An imidazole antithyroid agent. Carbimazole is metabolized to METHIMAZOLE, which is responsible for the antithyroid activity.
Agents that are used to treat hyperthyroidism by reducing the excessive production of thyroid hormones.
A hypermetabolic syndrome caused by excess THYROID HORMONES which may come from endogenous or exogenous sources. The endogenous source of hormone may be thyroid HYPERPLASIA; THYROID NEOPLASMS; or hormone-producing extrathyroidal tissue. Thyrotoxicosis is characterized by NERVOUSNESS; TACHYCARDIA; FATIGUE; WEIGHT LOSS; heat intolerance; and excessive SWEATING.
Hypersecretion of THYROID HORMONES from the THYROID GLAND. Elevated levels of thyroid hormones increase BASAL METABOLIC RATE.
A common form of hyperthyroidism with a diffuse hyperplastic GOITER. It is an autoimmune disorder that produces antibodies against the THYROID STIMULATING HORMONE RECEPTOR. These autoantibodies activate the TSH receptor, thereby stimulating the THYROID GLAND and hypersecretion of THYROID HORMONES. These autoantibodies can also affect the eyes (GRAVES OPHTHALMOPATHY) and the skin (Graves dermopathy).
A thioureylene antithyroid agent that inhibits the formation of thyroid hormones by interfering with the incorporation of iodine into tyrosyl residues of thyroglobulin. This is done by interfering with the oxidation of iodide ion and iodotyrosyl groups through inhibition of the peroxidase enzyme.
A thiourea antithyroid agent. Propythiouracil inhibits the synthesis of thyroxine and inhibits the peripheral conversion of throxine to tri-iodothyronine. It is used in the treatment of hyperthyroidism. (From Martindale, The Extra Pharmacopeoia, 30th ed, p534)
The major hormone derived from the thyroid gland. Thyroxine is synthesized via the iodination of tyrosines (MONOIODOTYROSINE) and the coupling of iodotyrosines (DIIODOTYROSINE) in the THYROGLOBULIN. Thyroxine is released from thyroglobulin by proteolysis and secreted into the blood. Thyroxine is peripherally deiodinated to form TRIIODOTHYRONINE which exerts a broad spectrum of stimulatory effects on cell metabolism.
An erythematous eruption commonly associated with drug reactions or infection and characterized by inflammatory nodules that are usually tender, multiple, and bilateral. These nodules are located predominantly on the shins with less common occurrence on the thighs and forearms. They undergo characteristic color changes ending in temporary bruise-like areas. This condition usually subsides in 3-6 weeks without scarring or atrophy.
A highly vascularized endocrine gland consisting of two lobes joined by a thin band of tissue with one lobe on each side of the TRACHEA. It secretes THYROID HORMONES from the follicular cells and CALCITONIN from the parafollicular cells thereby regulating METABOLISM and CALCIUM level in blood, respectively.
Maintenance of a constant blood glucose level by perfusion or infusion with glucose or insulin. It is used for the study of metabolic rates (e.g., in glucose, lipid, amino acid metabolism) at constant glucose concentration.
A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).
Glucose in blood.
A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.
Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS.
A syndrome with excessively high INSULIN levels in the BLOOD. It may cause HYPOGLYCEMIA. Etiology of hyperinsulinism varies, including hypersecretion of a beta cell tumor (INSULINOMA); autoantibodies against insulin (INSULIN ANTIBODIES); defective insulin receptor (INSULIN RESISTANCE); or overuse of exogenous insulin or HYPOGLYCEMIC AGENTS.
A test to determine the ability of an individual to maintain HOMEOSTASIS of BLOOD GLUCOSE. It includes measuring blood glucose levels in a fasting state, and at prescribed intervals before and after oral glucose intake (75 or 100 g) or intravenous infusion (0.5 g/kg).

Diabetic ketoacidosis precipitated by thyrotoxicosis. (1/89)

We report two patients with type 1 diabetes mellitus, previously well controlled with good compliance, presenting with unexplained diabetic ketoacidosis. Following initial correction of the metabolic disorder, persisting tachycardia lead to the diagnosis of thyrotoxicosis. In both cases, treatment with propranolol and carbimazole helped in the stabilization of their metabolic states. Although thyrotoxicosis is known to destabilize diabetes control, we can find no reports of it precipitating diabetic ketoacidosis.  (+info)

Insulin autoimmune syndrome: a rare cause of hypoglycaemia not to be overlooked. (2/89)

We report the case of a Caucasian patient with insulin autoimmune syndrome (IAS), defined as the association of hypoglycaemic attacks with insulin autoantibodies in individuals not previously treated with exogenous insulin. This rare syndrome (more than 200 published cases) has been reported mainly in Japan. Most affected patients present with other autoimmune disorders, most often Graves' disease. In most cases, insulin autoantibodies appear a few weeks after the beginning of treatment with a drug containing a sulphyldryl group. A significant increase in insulin and C-peptide plasma concentrations and the presence of other antiorgan antibodies are observed. The susceptibility haplotype is present in the Japanese population, which may account for the high frequency of IAS. Spontaneous remission is observed in 80% of cases, with cessation of hypoglycaemic attacks and disappearance of insulin autoantibodies some months after withdrawal of the drug. This rare cause of hypoglycaemia in Caucasian subjects should be considered in aetiologic investigation of spontaneous hypoglycaemia.  (+info)

Prevalence of positive anti-neutrophil cytoplasmic antibody (ANCA) in patients receiving anti-thyroid medication. (3/89)

OBJECTIVE: Vasculitis is a rare complication of anti-thyroid medications. There are 32 cases of anti-neutrophil cytoplasmic antibody (ANCA)-positive vasculitis in association with anti-thyroid medication reported in the English literature. The objectives of this study were to assess the frequency of positive ANCA in patients on long-term anti-thyroid medication, and to follow patients prospectively from commencement of medication to determine whether they became ANCA-positive after therapy. DESIGN: Prospectively collected cross-sectional study of two groups of patients: (i) who had received long-term (>18 months) anti-thyroid medication, and (ii) newly diagnosed thyrotoxicosis before commencement of anti-thyroid medication attending clinic between 28 April 1998 and 30 September 1998. Data were collected for age, sex, ethnicity, underlying thyroid disease, medication and duration, and symptomatology. RESULTS: Eight of 30 patients on long-term anti-thyroid medication (26.7%) were ANCA-positive. All ANCA-positive patients were female, seven were taking propylthiouracil (PTU) at the time of testing. ANCA-positive patients had taken PTU for a mean +/- s.d. of 7.9+/-10.2 years, compared with 0.8+/-2.2 years in ANCA-negative patients (Mann-Whitney, P<0.0001). The ten patients with newly diagnosed thyrotoxicosis were ANCA-negative before commencement of carbimazole. One (10%) became ANCA-positive within 8 months of therapy. CONCLUSIONS: In our population, ANCA-positivity in association with long-term anti-thyroid medication is common (26.7%). One patient who was ANCA-negative prior to anti-thyroid therapy has become ANCA-positive. ANCA should be tested in patients receiving long-term anti-thyroid medications, and in patients with adverse reactions. As PTU is more commonly associated with vasculitis and positive ANCA, carbimazole may be the preferred medication for long-term use. Patients with positive ANCA should be followed, and considered for definitive anti-thyroid therapy, to allow cessation of medication. ANCA-positivity may resolve after cessation of anti-thyroid medication.  (+info)

Platelet endothelial cell adhesion molecule-1 (PECAM-1) is a target glycoprotein in drug-induced thrombocytopenia. (4/89)

Drug-induced immune thrombocytopenia (DITP) is a serious complication of drug treatment. Previous studies demonstrated that most drug-dependent antibodies (DDAbs) react with the platelet membrane glycoprotein (GP) complexes IIb/IIIa and Ib/IX/V. We analyzed the sera from 5 patients who presented with DITP after intake of carbimazole. Notably, thrombocytopenia induced by carbimazole was relatively mild in comparison to patients with DITP induced by quinidine. The sera reacted with platelets in an immunoassay on addition of the drug. In immunoprecipitation experiments with biotin-labeled platelets and endothelial cells, reactivity with the platelet endothelial cell adhesion molecule-1 (PECAM-1, CD31) could be demonstrated, whereas neither GPIIb/IIIa nor GPIb/IX was precipitated in the presence of the drug. These results could be confirmed by GP-specific immunoassay (MAIPA) using monoclonal antibodies (mabs) against PECAM-1. In addition, the binding of DDAbs could be abolished by preincubation with soluble recombinant PECAM-1. Carbimazole-dependent antibodies showed similar reactivity with platelets carrying the Leu(125) and Val(125) PECAM-1 isoforms, indicating that this polymorphic structure, which is located in the first extracellular domain, is not responsible for the epitope formation. Binding studies with biotin-labeled mutants of PECAM-1 and analysis of sera with mabs against different epitopes on PECAM-1 in MAIPA assay suggested that carbimazole-dependent antibodies prominently bound to the second immunoglobulin homology domain of the molecule. Analysis of 20 sera from patients with quinidine-induced thrombocytopenia by MAIPA assay revealed evidence that DDAbs against PECAM-1 are involved in addition to anti-GPIb/IX and anti-GPIIb/IIIa. We conclude that PECAM-1 is an important target GP in DITP. (Blood. 2000;96:1409-1414)  (+info)

Successful treatment of amiodarone-induced thyrotoxicosis. (5/89)

BACKGROUND: Amiodarone-induced thyrotoxicosis (AIT) is a difficult management problem about which there are little published data. We examined whether continuing amiodarone or differentiating AIT into 2 subtypes affected outcome. METHODS AND RESULTS: The type and duration of antithyroid treatment and response were recorded in a consecutive series of 28 cases. Comparisons were made between those in whom amiodarone either was continued or stopped and between those with either possible type 1 or type 2 AIT. Of the 28 cases, 5 had spontaneous resolution of AIT; 23 received carbimazole (CBZ) alone as first-line therapy. Eleven achieved long-term euthyroidism off CBZ or on a maintenance dose. Five became hypothyroid and required long-term thyroxine. Five relapsed after stopping CBZ treatment and were rendered euthyroid with either long-term CBZ (n=3) or radioiodine (n=2). Four were intolerant of CBZ and received propylthiouracil (PTU), with good effect in 3. One was resistant to thionamide alone (CBZ then PTU) and responded to adjunctive steroids. No difference in presentation or outcome was noted between those in whom amiodarone was continued or stopped or between possible type 1 or type 2 AIT. CONCLUSIONS: Continuing amiodarone has no adverse influence on response to treatment of AIT. First-line therapy with a thionamide alone is appropriate in iodine-replete areas, thus avoiding potential complications of other drugs. Differentiating between 2 possible types of AIT does not influence management or outcome.  (+info)

Jaundice due to carbimazole. (6/89)

On three occasions, a 63 year old housewife with hyperthyroidism developed a reaction which included fever, pruritus, malaise, and, on one occasion, jaundice one to 17 days after taking carbimazole. Challenge with carbimazole was followed within 12 hours by abdominal pain, pruritus, and increased serum transaminase levels. Light microscopy of a liver biopsy showed increase of portal zone cellularity over the control and the electron microscopy revealed fine structural changes compatible with drug-related liver injury.  (+info)

The influence of preoperative drug treatment on the extent of hyperplasia of the thymus in primary thyrotoxicosis. (7/89)

Thymic biopsies taken from women at the beginning of the operation of subtotal thyroidectomy were studied by the point-counting histometric technique. In all patients with primary thyrotoxicosis, the thymus is hyperplastic. After pretreatment with antithyroid drugs, the pattern of thymic involution with age is similar to, but at higher levels, than that in control groups of patients with non-toxic goitre in whom there is no evidence of immunological abnormality. By contrast, after propranolol pretreatment very little age involution is seen. The differences in the appearance of the thymus in female primary thyrotoxixosis patients prepared for operation with different drug treatment regimes are probably related to the pharmacological actions of the drugs and may indicate an interaction between primary immunological and secondary endocrinological factors in the disease process.  (+info)

Acute pancreatitis, hepatic cholestasis, and erythema nodosum induced by carbimazole treatment for Graves' disease. (8/89)

A 33-year old female was diagnosed as Graves' disease and started on carbimazole. One month later when she was already euthyroid only on carbimazole therapy, she developed acute pancreatitis associated with mild cholestatic hepatitis and erythema nodosum. Carbimazole therapy was interrupted, pancreatic and liver function gradually improved and became normalized two weeks later. Other potential etiological causes of acute pancreatitis, hepatitis and erythema nodosum were excluded. Rechallenge with a single dose of carbimazole led to a new episode of acute pancreatitis and cholestatic hepatitis one day later. The appearance of different hypersensitivity reactions including pancreatitis, hepatitis and erythema nodosum, together with the observation that the interval between drug intake and onset of symptoms became shorter with repeated exposure to carbimazole, point to an immune-mediated mechanism. Carbimazole has to be added to the list of drugs capable of inducing acute pancreatitis, and should be emphasized the need to discontinue this medication as soon as there is evidence of pancreatic dysfunction.  (+info)

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.

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.

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.

Example of how to use 'Erythema Nodosum' in a sentence:

The patient presented with erythema nodosum on their shins, which was diagnosed as an adverse reaction to the new medication they had started taking.

There are several factors that can contribute to the development of insulin resistance, including:

1. Genetics: Insulin resistance can be inherited, and some people may be more prone to developing the condition based on their genetic makeup.
2. Obesity: Excess body fat, particularly around the abdominal area, can contribute to insulin resistance.
3. Physical inactivity: A sedentary lifestyle can lead to insulin resistance.
4. Poor diet: Consuming a diet high in refined carbohydrates and sugar can contribute to insulin resistance.
5. Other medical conditions: Certain medical conditions, such as polycystic ovary syndrome (PCOS) and Cushing's syndrome, can increase the risk of developing insulin resistance.
6. Medications: Certain medications, such as steroids and some antipsychotic drugs, can increase insulin resistance.
7. Hormonal imbalances: Hormonal changes during pregnancy or menopause can lead to insulin resistance.
8. Sleep apnea: Sleep apnea can contribute to insulin resistance.
9. Chronic stress: Chronic stress can lead to insulin resistance.
10. Aging: Insulin resistance tends to increase with age, particularly after the age of 45.

There are several ways to diagnose insulin resistance, including:

1. Fasting blood sugar test: This test measures the level of glucose in the blood after an overnight fast.
2. Glucose tolerance test: This test measures the body's ability to regulate blood sugar levels after consuming a sugary drink.
3. Insulin sensitivity test: This test measures the body's ability to respond to insulin.
4. Homeostatic model assessment (HOMA): This is a mathematical formula that uses the results of a fasting glucose and insulin test to estimate insulin resistance.
5. Adiponectin test: This test measures the level of adiponectin, a protein produced by fat cells that helps regulate blood sugar levels. Low levels of adiponectin are associated with insulin resistance.

There is no cure for insulin resistance, but it can be managed through lifestyle changes and medication. Lifestyle changes include:

1. Diet: A healthy diet that is low in processed carbohydrates and added sugars can help improve insulin sensitivity.
2. Exercise: Regular physical activity, such as aerobic exercise and strength training, can improve insulin sensitivity.
3. Weight loss: Losing weight, particularly around the abdominal area, can improve insulin sensitivity.
4. Stress management: Strategies to manage stress, such as meditation or yoga, can help improve insulin sensitivity.
5. Sleep: Getting adequate sleep is important for maintaining healthy insulin levels.

Medications that may be used to treat insulin resistance include:

1. Metformin: This is a commonly used medication to treat type 2 diabetes and improve insulin sensitivity.
2. Thiazolidinediones (TZDs): These medications, such as pioglitazone, improve insulin sensitivity by increasing the body's ability to use insulin.
3. Sulfonylureas: These medications stimulate the release of insulin from the pancreas, which can help improve insulin sensitivity.
4. DPP-4 inhibitors: These medications, such as sitagliptin, work by reducing the breakdown of the hormone incretin, which helps to increase insulin secretion and improve insulin sensitivity.
5. GLP-1 receptor agonists: These medications, such as exenatide, mimic the action of the hormone GLP-1 and help to improve insulin sensitivity.

It is important to note that these medications may have side effects, so it is important to discuss the potential benefits and risks with your healthcare provider before starting treatment. Additionally, lifestyle modifications such as diet and exercise can also be effective in improving insulin sensitivity and managing blood sugar levels.

In hyperinsulinism, the body produces too much insulin, leading to a range of symptoms including:

1. Hypoglycemia (low blood sugar): Excessive insulin can cause blood sugar levels to drop too low, leading to hypoglycemic symptoms such as shakiness, dizziness, confusion, and rapid heartbeat.
2. Weight gain: Hyperinsulinism can lead to weight gain due to the body's inability to effectively use glucose for energy production.
3. Fatigue: Excessive insulin can cause fatigue, as the body's cells are not able to effectively use glucose for energy production.
4. Mood changes: Hyperinsulinism can lead to mood changes such as irritability, anxiety, and depression.
5. Polycystic ovary syndrome (PCOS): Women with PCOS are at a higher risk of developing hyperinsulinism due to insulin resistance.
6. Gestational diabetes: Hyperinsulinism can occur during pregnancy, leading to gestational diabetes.
7. Acanthosis nigricans: A condition characterized by dark, velvety patches on the skin, often found in the armpits, neck, and groin area.
8. Cancer: Hyperinsulinism has been linked to an increased risk of certain types of cancer, such as breast, colon, and pancreatic cancer.
9. Cardiovascular disease: Excessive insulin can increase the risk of cardiovascular disease, including high blood pressure, heart disease, and stroke.
10. Cognitive impairment: Hyperinsulinism has been linked to cognitive impairment and an increased risk of dementia.

There are several causes of hyperinsulinism, including:

1. Insulin-producing tumors: Tumors that produce excessive amounts of insulin can lead to hyperinsulinism.
2. Familial hyperinsulinism: A genetic disorder that affects the regulation of insulin secretion and action.
3. Pancreatic beta-cell dysfunction: Dysfunction in the pancreatic beta cells, which produce insulin, can lead to hyperinsulinism.
4. Medications: Certain medications such as steroids and certain psychiatric drugs can cause hyperinsulinism.
5. Pituitary tumors: Tumors in the pituitary gland can lead to excessive secretion of growth hormone, which can stimulate insulin production.
6. Maternal diabetes during pregnancy: Women with diabetes during pregnancy may experience hyperinsulinism due to increased insulin resistance and higher insulin levels.
7. Gestational diabetes: High blood sugar during pregnancy can lead to hyperinsulinism.
8. Polycystic ovary syndrome (PCOS): Women with PCOS may experience hyperinsulinism due to insulin resistance and high insulin levels.
9. Cushing's syndrome: An endocrine disorder caused by excessive cortisol production can lead to hyperinsulinism.
10. Other medical conditions: Certain medical conditions such as thyroid disorders, adrenal gland disorders, and pituitary gland disorders can also cause hyperinsulinism.

It's important to note that some individuals with hyperinsulinism may not experience any symptoms, while others may experience a range of symptoms, including:

1. Weight gain
2. Fatigue
3. Headaches
4. Numbness or tingling in the hands and feet
5. Memory loss and difficulty concentrating
6. Mood changes, such as anxiety and depression
7. Skin problems, such as acne and thinning skin
8. Increased risk of heart disease and stroke
9. Growth retardation in children
10. Increased risk of developing type 2 diabetes

If you suspect that you or your child may have hyperinsulinism, it's important to consult with a healthcare professional for proper diagnosis and treatment. A doctor may perform a physical examination, take a medical history, and order blood tests to determine if hyperinsulinism is present and what may be causing it. Treatment options for hyperinsulinism will depend on the underlying cause of the condition. In some cases, medications such as metformin or other anti-diabetic drugs may be prescribed to help regulate blood sugar levels and reduce insulin production. In other cases, surgery or lifestyle changes may be necessary. With proper diagnosis and treatment, it is possible to manage hyperinsulinism and prevent or manage related health complications.

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These drugs (Methimazole and Propylthiouracil in the United States, Carbimazole in Europe) are usually very well tolerated. ... A total of 39 patients had agranulocytosis that was induced by antithyroid drugs (methimazole, 74%; carbimazole, 13%: and ... HLA-B*38:02:01 predicts carbimazole/ methimazole-induced agranulocytosis. Clin Pharmacol Ther 2016;99:555-61. Epub January 12, ... Agranulocytosis developed 19 patients taking methimazole or carbimazole and in 5 patients taking. Controls (those without ...
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  • Agranulocytosis developed 19 patients taking methimazole or carbimazole and in 5 patients taking. (
  • Controls (those without thyroid disease or agranulocytosis) included 387 randomly selected women from various other studies as well an additional group of 57 patients with Graves' disease who had been treated with methimazole or carbimazole for at least 3 months without agranulocytosis. (
  • The outcome of methimazole-induced cholestasis was generally benign, with self-resolution of symptoms and normalization of bilirubin levels and other liver function values 5 days to 6 months after stopping methimazole or carbimazole therapy. (
  • The antithyroid drugs include carbimazole, methimazole , and propylthiouracil ( PTU ). (
  • These drugs (Methimazole and Propylthiouracil in the United States, Carbimazole in Europe) are usually very well tolerated. (
  • Carbimazole, its active metabolite methimazole, and propylthiouracil all act by inhibiting the enzyme thyroid peroxidase and in that way they block the synthesis (the production) of thyroid hormone . (
  • Antithyroid medications (Carbimazole, Propylthiouracil, Methimazole. (
  • Pharmacokinetics of once daily prolonged-release carbimazole oral tablets in cats with hyperthyroidism. (
  • It also serves as a reference for Vidalta®(known as Vidalta® Vet in Belgium and Norway), MSD Animal Health's prolonged-release carbimazole for the management of hyperthyroidism in cats. (
  • In cases of hyperthyroidism, treatment options typically include anti-thyroid drugs, like carbimazole, radioactive iodine, beta blockers or in some cases surgery. (
  • Carbimazole on risk mitigation and analysis to handle specialty pharmacy ridgewood veterinary care for neurontin tablets after a promotional article. (
  • Prominent & Leading Exporter from Palghar, we offer chysin (trypsin chymotrypsin), dexamethasone tablets, dexamethasone tablet,dekot tablets 0.5mg, carbin-5 (carbimazole) and piroxicam capsules bp 40mg. (
  • 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. (
  • Methods: Patients commenced 0.75mg/kg carbimazole (CBZ) daily with randomisation to either BR or DT. (
  • Cet article procède à un examen des principales étapes dans l'histoire de la pathologie de la thyroïde, avec une brève discussion des aspects scientifiques concernant la glande thyroïde qui ont eu une importance historique, et de l'évolution de l'endocrinologie en tant que discipline à part entière. (
  • We report the case of a patient who developed jaundice, encephalopathy, a marked increase in serum aminotransferase activity and a decrease in prothrombin and proaccelerin levels, after 6 weeks' treatment with carbimazole and propranolol for hyperthyroidism. (
  • A 41-year-old Chinese man with a history of hyperthyroidism had been treated with carbimazole and propranolol for the past 5 years. (
  • Propylthiouracil, and methimazole, and carbimazole-related hepatotoxicity. (
  • 10. HLA-B*38:02:01 predicts carbimazole/methimazole-induced agranulocytosis. (
  • Carbimazole is metabolized to METHIMAZOLE , which is responsible for the antithyroid activity. (
  • Although there is increasing evidence of hepatotoxicity induced by bupropion, this is the first case of fatality that could have resulted from acute liver failure in a patient receiving bupropion while on concomitant treatment with carbimazole. (
  • Concomitant agranulocytosis and hepatotoxicity after treatment with carbimazole. (
  • 11. Spontaneous reporting of adverse reactions to carbimazole and propylthiouracil in the UK. (
  • 17. Propylthiouracil and carbimazole associated-antineutrophil cytoplasmic antibodies (ANCA) in patients with Graves' disease. (
  • Carbimazole-induced acute pancreatitis and cholestatic hepatitis. (
  • [ 1 ] Young women are advocated early definitive treatment to reduce the potential risk of congenital malformations in pregnant women on carbimazole (CBZ). (
  • Toxic hepatitis induced by antithyroid drugs: four cases including one with cross-reactivity between carbimazole and benzylthiouracil. (
  • To report a case of fatal liver failure possibly associated with concurrent use of bupropion and carbimazole. (