Propylthiouracil
Antithyroid Agents
Methimazole
Hyperthyroidism
Hypothyroidism
Thyroxine
Triiodothyronine
Triiodothyronine, Reverse
Graves Disease
Carbimazole
Thyroid Hormones
Thyroid Gland
Iodide Peroxidase
Thyrotropin
Thyrotoxicosis
Antibodies, Antineutrophil Cytoplasmic
Potassium Iodide
Goiter
Phenylthiourea
Perchlorates
Antimetabolites
Vasculitis, Leukocytoclastic, Cutaneous
Alternating antineutrophil cytoplasmic antibody specificity: drug-induced vasculitis in a patient with Wegener's granulomatosis. (1/453)
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)Stimulation of Na,K-ATPase by hypothyroidism in the thyroid gland. (2/453)
Although studies have documented the regulatory effects of thyroid hormones on the Na,K-ATPase in peripheral tissues, there is little information on the regulation of this transporter in the thyroid gland itself. Accordingly, we investigated the effects of thyroid status on Na,K-ATPase specific activity and the abundance of its constituent subunits in rat thyroid. Exogenous tri-iodothyronine (T3) was administered daily to produce hyperthyroidism. 6n-propyl-2-thiouracil (PTU), an inhibitor of thyroid hormone synthesis, was used to induce hypothyroidism. There was a four-fold increase in Na,K-ATPase specific activity in the follicular membranes from PTU-treated animals after 7 days. Enzymatic activities were not changed in the T3-treated glands. Immunoblotting of membranes from T3-treated rats revealed a 75% reduction in alpha1 subunit abundance and a slight, but nonsignificant reduction in beta1 abundance. On the other hand, the membranes from PTU-treated rats displayed 136 and 567% increases in the abundance of the alpha1 and beta1 subunits respectively. These data demonstrate that thyroid hormone status regulates Na,K-ATPase in the gland, but the effects are in direct contrast to those seen in the periphery. (+info)Na,K-ATPase mRNA beta 1 expression in rat myocardium--effect of thyroid status. (3/453)
The abundance of Na,K-ATPase and its alpha and beta subunit mRNAs is upregulated in cardiac and other target tissue by thyroid hormone (T3). Multiple Na,K-ATPase mRNA beta 1 species encoding an identical beta 1 polypeptide are expressed in the heart. The different mRNA beta 1 species result from utilization of two transcription start-sites in the first exon and multiple (five) poly(A) signals in the terminal exon of the beta 1 gene. In the present study we identify the mRNA beta 1 species that are expressed in rat ventricular myocardium under basal conditions, and determine whether they are differentially regulated by T3. mRNA beta 1 species were identified by 3'-RACE followed by DNA sequencing, and by Northern blotting using probes derived from different regions of rat cDNA beta 1. Five mRNA beta 1 species are expressed in rat heart: mRNA beta 1 species that are initiated at the first transcription start-site and end at the first, second and fifth poly(A) sites (resulting in mRNAs of 1630, 1810, and 2780 nucleotides), and mRNA beta 1 species initiated at the second transcription start-site and ending at the second and fifth poly(A) sites (resulting in mRNAs of 1500 and 2490 nucleotides); in order of increasing length, the five mRNAs constitute 0.04, 0.15, 0.38, 0.11 and 0.32 of total mRNA beta 1 content. In hypothyroid rats (induced by addition of propyl-thiouracil to the drinking water for 3 weeks), total mRNA beta 1 content decreased to 0.18 euthyroid levels, which was associated with a disproportionate 7.5-fold decrease in the abundance of the longest transcript (P < 0.05); transcripts initiating at the first transcription start-site and ending at the second poly(A) signal in hypothyroid hearts were 0.26 euthyroid levels (P < 0.05). Hyperthyroidism induced by injection of normal rats with three doses of 100 micrograms T3/100 g body weight every 48 h resulted in an overall approximately 2-fold increase in mRNA beta 1 content with no change in the fractional contribution of any of the mRNA beta 1 species. The results indicate a complex heterogeneity in the expression of mRNA beta 1 in myocardium. (+info)In vivo regulation of beta-MHC gene in rodent heart: role of T3 and evidence for an upstream enhancer. (4/453)
Cardiac beta-myosin heavy chain (beta-MHC) gene expression is mainly regulated through transcriptional processes. Although these results are based primarily on in vitro cell culture models, relatively little information is available concerning the interaction of key regulatory factors thought to modulate MHC expression in the intact rodent heart. Using a direct gene transfer approach, we studied the in vivo transcriptional activity of different-length beta-MHC promoter fragments in normal control and in altered thyroid states. The test beta-MHC promoter was fused to a firefly luciferase reporter gene, whereas the control alpha-MHC promoter was fused to the Renilla luciferase reporter gene and was used to account for variations in transfection efficiency. Absolute reporter gene activities showed that beta- and alpha-MHC genes were individually and reciprocally regulated by thyroid hormone. The beta-to-alpha ratios of reporter gene expression demonstrated an almost threefold larger beta-MHC gene expression in the longest than in the shorter promoter fragments in normal control animals, implying the existence of an upstream enhancer. A mutation in the putative thyroid response element of the -408-bp beta-MHC promoter construct caused transcriptional activity to drop to null. When studied in the -3, 500-bp beta-MHC promoter, construct activity was reduced ( approximately 100-fold) while thyroid hormone responsiveness was retained. These findings suggest that, even though the bulk of the thyroid hormone responsiveness of the gene is contained within the first 215 bp of the beta-MHC promoter sequence, the exact mechanism of triiodothyronine (T3) action remains to be elucidated. (+info)Clinical study on early changes in thyroid function of hyperthyroidism treated with propylthiouracil and a relatively small dose of iodide. (5/453)
In order to compare the acute effects of three kinds of antithyroid agents of iodide (I-), propylthiouracil (PTU) and PTU combined with iodide (PTU+I-) on thyroid function in hyperthyroid patients with diffuse goiter, serum concentrations of thyroxine (T4), triiodothyronine (T3), T3-resin sponge uptake (T3-RU) and free thyroxine index (FT4I) were employed as thyroid function parameters. In the group given iodine (1 mg/day) as iodinated-lecithine, the initial values of T4, T3, T3-RU and FT4I were 20.9 +/- 1.6 microng/100 ml (T4), greater than 740 ng/100 ml (T3), 49.5 +/- 2.3% (T3-RU) and 14.7 +/- 1.8 (FT4I). At the end of one week of therapy, they decreased clearly to 15.6 +/- 2.2 microng/100 ml, 457 +/- 87 ng/100 ml, 42.2 +/- 4.0% and 9.7 +/- 2.4. The so-called "escape phenomenon" from iodide inhibition was observed in serum T4, T3-RU and FT4I values at the end of two weeks of iodide therapy, while serum T3 continued to decrease but the value of T3 was far outside of the normal range. In the PTU group (300 mg/day), thyroid function parameters were 22.5 +/- 0.8 microng/100 ml (T4), greater than 592 ng/100 ml (T3), 54.9 +/- 1.0% (T3-RU) and 18.7 +/- 1.0 (FT4I) before treatment. They decreased continually week by week. At the end of four-week treatment with PTU, the value of each thyroid function parameter was 11.1 +/- 1.9 microng/100 ml, 229 +/- 56 ng/100 ml, 36.6 +/- 4.4% and 5.7 +/- 1.7. In the group of hyperthyroidism simultaneously given both PTU and iodide (300 mg/PTU and 1 mg/iodine), these thyroid function parameters decreased as well as in the group treated with PTU alone for more than two weeks. More rapid or significant decrease of T4, T3, T3-RU and ft4i in PTU+I- group than in PTU group was observed in the present study. These results suggested strongly that iodide alone was not an adequate therapy for hyperthyroidism as well known and they were also compatible with the idea that the concomitant administration of PTU and iodide was more effective in the early phase of therapy of hyperthyroidism than PTU alone. (+info)Tri-iodothyronine increases insulin-like growth factor binding protein-2 expression in cultured hepatocytes from hypothyroid rats. (6/453)
Previous evidence suggests the existence of a thyroid hormone-IGF axis in the liver and changes in hepatic insulin-like growth factor binding protein (IGFBP) expression in rats with altered thyroid status have been previously reported. The aim of this study was to check if the higher IGFBP-2 mRNA levels observed in liver of hypothyroid rats could be due to a direct effect of thyroid hormone on the IGFBP-2 gene. In our experiments, cultured hepatocytes isolated from normal and hypothyroid adult rats were used. Northern blot analysis revealed barely detectable IGFBP-2 mRNA in normal rat hepatocytes, but easily detectable signal in hypothyroid rat cells. Therefore, the effect of tri-iodothyronine (T3) was investigated using cultured hepatocytes from hypothyroid rats as an in vitro model. The IGFBP-2 message was increased in a dose-dependent manner in hepatocytes cultured for 12-24 h in the presence of T3. A similar increase occurred in accumulation of IGFBP-2 in the culture medium, as measured by RIA. The effect of T3 on IGFBP-2 transcript levels appeared to consist of enhanced gene transcription and was independent of ongoing protein synthesis, but it was completely abolished by the incubation of hepatocytes with insulin. The latter result confirmed the dominant role of insulin in regulating IGFBP-2 expression by cultured hepatocytes. In vivo experiments confirmed an increase in hepatic IGFBP-2 mRNA and serum IGFBP-2 levels in hypothyroid rats and demonstrated, in addition, a significant increase in these measures in T3-treated rats. Taken together, our in vitro and in vivo results support a role for a thyroid hormone-IGF axis in the liver and suggest that other factors, such as insulin, interact in vivo with thryoid hormone in regulating hepatic IGFBP-2 expression. (+info)Improved suppression by dietary taurine of the fecal excretion of bile acids from hypothyroid rats. (7/453)
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. (8/453)
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)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.
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.
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.
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.
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.
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.
Reverse Triiodothyronine (rT3) is a thyroid hormone that is chemically identical to triiodothyronine (T3), but has a reverse configuration at one end of the molecule. It is produced in smaller quantities compared to T3 and its function is not well understood. In some cases, increased levels of rT3 have been associated with decreased thyroid hormone action, such as in non-thyroidal illnesses or during calorie restriction. However, the clinical significance of rT3 levels remains a topic of ongoing research and debate.
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.
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.
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.
Iopanoic acid is a contrast medium, specifically a radiocontrast agent, that is used during imaging examinations such as X-rays and CT scans to help improve the visibility of internal body structures. It works by blocking the absorption of X-rays in the digestive tract, making it possible to visualize the gastrointestinal tract more clearly on imaging studies. Iopanoic acid is typically given orally before the examination.
It's important to note that the use of iopanoic acid and other radiocontrast agents should be carefully weighed against the potential risks, as they can cause allergic reactions, kidney damage, and other complications in some individuals. Therefore, it is usually reserved for situations where the benefits of improved imaging outweigh these potential risks.
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).
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.
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.
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.
Antineutrophil cytoplasmic antibodies (ANCAs) are a type of autoantibody that specifically target certain proteins in the cytoplasm of neutrophils, which are a type of white blood cell. These antibodies are associated with several types of vasculitis, which is inflammation of the blood vessels.
There are two main types of ANCAs: perinuclear ANCAs (p-ANCAs) and cytoplasmic ANCAs (c-ANCAs). p-ANCAs are directed against myeloperoxidase, a protein found in neutrophil granules, while c-ANCAs target proteinase 3, another protein found in neutrophil granules.
The presence of ANCAs in the blood can indicate an increased risk for developing certain types of vasculitis, such as granulomatosis with polyangiitis (GPA), eosinophilic granulomatosis with polyangiitis (EGPA), and microscopic polyangiitis (MPA). ANCA testing is often used in conjunction with other clinical findings to help diagnose and manage these conditions.
It's important to note that while the presence of ANCAs can indicate an increased risk for vasculitis, not everyone with ANCAs will develop the condition. Additionally, ANCAs can also be found in some individuals without any associated disease, so their presence should be interpreted in the context of other clinical findings.
Potassium iodide is an inorganic, non-radioactive salt of iodine. Medically, it is used as a thyroid blocking agent to prevent the absorption of radioactive iodine in the event of a nuclear accident or radiation exposure. It works by saturating the thyroid gland with stable iodide, which then prevents the uptake of radioactive iodine. This can help reduce the risk of thyroid cancer and other thyroid related issues that may arise from exposure to radioactive materials. Potassium iodide is also used in the treatment of iodine deficiency disorders.
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.
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.
Phenylthiourea is not typically considered a medical term, but it is a chemical compound that is used in scientific research and has been studied in the context of medicine. Here's a definition from a chemistry perspective:
Phenylthiourea (PTU) is an organic compound with the formula C6H5NCS. It is a derivative of thiourea, where one hydrogen atom is replaced by a phenyl group. PTU is a white crystalline powder that is soluble in water and alcohol.
In medical terms, PTU has been used as a medication to treat hyperthyroidism (overactive thyroid gland) because it can inhibit the production of thyroid hormones. However, its use as a therapeutic agent has declined due to the availability of other medications with fewer side effects. It is still used in research settings to study various biological processes and diseases.
It's important to note that PTU should only be administered under the supervision of a healthcare professional, as it can have adverse effects if not used properly.
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.
Antimetabolites are a class of drugs that interfere with the normal metabolic processes of cells, particularly those involved in DNA replication and cell division. They are commonly used as chemotherapeutic agents to treat various types of cancer because many cancer cells divide more rapidly than normal cells. Antimetabolites work by mimicking natural substances needed for cell growth and division, such as nucleotides or amino acids, and getting incorporated into the growing cells' DNA or protein structures, which ultimately leads to the termination of cell division and death of the cancer cells. Examples of antimetabolites include methotrexate, 5-fluorouracil, and capecitabine.
Leukocytoclastic vasculitis, cutaneous is a type of vasculitis that is limited to the skin. Vasculitis refers to inflammation of the blood vessels, which can cause damage to the vessel walls and impair blood flow to various tissues in the body. In leukocytoclastic vasculitis, the small blood vessels (capillaries and venules) in the skin become inflamed, leading to damage and destruction of the vessel walls.
The term "leukocytoclastic" refers to the presence of nuclear debris from white blood cells (leukocytes) that have been destroyed within the affected blood vessels. This type of vasculitis is often associated with the deposition of immune complexes (formed by the interaction between antibodies and antigens) in the walls of the blood vessels, which triggers an inflammatory response.
Cutaneous leukocytoclastic vasculitis typically presents as palpable purpura (small to large, raised, purple or red spots on the skin), usually located on the lower extremities, but can also affect other areas of the body. Other symptoms may include burning or itching sensations in the affected area, and in some cases, ulcers or necrosis (tissue death) may occur.
The diagnosis of cutaneous leukocytoclastic vasculitis is typically made based on clinical presentation, laboratory tests, and histopathological examination of a skin biopsy specimen. Treatment usually involves addressing any underlying causes or triggers, as well as managing symptoms with medications such as corticosteroids or immunosuppressive agents.
Iodides are chemical compounds that contain iodine in the form of an iodide ion (I-). Iodide ions are negatively charged ions that consist of one iodine atom and an extra electron. Iodides are commonly found in dietary supplements and medications, and they are often used to treat or prevent iodine deficiency. They can also be used as expectorants to help thin and loosen mucus in the respiratory tract. Examples of iodides include potassium iodide (KI) and sodium iodide (NaI).
Taste threshold is the minimum concentration of a taste substance that can be detected by the taste buds. It is the point at which a person can just discriminate the presence of a specific taste (sweet, salty, sour, bitter, or umami) from plain water or another tastant. The taste threshold can be measured through various methods, such as whole-mouth tastings or using specialized taste strips, and it can vary among individuals due to factors like age, genetics, and exposure to certain chemicals or medications.