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
Hashimoto Disease
Methylthiouracil
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)Grave's disease is the most common cause of hyperthyroidism and affects about 1 in 200 people. It can occur at any age but is more common in women and tends to run in families. The exact cause of Grave's disease is not known, but it may be related to a combination of genetic and environmental factors.
Symptoms of Grave's disease can vary from person to person, but common signs include:
* Weight loss
* Nervousness or anxiety
* Irregular heartbeat (palpitations)
* Increased sweating
* Heat intolerance
* Fatigue
* Changes in menstrual cycle in women
* Enlargement of the thyroid gland, known as a goiter
* Bulging eyes (exophthalmos)
Grave's disease can be diagnosed through blood tests and scans. Treatment options include medication to reduce the production of thyroxine, radioactive iodine therapy to destroy part of the thyroid gland, and surgery to remove part or all of the thyroid gland.
It is important to seek medical attention if you experience any symptoms of Grave's disease, as untreated hyperthyroidism can lead to complications such as heart problems, osteoporosis, and eye problems. With proper treatment, most people with Grave's disease can manage their symptoms and lead a normal life.
The most common cause of hyperthyroidism is an autoimmune disorder called Graves' disease, which causes the thyroid gland to produce too much thyroxine (T4) and triiodothyronine (T3). Other causes include inflammation of the thyroid gland (thyroiditis), thyroid nodules, and certain medications.
Symptoms of hyperthyroidism can vary depending on the severity of the condition, but may include:
* Rapid weight loss
* Nervousness or irritability
* Increased heart rate
* Heat intolerance
* Changes in menstrual cycle
* Fatigue
* Muscle weakness
* tremors
If left untreated, hyperthyroidism can lead to more serious complications such as heart problems, bone loss, and eye problems. Treatment options for hyperthyroidism include medications to reduce hormone production, radioactive iodine therapy to destroy part of the thyroid gland, and surgery to remove part or all of the thyroid gland.
In pregnant women, untreated hyperthyroidism can increase the risk of miscarriage, preterm labor, and intellectual disability in the baby. Treatment options for pregnant women with hyperthyroidism are similar to those for non-pregnant adults, but may need to be adjusted to avoid harm to the developing fetus.
It is important for individuals suspected of having hyperthyroidism to seek medical attention as soon as possible to receive proper diagnosis and treatment. Early treatment can help prevent complications and improve quality of life.
The most common cause of thyrotoxicosis is an overactive thyroid gland, known as hyperthyroidism. This can be caused by a variety of factors, including:
* Graves' disease: An autoimmune disorder that causes the thyroid gland to produce too much thyroid hormone.
* Toxic multinodular goiter: A condition in which one or more nodules in the thyroid gland become overactive and produce excessive amounts of thyroid hormone.
* Thyroid adenoma: A benign tumor of the thyroid gland that can cause hyperthyroidism.
* Thyroid cancer: A malignant tumor of the thyroid gland that can cause hyperthyroidism.
Symptoms of thyrotoxicosis can vary depending on the severity of the condition and the individual affected, but may include:
* Weight loss
* Increased heart rate
* Anxiety
* Sweating
* Tremors
* Nervousness
* Fatigue
* Heat intolerance
* Increased bowel movements
* Muscle weakness
Thyrotoxicosis can be diagnosed through a series of tests, including:
* Blood tests: To measure thyroid hormone levels in the blood.
* Thyroid scan: To visualize the thyroid gland and identify any nodules or tumors.
* Ultrasound: To evaluate the structure of the thyroid gland and detect any abnormalities.
Treatment for thyrotoxicosis depends on the underlying cause, but may include:
* Medications to reduce thyroid hormone production.
* Radioactive iodine therapy to destroy part or all of the thyroid gland.
* Surgery to remove part or all of the thyroid gland.
It is important to note that untreated thyrotoxicosis can lead to complications such as heart problems, osteoporosis, and eye problems, so it is important to seek medical attention if symptoms persist or worsen over time.
Hypothyroidism can be diagnosed through a series of blood tests that measure the levels of thyroid hormones in the body. Treatment typically involves taking synthetic thyroid hormone medication to replace the missing hormones. With proper treatment, most people with hypothyroidism can lead normal, healthy lives.
Hypothyroidism is a relatively common condition, affecting about 4.6 million people in the United States alone. Women are more likely to develop hypothyroidism than men, and it is most commonly diagnosed in middle-aged women.
Some of the symptoms of Hypothyroidism include:
1. Fatigue or tiredness
2. Weight gain
3. Dry skin
4. Constipation
5. Depression or anxiety
6. Memory problems
7. Muscle aches and stiffness
8. Heavy or irregular menstrual periods
9. Pale, dry, or rough skin
10. Hair loss or thinning
11. Cold intolerance
12. Slowed speech and movements
It's important to note that some people may not experience any symptoms at all, especially in the early stages of the condition. However, if left untreated, hypothyroidism can lead to more severe complications such as heart disease, mental health problems, and infertility.
This condition can be caused by various factors such as genetic mutations, infections, autoimmune disorders, and certain medications. In severe cases, agranulocytosis can lead to life-threatening infections that require prompt medical treatment.
Some of the common symptoms of agranulocytosis include fever, chills, sore throat, fatigue, and recurring infections. Diagnosis is typically made through blood tests that measure the number and function of white blood cells, including granulocytes. Treatment options for agranulocytosis depend on the underlying cause, but may include antibiotics, antiviral medications, and immunoglobulin replacement therapy in severe cases.
1. Hypothyroidism: This is a condition where the thyroid gland does not produce enough thyroid hormones. Symptoms can include fatigue, weight gain, dry skin, constipation, and depression.
2. Hyperthyroidism: This is a condition where the thyroid gland produces too much thyroid hormone. Symptoms can include weight loss, anxiety, tremors, and an irregular heartbeat.
3. Thyroid nodules: These are abnormal growths on the thyroid gland that can be benign or cancerous.
4. Thyroid cancer: This is a type of cancer that affects the thyroid gland. There are several types of thyroid cancer, including papillary, follicular, and medullary thyroid cancer.
5. Goiter: This is an enlargement of the thyroid gland that can be caused by a variety of factors, including hypothyroidism, hyperthyroidism, and thyroid nodules.
6. Thyrotoxicosis: This is a condition where the thyroid gland produces too much thyroid hormone, leading to symptoms such as weight loss, anxiety, tremors, and an irregular heartbeat.
7. Thyroiditis: This is an inflammation of the thyroid gland that can cause symptoms such as pain, swelling, and difficulty swallowing.
8. Congenital hypothyroidism: This is a condition where a baby is born without a functioning thyroid gland or with a gland that does not produce enough thyroid hormones.
9. Thyroid cancer in children: This is a type of cancer that affects children and teenagers, usually in the form of papillary or follicular thyroid cancer.
10. Thyroid storm: This is a life-threatening condition where the thyroid gland produces an excessive amount of thyroid hormones, leading to symptoms such as fever, rapid heartbeat, and cardiac arrest.
These are just a few examples of the many conditions that can affect the thyroid gland. It's important to be aware of these conditions and seek medical attention if you experience any symptoms or concerns related to your thyroid health.
Causes: Thyroiditis can be caused by a viral or bacterial infection, autoimmune disorders, or radiation exposure.
Symptoms: Symptoms of thyroiditis may include pain and swelling in the neck, difficulty swallowing, hoarseness, fatigue, weight gain, muscle weakness, and depression.
Types: There are several types of thyroiditis, including subacute thyroiditis, silent thyroiditis, and postpartum thyroiditis.
Diagnosis: Thyroiditis is typically diagnosed through a combination of physical examination, blood tests, and imaging studies such as ultrasound or CT scans.
Treatment: Treatment for thyroiditis usually involves antibiotics to treat any underlying infection, pain relief medication to manage neck swelling and discomfort, and hormone replacement therapy to address hormonal imbalances. In some cases, surgery may be necessary to remove part or all of the affected thyroid gland.
Complications: Untreated thyroiditis can lead to complications such as hypothyroidism (underactive thyroid), hyperthyroidism (overactive thyroid), and thyroid nodules or cancer.
Prevention: Preventing thyroiditis is challenging, but maintaining good overall health, avoiding exposure to radiation, and managing any underlying autoimmune disorders can help reduce the risk of developing the condition.
Prognosis: With proper treatment, most people with thyroiditis experience a full recovery and normalization of thyroid function. However, in some cases, long-term hormone replacement therapy may be necessary to manage persistent hypothyroidism or hyperthyroidism.
1. Hypothyroidism: An underactive thyroid gland can cause the gland to become enlarged as it tries to produce more hormones to compensate for the lack of production.
2. Hyperthyroidism: An overactive thyroid gland can also cause the gland to become enlarged as it produces excessive amounts of hormones.
3. Thyroid nodules: These are abnormal growths within the thyroid gland that can cause the gland to become enlarged.
4. Thyroiditis: This is an inflammation of the thyroid gland that can cause it to become enlarged.
5. Iodine deficiency: Iodine is essential for the production of thyroid hormones, and a lack of iodine in the diet can cause the gland to become enlarged as it tries to produce more hormones.
6. Pituitary gland problems: The pituitary gland, located at the base of the brain, regulates the production of thyroid hormones. Problems with the pituitary gland can cause the thyroid gland to become enlarged.
7. Genetic conditions: Some genetic conditions, such as familial goiter, can cause the thyroid gland to become enlarged.
Symptoms of goiter may include:
* A noticeable lump in the neck
* Difficulty swallowing or breathing
* Hoarseness or vocal cord paralysis
* Fatigue
* Weight gain
* Cold intolerance
Goiter can be diagnosed through a physical examination, blood tests to measure thyroid hormone levels, and imaging studies such as ultrasound or radionuclide scans to evaluate the size and function of the gland. Treatment options for goiter depend on the underlying cause and may include medication, surgery, or radioactive iodine therapy.
The disease is named after Hakama Hashimoto, a Japanese physician who first described it in 1912. It is characterized by the presence of inflammatory cells in the thyroid gland, which can lead to damage to the gland and disrupt its ability to produce thyroid hormones.
The symptoms of Hashimoto's disease are similar to those of hypothyroidism and can include fatigue, weight gain, cold intolerance, dry skin, constipation, and depression. The disease is more common in women than men and typically affects people between the ages of 30 and 50.
Hashimoto's disease is diagnosed based on a combination of symptoms, physical examination findings, and laboratory tests, such as blood tests to measure thyroid hormone levels and an ultrasound or biopsy to examine the thyroid gland. Treatment typically involves replacing missing thyroid hormones with synthetic hormones, but in some cases, surgery may be necessary to remove part or all of the thyroid gland.
While Hashimoto's disease is a chronic condition and cannot be cured, it can be effectively managed with appropriate treatment. With early diagnosis and proper management, most people with Hashimoto's disease can lead normal, healthy lives.
Antithyroid agent
Halocarbon
Thyroid peroxidase
2-Thiouracil
Causes of autism
Potassium perchlorate
Govindasamy Mugesh
Propylthiouracil
List of MeSH codes (D27)
Glucosinolate
ATD
Basal metabolic rate
Medication
Hyperthyroidism
Infertility
Amphenone B
Amiodarone
Hashimoto's encephalopathy
Scott Rivkees
Hashimoto's thyroiditis
Agranulocytosis
Tricyanoaminopropene
Miscarriage
Sum activity of peripheral deiodinases
Lugol's iodine
Wolff-Chaikoff effect
Thyroid cancer
Endocrine disruptor
4-Aminosalicylic acid
Acquired non-inflammatory myopathy
Graves' disease
Thyroid
Preterm birth
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Hyperthyroidism6
- Antithyroid medications are used mostly as a temporizing measure in preparation for surgery or radioactive iodine, or when the hyperthyroidism is thought to be temporary and self-limiting (as in subacute thyroiditis). (nih.gov)
- 14. Characteristics of Antithyroid Drug-Induced Agranulocytosis in Patients with Hyperthyroidism: A Retrospective Analysis of 114 Cases in a Single Institution in China Involving 9690 Patients Referred for Radioiodine Treatment Over 15 Years. (nih.gov)
- Thy- roidectomy for hyperthyroidism was first performed in 1880, and antithyroid drugs and radioiodine therapy were developed in the early 1940s. (who.int)
- Agents that are used to treat hyperthyroidism by reducing the excessive production of thyroid hormones. (nih.gov)
- Objective: Remission rates in young people with Graves hyperthyroidism are 25% or less after a 2-yr course of thionamide antithyroid drug (ATD). (eurospe.org)
- It seems that the prolonged pharmacotherapy with antithyroid drugs, followed by observation after remission of hyperthyroidism, may be an appropriate therapeutic option at least in some children with GD as they can be cured without radical therapy and the potential risks of such treatment. (nel.edu)
Propylthiouracil4
- The major antithyroid medications used are all thionamides and include propylthiouracil (PTU, 1947), carbimazole and methimazole (Tapazol, 1950, as known as thiamazole). (nih.gov)
- Propylthiouracil is in a class of medications called antithyroid agents. (medlineplus.gov)
- Propylthiouracil is an antithyroid drug administered orally. (nih.gov)
- In the United States two antithyroid drugs are available for treating Graves' disease: Propylthiouracil (PTU) and Methimazole (1-methyl-2-mercaptoimidazole or MMI, Tapazole). (elaine-moore.com)
Drugs4
- 15. [Retrospective analysis of 18 cases with agranulocytosis induced by antithyroid drugs]. (nih.gov)
- In all the girls, antithyroid drugs were administered and euthyroid state was achieved during the first 2.0-3.5 months of the treatment. (nel.edu)
- Conventional medicine offers three major options for treating GD: 1) the medical administration of antithyroid drugs (ATD's) which inhibit thyroid hormone synthesis, 2) partial or complete surgical removal of the thyroid gland, and 3) radioiodine ablation. (elaine-moore.com)
- Antithyroid drugs (ATDs) have been a mainstay in the management of Graves' disease since their introduction in the mid-1940's. (elaine-moore.com)
Autoimmune1
- Antithyroid antibody studies are used to evaluate for autoimmune thyroid problems. (medscape.com)
Antigen1
- Disorder characterized by a vasculitic syndrome associated with exposure to an antigen such as a drug, infectious agent, or other foreign or endogenous substance. (lookformedical.com)
Methimazole1
- Some experts now recommend that methimazole should be considered the antithyroid drug of choice in nursing mothers. (nih.gov)
Inhibit2
- These agents inhibit cell growth and proliferation. (medscape.com)
- Contrast solutions include barium, water-based gastrografin, saline, and hypertonic sodium bicarbonate is controlled by hormones and locally produced agents that inhibit the efficiency of sexual hair. (albionfoundation.org)
Hyperthyroid1
- Changes in liver biochemical test results have been described in hyperthyroid patients before and after antithyroid therapy. (nih.gov)
Drug8
- 3. Treatment of antithyroid drug-induced agranulocytosis by granulocyte colony-stimulating factor: a case of primum non nocere. (nih.gov)
- 6. Granulocyte colony-stimulating factor treatment of antithyroid drug-induced granulocytopenia. (nih.gov)
- 7. Usefulness of granulocyte count measurement four hours after injection of granulocyte colony-stimulating factor for detecting recovery from antithyroid drug-induced granulocytopenia. (nih.gov)
- 11. Serum concentrations of granulocyte colony-stimulating factor (G-CSF) in antithyroid drug-induced agranulocytosis. (nih.gov)
- 13. [Granulocyte colony-stimulating factor treatment (G-CSF) of antithyroid drug-induced granulocytopenia: granulocyte count measurement after 4 hours of G-CSF injection is useful for the detection of recovery from granulocytopenia]. (nih.gov)
- 18. Antithyroid drug-induced agranulocytosis: clinical experience with ten patients treated at one institution and review of the literature. (nih.gov)
- Since the discovery of TSAb as the causative agent of GD, there have been numerous studies that have demonstrated the significance of the levels of these Ab during the course of the disease as well as during antithyroid drug treatment in both adults and children ( 2 , 3 ). (frontiersin.org)
- Background: First line treatment for thyrotoxicosis is thionamide (TA) antithyroid drug therapy. (eurospe.org)
Therapy1
- 16. Agranulocytosis induced by antithyroid therapy: effects of treatment with granulocyte colony stimulating factor. (nih.gov)
Thyroid agents1
- thyroid agents decrease uptake of sodium iodide I-131 by the thyroid gland. (medscape.com)
Treatment1
- In particular, the analytical performance and clinical utility of a FDA-cleared, stimulatory TSH-R bioassay in a large collective of patients with GD, both prior to as well as during medical antithyroid treatment, has been shown ( 12 ). (frontiersin.org)
Infectious1
- 8.All the samples, washing buffer and wastes should be treated as infectious agents. (andygene.com)
Results1
- An agent that disrupts healthy embryonic development and results in congenital defects is known as a teratogen. (journals-times.com)
Blood1
- Clotting agents (blood thinners). (journals-times.com)
Hyperthyroidism3
- Antithyroid medications are used mostly as a temporizing measure in preparation for surgery or radioactive iodine, or when the hyperthyroidism is thought to be temporary and self-limiting (as in subacute thyroiditis). (nih.gov)
- Thy- roidectomy for hyperthyroidism was first performed in 1880, and antithyroid drugs and radioiodine therapy were developed in the early 1940s. (who.int)
- Agents that are used to treat hyperthyroidism by reducing the excessive production of thyroid hormones. (nih.gov)
Medications3
- Medications used in iodine deficiency include antithyroid agents (potassium iodide) and thyroid products (levothyroxine). (medscape.com)
- The major antithyroid medications used are all thionamides and include propylthiouracil (PTU, 1947), carbimazole and methimazole (Tapazol, 1950, as known as thiamazole). (nih.gov)
- Propylthiouracil is in a class of medications called antithyroid agents. (medlineplus.gov)
Thyroid hormones1
- A thioureylene antithyroid agent that inhibits the formation of thyroid hormones by interfering with the incorporation of iodine into tyrosyl residues of thyroglobulin. (bvsalud.org)
Graves2
- 12. Hypothyroidism as a late sequela in patient with Graves' disease treated with antithyroid agents. (nih.gov)
- RÉSUMÉ La première description des pathologies thyroïdiennes, telles qu'on les connaît aujourd'hui, a été celle de la maladie de Graves par Caleb Parry en 1786, mais la pathogenèse de l'affection thyroïdienne n'a pas été découverte avant 1882-1886. (who.int)
Patient1
- The patient was diagnosed with GD, which improved with antithyroid agent administration. (bvsalud.org)