyroid cancer.
Thyroidectomy may be recommended for various reasons, such as treating thyroid nodules, goiter, hyperthyroidism (overactive thyroid), or thyroid cancer. Potential risks and complications of the procedure include bleeding, infection, damage to nearby structures like the parathyroid glands and recurrent laryngeal nerve, and hypoparathyroidism or hypothyroidism due to removal of or damage to the parathyroid glands or thyroid gland, respectively. Close postoperative monitoring and management are essential to minimize these risks and ensure optimal patient outcomes.
Hashimoto's disease, also known as chronic lymphocytic thyroiditis, is an autoimmune disorder in which the immune system mistakenly attacks and damages the thyroid gland. The resulting inflammation often leads to an underactive thyroid gland (hypothyroidism). It primarily affects middle-aged women but can also occur in men and women of any age and in children.
The exact cause of Hashimoto's disease is unclear, but it appears to involve interactions between genetic and environmental factors. The disorder tends to run in families, and having a family member with Hashimoto's disease or another autoimmune disorder increases the risk.
Symptoms of hypothyroidism include fatigue, weight gain, constipation, cold intolerance, joint and muscle pain, dry skin, thinning hair, irregular menstrual periods, and depression. However, some people with Hashimoto's disease may have no symptoms for many years.
Diagnosis is typically based on a combination of symptoms, physical examination findings, and laboratory test results. Treatment usually involves thyroid hormone replacement therapy, which can help manage symptoms and prevent complications of hypothyroidism. Regular monitoring of thyroid function is necessary to adjust the dosage of medication as needed.
Methimazole (brand name Tapazole) is often used instead of methylthiouracil in current clinical practice due to its more favorable side effect profile. However, I will provide the medical definition for methylthiouracil as you requested:
Methylthiouracil is an anti-thyroid medication primarily used to manage hyperthyroidism (overactive thyroid gland). It works by inhibiting the enzyme thyroperoxidase, which is essential for the production of thyroid hormones triiodothyronine (T3) and thyroxine (T4). By blocking this enzyme, methylthiouracil helps reduce the levels of these hormones in the body.
Methylthiouracil has additional immunomodulatory effects that can help suppress the autoimmune response responsible for some forms of hyperthyroidism, such as Graves' disease. It may be used to prepare patients for thyroid surgery or radioactive iodine therapy, or it can be employed as a long-term treatment option in certain cases.
Common side effects of methylthiouracil include nausea, vomiting, skin rashes, and joint pain. Rare but serious side effects may include agranulocytosis (a severe decrease in white blood cells), hepatotoxicity (liver damage), and vasculitis (inflammation of the blood vessels). Due to these potential adverse reactions, methylthiouracil is generally used less frequently than methimazole in current clinical practice.
Iodide peroxidase, also known as iodide:hydrogen peroxide oxidoreductase, is an enzyme that belongs to the family of oxidoreductases. Specifically, it is a peroxidase that uses iodide as its physiological reducing substrate. This enzyme catalyzes the oxidation of iodide by hydrogen peroxide to produce iodine, which plays a crucial role in thyroid hormone biosynthesis.
The systematic name for this enzyme is iodide:hydrogen-peroxide oxidoreductase (iodinating). It is most commonly found in the thyroid gland, where it helps to produce and regulate thyroid hormones by facilitating the iodination of tyrosine residues on thyroglobulin, a protein produced by the thyroid gland.
Iodide peroxidase requires a heme cofactor for its enzymatic activity, which is responsible for the oxidation-reduction reactions it catalyzes. The enzyme's ability to iodinate tyrosine residues on thyroglobulin is essential for the production of triiodothyronine (T3) and thyroxine (T4), two critical hormones that regulate metabolism, growth, and development in mammals.
Perchlorates are chemical compounds containing the perchlorate ion (ClO4-). Perchloric acid is the parent compound and has the formula HClO4. Perchlorates contain chlorine in its highest oxidation state (+7) and are strong oxidizing agents. They have been used in various industrial and military applications, such as in explosives, rocket propellants, and matches.
In a medical context, perchlorates can be relevant due to their potential health effects. Exposure to high levels of perchlorates can affect the thyroid gland's function because they can compete with iodide ions for uptake by the thyroid gland. Iodide is an essential component of thyroid hormones, and disruption of iodide uptake may lead to hypothyroidism, particularly in individuals who are iodine-deficient. However, it's important to note that the evidence for adverse health effects in humans from environmental exposures to perchlorates is still a subject of ongoing research and debate.
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