In addition to methimazole, a symptomatic patient with hyperthyroidism may need a prescription for:

Methimazole is an oral thioimidazole antithyroid agent. Antithyroid agents are indicated for various hyperthyroid conditions including maintenance of a euthyroid state in patients with Graves' disease until spontaneous remission occurs. Methimazole is less likely to induce hepatotoxicity than propylthiouracil, especially in pediatric patients. The drug is the preferred antithyroid agent for hyperthyroidism treatment when drug therapy must be used, except in the first trimester of pregnancy, where teratogenesis is a concern, or in cases of drug allergy or intolerance. Methimazole was approved by the FDA in 1950.

General Administration Information
For storage information, see the specific product information within the How Supplied section.
Hazardous Drugs Classification
-NIOSH 2016 List: Group 2
-NIOSH (Draft) 2020 List: Table 2
-Observe and exercise appropriate precautions for handling, preparation, administration, and disposal of hazardous drugs.
-Use gloves to handle. Cutting, crushing, or otherwise manipulating tablets/capsules will increase exposure and require additional protective equipment. Oral liquid drugs require double chemotherapy gloves and protective gown; may require eye/face protection.

Route-Specific Administration

Oral Administration
-Administer orally at the same time(s) each day in relation to meals.

Minor adverse dermatologic reactions including rash (unspecified), alopecia, skin hyperpigmentation, urticaria, and pruritus occur in approximately 3-5% of patients receiving methimazole. Other cutaneous reactions occur less frequently. Rashes are often self-limiting and may be symptomatically managed. Exfoliative dermatitis, a severe cutaneous eruption, requires discontinuance of the drug.

Hematologic toxicity can occur during therapy with methimazole, although some clinicians believe this risk is less with methimazole than with propylthiouracil. Leukopenia occurs in up to 15% of adults and 25% of children taking methimazole. It is usually asymptomatic but can be associated with fever or chills, throat infection, cough, mouth sores, or hoarseness. Approximately 10% of patients with untreated hyperthyroidism have leukopenia with neutropenia, which should be considered when evaluating this adverse reaction. Therapy usually can be continued, but WBC counts should be monitored. Agranulocytosis, granulocytopenia, thrombocytopenia, pancytopenia, and aplastic anemia can occur because of inhibition of myelopoiesis. Most cases of agranulocytosis occur during the first 2 months of therapy and diminish significantly by 4 months of treatment. Methimazole-induced agranulocytosis is generally associated with doses of 40 mg or more in patients older than 40 years of age. Exercise particular care with patients who are receiving additional drugs known to cause agranulocytosis. Methimazole may also cause hypoprothrombinemia and bleeding; monitor prothrombin time during therapy, especially before surgical procedures. Monitor the patient's bone marrow function and determine white blood cell and differential counts. Discontinue methimazole if aplastic anemia, pancytopenia, or agranulocytosis develop.

Hypothyroidism can occur with prolonged use of methimazole although the incidence appears to be low. Periodic monitoring of thyroid function is warranted, and the finding of an elevated TSH warrants a decrease in the methimazole dosage. The incidence of this adverse reaction can be minimized by using the smallest dose that controls thyrotoxicosis once euthyroidism is achieved. Some clinicians continue with the initial dosage and supplement methimazole therapy with levothyroxine.

Adverse events noted with methimazole include arthralgia, vasculitis, myalgia, edema, nephrotic syndrome, drug fever, lupus-like symptoms, insulin autoimmune syndrome (hypoglycemia and hypoglycemic coma), lymphadenopathy, periarteritis, and sialadenitis. Arthralgia can occur in up to 5% of patients who receive methimazole and can occur more frequently when higher doses are used. Children may have a higher incidence of myalgia and arthralgia reactions. Discontinue methimazole in the presence of ANCA-positive vasculitis.

Drowsiness, neuritis, paresthesias, headache, and vertigo have occurred in patients receiving methimazole. The incidence of methimazole-induced peripheral neuropathy is extremely low but may require discontinuation of methimazole.

Hepatotoxicity occurs rarely during therapy with methimazole but can be fatal. Methimazole-induced hepatotoxicity can manifest as jaundice, hepatic encephalopathy, hepatic necrosis, and/or hepatitis. Promptly evaluate liver function for symptoms such as anorexia, pruritus, and right upper quadrant pain. Promptly discontinue methimazole for hepatitis or if clinically significant evidence of liver abnormality develops such as elevated hepatic enzymes more than 3 times the upper limit of normal. Jaundice may persist for several weeks after methimazole discontinuation.

Gastrointestinal adverse reactions noted with methimazole include nausea, vomiting, dysgeusia, and epigastric distress.

Teratogenesis is a serious concern with methimazole if administered during early pregnancy during the period of organogenesis. Methimazole crosses the placental membranes and can cause fetal harm when administered in the first trimester of pregnancy. Rare instances of congenital defects, including aplasia cutis, craniofacial malformations (facial dysmorphism; choanal atresia), gastrointestinal malformations (esophageal atresia with or without tracheoesophageal fistula), omphalocele and abnormalities of the omphalomesenteric duct have occurred in infants born to mothers who received methimazole in the first trimester of pregnancy. Because of the risk for congenital malformations associated with use of methimazole in the first trimester of pregnancy, the use other agents (e.g., propylthiouracil) is preferred in the first trimester. However, given the potential maternal adverse effects of propylthiouracil (e.g., hepatotoxicity), it is often preferable to switch therapy to methimazole for the second and third trimesters. Because methimazole crosses placental membranes and can induce goiter and cretinism in the developing fetus, hyperthyroidism should be closely monitored in pregnant women and treatment adjusted such that a sufficient, but not excessive, dose is given.

Antithyroid agents should be discontinued at least 3-4 days prior to treatment with radioiodine (sodium iodide, I-131). Typically, antithyroid agents are not reintroduced until 1 week after the radioiodine treatment.

Methimazole is contraindicated in patients with a history of hypersensitivity to the drug, including a history of serious rash or skin eruption, drug-induced liver disease, or drug-induced agranulocytosis. Cross-hypersensitivity occurs in roughly 50% of patients who have previously exhibited a major hypersensitivity to an antithyroid thioamide medication (like propylthiouracil). Agranulocytosis (severe neutropenia) is the most serious adverse reaction of methimazole, and is most likely immune-mediated. Patients should report symptoms of sore throat, fever, and general malaise promptly to their prescriber for evaluation. Thrombocytopenia, and aplastic anemia (pancytopenia) may also occur. Methimazole should be used cautiously in other patients with bone marrow suppression or risk factors for methimazole hematologic toxicity. Use with caution in adults 40 years of age or older, including the geriatric adult. Doses of greater than 40 mg/day should generally be avoided, if possible, due to the increased risk of agranulocytosis. Use methimazole with extreme caution in combination with other drugs known to cause agranulocytosis. Leukopenia occurs in 10% of untreated hyperthyroid patients and is not a contraindication for use of methimazole, however, CBCs and differentials should be monitored closely. The drug should be discontinued in the presence of agranulocytosis, aplastic anemia (pancytopenia), ANCA-positive vasculitis, hepatitis, or exfoliative dermatitis and the patient's complete blood counts (CBC) should be monitored.

In general, use methimazole with caution in patients with pre-existing hepatic disease. Although there have been reports of hepatotoxicity (including acute liver failure) associated with methimazole, the risk of hepatotoxicity is less with methimazole than with propylthiouracil, especially in the pediatric population. Symptoms suggestive of hepatic dysfunction (anorexia, jaundice, pruritus, right upper quadrant pain, etc.) should prompt evaluation of liver function tests (i.e., bilirubin, alkaline phosphatase, ALT, AST). Drug treatment should be discontinued promptly in the event of clinically significant evidence of liver abnormality including hepatic transaminase values exceeding 3 times the upper limit of normal (ULN). The drug should be discontinued in the presence of apparent drug-induced hepatitis and the patient's complete blood counts (CBC) should be monitored.

Females of childbearing potential who are taking methimazole should inform their prescriber if they desire to become pregnant or think they may be pregnant. Teratogenesis is a serious concern with methimazole if administered during early pregnancy during the period of organogenesis. Methimazole crosses the placental membranes and can cause fetal harm when administered in the first trimester of pregnancy. Rare instances of congenital defects, including aplasia cutis, craniofacial malformations (facial dysmorphism; choanal atresia), gastrointestinal malformations (esophageal atresia with or without tracheoesophageal fistula), omphalocele and abnormalities of the omphalomesenteric duct have occurred in babies born to mothers who received methimazole in the first trimester of pregnancy. Because of the risk for congenital malformations associated with the use of methimazole in the first trimester of pregnancy, the use of other agents (e.g., propylthiouracil) is preferred in the first trimester. However, given the potential maternal adverse effects of propylthiouracil (e.g., hepatotoxicity), it is often preferable to switch therapy to methimazole for the second and third trimesters. Because methimazole crosses placental membranes and can induce goiter and cretinism in the developing fetus, pregnant patients with hyperthyroidism should be closely monitored and treatment adjusted such that a sufficient, but not excessive, the dose is given. Because thyroid dysfunction may improve as pregnancy proceeds in some patients, it may be possible to discontinue antithyroid therapy 2 to 3 months prior to delivery after careful clinical evaluation of thyroid function.

Methimazole is considered compatible for use during breast-feeding. Methimazole is present in breast milk. However, several studies found no effect on clinical status in nursing infants of mothers taking methimazole. A long-term study of 139 thyrotoxic lactating mothers and their infants failed to demonstrate toxicity in infants who are nursed by mothers receiving treatment with methimazole. Monitor thyroid function at frequent (weekly or biweekly) intervals. The American Thyroid Association (ATA) guidelines recommend that low to moderate doses(e.g., methimazole 20 to 30 mg/day) be used during lactation. The ATA also recommends that the infant's thyroid function be monitored regularly and that the mothers take their thyroid medication in divided doses, with doses taken immediately following a feeding.

For the treatment of hyperthyroidism, including Graves' disease or toxic multinodular goiter when surgery or radioactive iodine therapy (RAI) is not appropriate, or for symptomatic treatment in preparation for thyroidectomy or RAI:
Oral dosage:
Adults: Initially, 15 mg/day PO for mild hyperthyroidism, 30 to 40 mg/day PO for moderately severe hyperthyroidism, and 60 mg/day PO for severe hyperthyroidism. Daily doses are divided into 3 doses and given at approximately 8-hour intervals. Once clinical evidence of hyperthyroidism has resolved, a rising serum TSH indicates that a lower maintenance dose should be employed. The usual maintenance dosage is 5 to 15 mg daily, given in 3 divided doses.
Infants, Children, and Adolescents: Initially, give 0.4 mg/kg/day PO, divided into 3 doses and given at approximately 8-hour intervals. Once clinical evidence of hyperthyroidism has resolved, a rising serum TSH indicates that a lower maintenance dose should be used. The maintenance dosage is approximately one-half of the initial dose, or approximately 0.2 mg/kg/day PO, given in divided doses. Alternatively, guidelines state the usual weight based dose range is 0.2 mg/kg to 0.5 mg/kg PO daily (range from 0.1 to 1 mg/kg PO daily). One approach is to initiate dosing based on age: infants, 1.25 mg/day; 1 to 5 years, 2.5 to 5 mg/day; 5 to 10 years, 5 mg to 10 mg/day; and 10 and older: 10 to 20 mg/day. Daily doses can be given once daily or divided. Guidelines note that in severe hyperthyroidism, doses that are 50% to 100% higher than those listed may be needed, then, when thyroid hormone levels normalize, doses can be reduced by 50% or more to maintain a euthyroid state.

For the treatment of thyrotoxicosis* (thyroid storm*):
Oral dosage:
Adults: Guidelines note that 60 to 80 mg/day PO is a usual dosage range during thyrotoxicosis until control is achieved; doses are divided and given at 8-hour intervals. Adjust subsequent doses and duration of treatment based on patient response.
Infants, Children, and Adolescents: Initially 0.4 mg/kg/day (range: 0.4 to 1 mg/kg/day) PO given in 3 equally divided doses at 8-hour intervals. Guidelines note that doses may be 50% to 100% higher than the usual initial dosage range during severe hyperthyroidism. Adjust subsequent doses and duration of treatment based on patient response.

Maximum Dosage Limits:
Methimazole has a narrow therapeutic window; individualize dosage. General maximum doses for routine treatment of hyperthyroidism are listed. Higher dosages may be used short-term in the emergent treatment of thyrotoxicosis.
-Adults
40 mg/day PO; 60 mg/day in severe disease.
-Geriatric
40 mg/day PO; 60 mg/day in severe disease.
-Adolescents
Maintenance doses rarely exceed 30 mg/day PO; 1 mg/kg/day PO in severe hyperthyroidism. In some patients in whom growth is complete, doses may approach adult dosing.
-Children
Maintenance doses rarely exceed 30 mg/day PO; 1 mg/kg/day for severe hyperthyroidism.
-Infants
1 mg/kg/day for severe hyperthyroidism.

Patients with Hepatic Impairment Dosing
No specific recommendations for dosage adjustments are available. Discontinue if clinically important evidence of hepatic dysfunction (e.g., LFT elevation) occurs during use.

Patients with Renal Impairment Dosing
Specific guidelines for dosage adjustments in renal impairment are not available; it appears that no dosage adjustments are needed.

*non-FDA-approved indication

Acebutolol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Amiodarone: (Moderate) In hyperthyroid patients, the combination of amiodarone and methimazole has been associated with a greater decrease in serum triiodothyronine and thyroxine levels, as compared to the administration of methimazole alone. This may be due to increased iodide release associated with amiodarone. Monitor serum T3 and T4 levels in patients receiving combination therapy.

Atenolol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Atenolol; Chlorthalidone: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Bendroflumethiazide; Nadolol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Beta-blockers: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Betaxolol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Bisoprolol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Bisoprolol; Hydrochlorothiazide, HCTZ: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Brimonidine; Timolol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Carteolol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Carvedilol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Deferiprone: (Major) Avoid concomitant use of deferiprone with other drugs known to be associated with neutropenia or agranulocytosis, such as methimazole; however, if this is not possible, closely monitor the absolute neutrophil count and interrupt deferiprone therapy if neutropenia develops.

Digoxin: (Minor) Serum concentrations of digoxin can increase as hyperthyroidism is corrected. In patients receiving antithyroid therapy, the dosage of digoxin may need to be reduced as the patient becomes euthyroid.

Dorzolamide; Timolol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Esmolol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Iodine; Potassium Iodide, KI: (Moderate) Potassium iodide should not be used concurrently with other antithyroid agents. Agents such as methimazole and propylthiouracil, PTU can increase the likelihood of hypothyroidism when used in combination with potassium iodide.

Iodoquinol: (Moderate) Iodoquinol should be used with caution in patients treated with thyroid agents. Iodine-containing compounds like iodoquinol may result in overt thyroid disease.

Labetalol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Levobetaxolol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Levobunolol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Macimorelin: (Major) Avoid use of macimorelin with drugs that may blunt the growth hormone response to macimorelin, such as antithyroid agents. Healthcare providers are advised to discontinue antithyroid therapy at least 1 week before administering macimorelin. Use of these medications together may impact the accuracy of the macimorelin growth hormone test.

Metoprolol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Metoprolol; Hydrochlorothiazide, HCTZ: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Nadolol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Nebivolol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Nebivolol; Valsartan: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Penbutolol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Pindolol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Potassium Iodide, KI: (Moderate) Potassium iodide should not be used concurrently with other antithyroid agents. Agents such as methimazole and propylthiouracil, PTU can increase the likelihood of hypothyroidism when used in combination with potassium iodide.

Propranolol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Propranolol; Hydrochlorothiazide, HCTZ: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Sodium Iodide: (Contraindicated) The recent intake of antithyroid agents will affect the uptake of radioiodide from sodium iodide, I-131; patients must discontinue all medications and supplements that may interfere with iodide uptake into thyroid tissue prior to therapy with sodium iodide I-131. Various protocols are used. Many manufacturers state that concurrent antithyroid agents should be discontinued at least 3 to 4 days before administration of radioiodide. The following withdrawal timing recommendations were set forth in a procedure guideline published by the Society of Nuclear Medicine in February 2002. Antithyroid agents may affect iodide protein binding for an average of 5 days after administration; allow a 3 day wash out period for the antithyroid agent (e.g., PTU, methimazole) prior to sodium iodide I-131 administration. The antithyroid agent may be resumed 2 to 3 days after treatment. When patients are taking sodium iodide (non-radioiodide) for supplementation in TPN, the effect of the iodide on antithyroid therapy should be considered.

Sotalol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Theophylline, Aminophylline: (Minor) Patients with hyperthyroidism may exhibit accelerated clearance of theophylline. Correction of hyperthyroidism can lead to a decrease in theophylline clearance. Theophylline serum concentrations should be monitored closely during the initial stages of treatment for hyperthyroidism.

Timolol: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.

Warfarin: (Moderate) The interaction between thioamine antithyroid agents and warfarin is variable. The effects of warfarin can be enhanced due to the vitamin K antagonistic properties of methimazole or propylthiouracil, PTU. Isolated cases have reported hypoprothrombinemia due to methimazole or propylthiouracil, which may be additive with warfarin. In addition, as hyperthyroidism is corrected, the anticoagulant effect of warfarin can diminish due to a change in the clearance rate of endogenous clotting factors. Thus, administration of antithyroid agents such as methimazole or PTU can also reduce the effectiveness of warfarin. INRs should be monitored closely whenever methimazole is added or discontinued during warfarin therapy or when the thyroid status of a patient is expected to change. Warfarin dosage should be adjusted accordingly based on the INR and the clinical goals for the patient.

Methimazole directly interferes with the first step in thyroid hormone biosynthesis in the thyroid gland. By acting as a substrate for the catalyst thyroid peroxidase, methimazole inhibits the incorporation of iodide into the thyroid hormone precursor, thyroglobulin. Consequently, the drug is iodinated and degraded within the thyroid gland. Oxidized iodine is diverted away from thyroglobulin, which effectively diminishes the biosynthesis of thyroid hormone. An additional mechanism is the inhibition of iodotyrosyl residues coupling to form thyroglobulin. Methimazole may interfere with the oxidation of the iodide ion and iodotyrosyl groups. Eventually, thyroglobulin is depleted and circulating thyroid hormone levels diminish. Methimazole does not alter the action of existing thyroxine (T4) and triiodothyronine (T3) in the circulation or stored in the thyroid gland. Similarly, no alterations in the effectiveness of exogenously administered thyroid hormones have been observed.

Methimazole is administered orally. Once absorbed, methimazole is actively concentrated by the thyroid gland. Protein binding is insignificant, as a result, methimazole is excreted more readily into breast milk than other drugs in its class. The drug also readily crosses the placenta.

Methimazole undergoes hepatic metabolism with no active metabolites. Renal excretion is < 10%. The elimination half-life is approximately 5-9 hours. However, the intrathyroidal residence of methimazole is roughly 20 hours, and the duration of action 40 hours, which allows once-daily dosing some patients. The plasma elimination half-life of methimazole is not appreciably altered by the patient's thyroid status.

-Route-Specific Pharmacokinetics
Oral Route
Methimazole is rapidly absorbed from the gastrointestinal tract, reaching peak serum concentrations within 1-2 hours after administration. However, it usually takes 2-4 months of treatment to achieve initial euthyroid status; response rates are dependent on several pharmacodynamic and patient variables.

-Special Populations
Hepatic Impairment
Interpatient variables, such as hepatic disease, may alter methimazole's clearance, but specific recommendations for dosage adjustment have not been established.

Renal Impairment
The plasma half-life of methimazole is not significantly altered in patients with end-stage renal disease. It is not known if methimazole is dialyzable.