Class: Antithyroid Agents
ATC Class: H03BA02
VA Class: HS852
CAS Number: 51-52-5
Severe liver injury and acute liver failure, in some cases requiring liver transplantation or resulting in death, reported in adult and pediatric patients. (See Hepatotoxicity under Cautions.)
Reserve propylthiouracil for patients who cannot tolerate methimazole and for whom radioactive iodine therapy or surgery are not appropriate for the management of hyperthyroidism. (See Hyperthyroidism under Uses.)
Propylthiouracil may be the treatment of choice when an antithyroid drug is indicated during or just prior to the first trimester of pregnancy because of the risk of fetal abnormalities associated with methimazole. (See Fetal/Neonatal Morbidity and also see Pregnancy under Cautions.)
Antithyroid agent; thiourea-derivative.
Uses for Propylthiouracil
Used in patients with Graves’ disease with hyperthyroidism or toxic multinodular goiter who are intolerant of methimazole and for whom surgery or radioactive iodine therapy is not an appropriate treatment option.
Amelioration of symptoms of hyperthyroidism in preparation for thyroidectomy or radioactive iodine therapy in patients who are intolerant of methimazole.
Propylthiouracil is associated with a higher risk for clinically serious or fatal liver injury compared with methimazole in adult and pediatric patients; therefore, when initiating hyperthyroid treatment, reserve propylthiouracil for patients who cannot tolerate methimazole and for whom radioactive iodine therapy or surgery are not appropriate for the management of hyperthyroidism. (See Boxed Warning and also see Hepatotoxicity under Cautions.)
Not recommended for use in pediatric patients except in rare instances in which methimazole is not well tolerated and surgery or radioactive iodine therapy are not appropriate therapies. (See Pediatric Use under Cautions.)
Preferred agent when an antithyroid drug is indicated during or just prior to the first trimester of pregnancy because of the risk of fetal abnormalities associated with methimazole. For second and third trimesters (i.e., after first trimester), may be preferable to switch from propylthiouracil to methimazole because of the risk of adverse maternal effects associated with propylthiouracil (e.g., hepatotoxicity). (See Fetal/Neonatal Morbidity and also see Pregnancy under Cautions.)
Therapy with thioamide antithyroid agents (e.g., propylthiouracil, methimazole) maintains patients with Graves’ disease in euthyroid state for a period of several (generally 1–2) years until spontaneous remission occurs; however, spontaneous remission does not occur in all patients, and most eventually require ablative therapy (i.e., surgery, radioactive iodine). Thioamide antithyroid agents do not affect underlying cause of hyperthyroidism. Minimum duration of therapy necessary before assessing whether spontaneous remission has occurred not clearly established; however, some clinicians consider a treatment duration of 12–18 months to be optimal.
Therapy with propylthiouracil returns hyperthyroid patient to a normal metabolic state prior to thyroidectomy and controls the thyrotoxic crisis that may accompany thyroidectomy.
Therapy with propylthiouracil controls the symptoms of hyperthyroidism before and after radioactive iodine therapy until the ablative effects of iodine occur. However, beneficial and detrimental effects and optimal sequencing of antithyroid drugs before or after radioactive iodine therapy not clearly established. Pretreatment with propylthiouracil may increase radioresistance of thyroid and risk of radioactive iodine treatment failure.
Does not induce remission in patients with nodular thyroid disease (i.e., toxic adenoma†, toxic multinodular goiter); discontinuance of therapy results in relapse. Therefore, some clinicians suggest that adults with overt toxic adenoma or toxic multinodular goiter be treated with either radioactive iodine therapy or thyroidectomy.
May be used for management of thyrotoxic crisis; preferred over methimazole because of its ability to inhibit peripheral conversion of thyroxine [T4] to triiodothyronine [T3]. Usually initiated before iodide (e.g., potassium iodide, strong iodine solution) therapy.
Alcoholic Liver Disease
Has been studied in patients with alcoholic liver disease†.
No substantial benefit has been demonstrated on any clinically important outcomes of alcoholic liver disease (e.g., all-cause mortality, liver-related mortality, complications associated with the liver disease, liver histology); currently available evidence does not support its use outside of randomized clinical studies.
Propylthiouracil Dosage and Administration
May use a β-adrenergic blocking agent (e.g., propranolol) concomitantly to manage peripheral signs and symptoms of hyperthyroidism, particularly cardiovascular effects (e.g., tachycardia).
Manufacturer recommends administering total daily dosage in 3 equally divided doses at approximately 8-hour intervals. More frequent administration (e.g., at 4- or 6-hour intervals) may be necessary in some cases.
Generally not recommended for use in pediatric patients except in rare instances in which alternative therapies are not appropriate options. (See Pediatric Use under Cautions.) Although studies evaluating appropriate dosage regimens not conducted in pediatric population, manufacturer states that general practice would suggest initiation of therapy in children ≥6 years of age at 50 mg daily with careful upward titration based on clinical response and evaluation of TSH and free T4 concentrations.
Severe liver injury reported with dosages as low as 50 mg daily, but most cases were associated with dosages of ≥300 mg daily. (See Hepatotoxicity under Cautions.)
Graves’ Disease with Hyperthyroidism or Toxic Multinodular GoiterOral
Initially, 300 mg daily, usually given in 3 equally divided doses at approximately 8-hour intervals. For patients with severe hyperthyroidism and/or very large goiters, initial dosage may be increased to 400 mg daily; occasionally, an initial dosage of 600–900 mg daily may be required. Alternatively, for treatment of Graves’ disease, some clinicians recommend an initial dosage of 50–150 mg 3 times daily, depending on severity of hyperthyroidism.
Considerable improvement or normal thyroid function generally achieved following 4–12 weeks of therapy, after which dosage may be decreased while maintaining normal thyroid function. Carefully adjust subsequent dosage according to patient’s tolerance and therapeutic response. (See Laboratory Monitoring under Cautions.)
Usual maintenance dosage: Manufacturer recommends 100–150 mg daily, usually given in 3 equally divided doses at approximately 8-hour intervals. Alternatively, as clinical findings and thyroid function tests return to normal, some clinicians suggest a maintenance dosage of 50 mg 2 or 3 times daily.
Optimum duration of antithyroid therapy not clearly established. However, some clinicians consider a treatment duration 12–18 months to be optimal in patients with Graves’ disease.
Preparation for ThyroidectomyOral
Initially, 300 mg daily, usually given in 3 equally divided doses at approximately 8-hour intervals. For patients with severe hyperthyroidism and/or very large goiters, initial dosage may be increased to 400 mg daily; occasionally, an initial dosage of 600–900 mg daily may be required.
Discontinue propylthiouracil at time of procedure.
Preparation for Radioactive Iodine TherapyOral
Initially, 300 mg daily, usually given in 3 equally divided doses at approximately 8-hour intervals. For patients with severe hyperthyroidism and/or very large goiters, usual initial dosage may be increased to 400 mg daily; occasionally, an initial dosage of 600–900 mg daily may be required.
Some clinicians recommend discontinuing propylthiouracil 2–7 days before administration of radioactive iodine; may restart propylthiouracil 3–7 days after radioactive iodine therapy, then discontinue propylthiouracil once thyroid function normalizes.
Some clinicians recommend a loading dose of 500 mg to 1 g, followed by 250 mg every 4 hours.
No specific dosage recommendations at this time.
No specific dosage recommendations at this time.
Select dosage with caution because of the greater frequency of decreased hepatic, renal, and/or cardiac function and of concomitant disease and drug therapy. (See Geriatric Use under Cautions.)
If used during pregnancy for management of hyperthyroidism, a sufficient, but not excessive, dosage is necessary. Thyroid dysfunction diminishes in many women as pregnancy proceeds; reduction in dosage may be possible, and, in some patients, propylthiouracil can be discontinued several weeks or months before delivery. (See Pregnancy under Cautions and also see Hepatotoxicity under Cautions.)
Cautions for Propylthiouracil
Known hypersensitivity to propylthiouracil or any ingredient in the formulation.
Liver injury (including severe liver injury) resulting in hepatitis, liver failure (including acute liver failure), liver transplantation, or death reported in adult and pediatric patients. (See Boxed Warning.) FDA has concluded that use of propylthiouracil is associated with a higher risk for clinically serious or fatal liver injury compared with methimazole in both adult and pediatric patients.
No cases of liver failure reported with use of methimazole in pediatric patients; therefore, propylthiouracil not recommended for use in pediatric patients except in rare instances in which methimazole is not well tolerated and surgery or radioactive iodine therapy are not appropriate therapies. (See Pediatric Use under Cautions.)
Cases of liver injury, including liver failure and death, reported in women receiving propylthiouracil during pregnancy. Two cases of in utero exposure with liver failure and death of a newborn also reported. Use of an alternative antithyroid drug (e.g., methimazole) may be advisable after the first trimester of pregnancy. (See Fetal/Neonatal Morbidity and also see Pregnancy under Cautions.)
Extent of propylthiouracil-induced hepatitis and true incidence of severe liver injury not known.
Propylthiouracil-induced liver failure may occur at any time during therapy with a sudden onset, rapid progression, and a low chance of reversibility; liver failure has been observed after 6–450 days of propylthiouracil therapy (median: 120 days).
Effect of dosage on risk of hepatotoxicity not clearly elucidated; however, reported average daily dosage associated with liver failure was approximately 300 mg in both children and adults.
Perform liver function tests (e.g., alkaline phosphatase, aminotransferase, bilirubin) prior to initiating therapy in patients with Graves’ disease.
Routine biochemical monitoring of liver function (bilirubin, alkaline phosphatase) and hepatocellular integrity (ALT, AST) may not be effective in identifying patients at risk of liver failure and is not expected to attenuate risk of severe liver injury due to its rapid and unpredictable onset; however, should be performed in symptomatic patients.
Closely monitor patients for signs and symptoms of liver injury (e.g., fatigue, weakness, vague abdominal pain, right upper quadrant pain, anorexia, pruritus, easy bruising, jaundice, pruritic rash, light-colored stool, dark urine, joint pain, bloating, nausea), particularly during the first 6 months following initiation of therapy. If such symptoms occur, immediately discontinue the drug, evaluate the patient for evidence of liver injury (including evaluation of liver function [bilirubin, alkaline phosphatase] and hepatocellular integrity [ALT, AST]), and provide supportive care.
Some clinicians recommend discontinuing propylthiouracil if aminotransferase concentrations (whether elevated at initiation of therapy, found incidentally, or measured as clinically indicated) increase to 2–3 times the ULN and fail to improve within 1 week with repeat testing. After discontinuing the drug, monitor liver function (i.e., alkaline phosphatase, bilirubin, transaminases) weekly until there is evidence of resolution. If resolution is not evident, promptly refer patient to a gastroenterologist or hepatologist.
Risk of agranulocytosis; usually occurs within first 3 months of therapy, but rarely may occur after 4 months of therapy. May occur irrespective of dosage, length of treatment, or previous exposure to antithyroid drug, and may occur more frequently in geriatric patients.
Leukopenia, thrombocytopenia, and aplastic anemia (pancytopenia) may occur. Hypoprothrombinemia and bleeding also may occur. (See Laboratory Monitoring under Cautions.)
Perform baseline CBC, including white count with differential, prior to initiating therapy in patients with Graves’ disease.
Monitor patient carefully for signs or symptoms of illness (e.g., sore throat, skin eruptions, fever, chills, headache, general malaise), particularly during the early stages of therapy. If fever, sore throat, or other signs or symptoms of illness occur, determine leukocyte and differential counts to assess whether agranulocytosis has developed. When evaluating myelopoietic response to propylthiouracil, consider that leukopenia (i.e., WBC <4000/mm3) occurs in 10% of untreated hyperthyroid patients and is often associated with relative granulocytopenia.
If agranulocytosis, aplastic anemia (pancytopenia), or fever is suspected, discontinue propylthiouracil and obtain bone marrow indices. In patients who develop agranulocytosis or other serious adverse effects while receiving propylthiouracil or methimazole, use of the other drug is contraindicated because of risk of cross-sensitivity between the two drugs.
May cause hypothyroidism necessitating routine monitoring of TSH and free T4 concentrations with dosage adjustments to maintain a euthyroid state.
May cause fetal goiter and cretinism when administered to a pregnant woman, because the drug readily crosses the placenta. (See Fetal/Neonatal Morbidity and also see Pregnancy under Cautions.)
May cause fetal harm (i.e., induction of goiter, hypothyroidism, or cretinism).
Congenital malformations reported approximately 3 times more often with prenatal exposure to methimazole compared with propylthiouracil. Distinct and consistent pattern of congenital malformations associated with the use of methimazole, but not with propylthiouracil, particularly craniofacial malformations (e.g., scalp epidermal aplasia [aplasia cutis], facial dysmorphism, choanal atresia). Specific birth defects were associated with use of methimazole during the first trimester of pregnancy and not found when the drug was administered later in pregnancy. FDA has not found a consistent pattern of birth defects associated with use of propylthiouracil and has concluded there is no convincing evidence of an association between propylthiouracil use and congenital malformations, even with use during the first trimester. (See Pregnancy under Cautions and also see Distribution under Pharmacokinetics.)
If used during pregnancy or if pregnancy occurs during therapy, apprise of rare potential hazard to the mother and fetus of liver damage; inform the patient of these potential risks and risks of methimazole-associated fetal malformations when considering antithyroid drug use during pregnancy. (See Hepatotoxicity under Cautions.)
Cross-sensitivity between thioamides may occur (i.e., in approximately 50% of patients switched from one thioamide agent to the other).
In patients who develop serious adverse effects (e.g., agranulocytosis) while receiving either propylthiouracil or methimazole, use of other drug also is contraindicated, because of risk of cross-sensitivity between the two drugs. In patients experiencing serious allergic reactions to propylthiouracil, use of the alternative antithyroid drug (i.e., methimazole) not recommended.
Before initiating thioamide therapy in patients with Graves’ disease, some clinicians recommend obtaining baseline free T4 and TSH concentrations; CBC, including white count and differential; and liver function tests (e.g., alkaline phosphatase, aminotransferase, bilirubin). Routine biochemical monitoring of liver function (bilirubin, alkaline phosphatase) and hepatocellular integrity (ALT, AST) not expected to attenuate risk of severe liver injury, but should be performed in symptomatic patients. (See Hepatotoxicity under Cautions.)
Monitor thyroid function (e.g., serum free T4, serum free or total T3, TSH) periodically (e.g., every 4–8 weeks [with subsequent dosage adjustments as needed] until thyroid function is stable or patient is euthyroid); once euthyroidism is achieved, monitor thyroid function every 2–3 months. Serum TSH not a reliable parameter to monitor early in therapy because it may remain suppressed for several months after initiation of therapy despite normalization of free T4 concentrations. A suppressed TSH concentration during this period does not indicate a need for dosage increase. However, once hyperthyroidism resolves, decrease maintenance dosage if serum TSH is elevated. Monitoring serum T3 concentrations may sometimes be useful for dosage adjustment; if total or free T3 concentrations remain elevated despite low, normal, or reduced free T4 concentrations, may need to increase antithyroid dosage.
Determine leukocyte and differential counts in patients who develop any signs or symptoms of illness (e.g., fever, sore throat) during therapy.
Consider monitoring PT during therapy, particularly before surgical procedures, because of possible risk of hypoprothrombinemia and bleeding.
Exfoliative dermatitis reported. If exfoliative dermatitis is suspected, discontinue propylthiouracil.
Vasculitic syndrome associated with the presence of antineutrophil cytoplasmic antibody (ANCA) reported. Manifestations of ANCA-positive vasculitis may include rapidly progressive glomerulonephritis (crescentic and pauci-immune necrotizing glomerulonephritis) sometimes leading to acute renal failure, pulmonary infiltrates or alveolar hemorrhage, skin ulcers, and leukocytoclastic vasculitis. If ANCA-positive vasculitis is suspected, discontinue propylthiouracil.
Interstitial pneumonitis reported. If interstitial pneumonitis is suspected, discontinue propylthiouracil.
Category D. (See Fetal/Neonatal Morbidity under Cautions and also see Distribution under Pharmacokinetics.)
Despite potential fetal hazard, antithyroid agents still considered therapy of choice for management of hyperthyroidism during pregnancy. Since methimazole may be associated with the rare development of fetal abnormalities (e.g., aplasia cutis, choanal atresia), propylthiouracil is preferred when an antithyroid drug is indicated during organogenesis, in the first trimester of pregnancy, or just prior to the first trimester of pregnancy. (See Boxed Warning and also see Fetal/Neonatal Morbidity under Cautions.) Switch patients receiving methimazole to propylthiouracil if pregnancy is confirmed in first trimester. May be preferable to switch from propylthiouracil to methimazole for the second and third trimesters (i.e., after the first trimester), because of potential adverse maternal effects of propylthiouracil (e.g., hepatotoxicity). (See Hepatotoxicity under Cautions.) If switching from propylthiouracil to methimazole, assess thyroid function after 2 weeks and then every 2–4 weeks thereafter. Not known if risk of methimazole-induced aplasia cutis or embryopathy outweighs risk of propylthiouracil-induced hepatotoxicity.
If used during pregnancy, a sufficient, but not excessive, dosage is necessary. Initiate or adjust antithyroid drug therapy to maintain maternal free T4 concentrations at or just above the ULN of nonpregnant reference range, or to maintain total T4 concentrations at 1.5 times the ULN or the free T4 index in the ULN, while using lowest possible dosage. As thyroid dysfunction diminishes in many women as pregnancy proceeds, may be possible to reduce propylthiouracil dosage; in some patients, may discontinue propylthiouracil several weeks or months before delivery.
If used during pregnancy or if patient becomes pregnant while receiving the drug, apprise of rare potential hazard to the mother and fetus of liver damage; inform the patient of these potential risks and risks of methimazole-associated fetal malformations when considering antithyroid drug use during pregnancy. Although liver toxicity may appear abruptly, it is reasonable to monitor liver function every 3–4 weeks in pregnant women receiving propylthiouracil and to encourage patients to promptly report any new symptoms.
Distributed into milk to a small extent and, therefore, likely does not result in clinically important doses to the nursing infant. Mean amount of propylthiouracil distributed into milk during 4 hours following single oral 400-mg dose in 9 lactating women was 0.025% (range: 0.007–0.077%) of the administered dose.
Generally compatible with breast-feeding; moderate dosages (i.e., <300 mg daily) appear to be safe. However, considered by some clinicians to be a second-line agent in nursing women because of concerns regarding severe hepatotoxicity (i.e., hepatic necrosis in either woman or child); methimazole is the preferred antithyroid drug in nursing women. If antithyroid drug is used in nursing women, some clinicians recommend administering drug after a feeding and in divided doses, and monitoring thyroid function of nursing infants.
Postmarketing cases of severe liver injury, including hepatic failure requiring liver transplantation or resulting in death, reported in pediatric patients; however, no such reports observed with methimazole. Propylthiouracil not recommended for use in pediatric patients except in rare instances in which methimazole is not well tolerated and surgery or radioactive iodine therapy are not appropriate therapies. In addition, some experts state that alternative therapy should be considered for children who are currently receiving propylthiouracil and that it is reasonable and prudent to discontinue propylthiouracil use in children receiving this drug for the treatment of Graves’ disease.
When propylthiouracil is used in children, inform parents and patients of risk of liver failure. If patients develop tiredness, nausea, anorexia, fever, pharyngitis, or malaise, immediately discontinue the drug, contact a clinician, and obtain WBC count, liver function tests, and transaminase concentrations. (See Hepatotoxicity under Cautions.)
Insufficient experience in patients ≥65 years of age to determine whether geriatric patients respond differently than younger adults. Select dosage with caution due to greater frequency of decreased hepatic, renal, and/or cardiac function and of concomitant disease and drug therapy.
Common Adverse Effects
Rash, urticaria, pruritus, abnormal hair loss, skin pigmentation, edema, nausea, vomiting, epigastric distress, loss of taste, taste perversion, arthralgia, myalgia, paresthesia, headache, drowsiness, neuritis, vertigo, jaundice, sialadenopathy, lymphadenopathy.
Interactions for Propylthiouracil
Drugs Known to be Associated with Agranulocytosis
Use concomitantly with extreme caution. (See Hematologic Effects under Cautions.)
Anticoagulants, oral (e.g., warfarin)
Activity of oral anticoagulants (e.g., warfarin) may be increased because of potential inhibition of vitamin K activity by propylthiouracil; however, anticoagulant effect of warfarin also may be decreased
Consider additional monitoring of PT/INR, particularly prior to surgery; adjustment of warfarin dosage may be needed
β-Adrenergic blocking agents (e.g., propranolol)
Possible increased clearance of β-adrenergic blocking agents with a high extraction ratio during hyperthyroid state
Reduction of β-blocker dosage may be needed when patient becomes euthyroid
Possible increased serum digitalis concentrations when hyperthyroid patients receiving a stable digitalis glycoside regimen become euthyroid
Reduction of digitalis glycoside dosage may be needed when patient becomes euthyroid
Possible decreased theophylline clearance when hyperthyroid patients on a stable theophylline regimen become euthyroid
Reduction of theophylline dosage may be needed when patient becomes euthyroid
Rapidly and readily absorbed from the GI tract following oral administration. Peak plasma concentrations attained within 1–1.5 hours; however, plasma concentrations do not appear to correlate with therapeutic effects.
Bioavailability is approximately 75%.
Distribution into human body tissues and fluids not fully characterized; however, drug appears to be concentrated in the thyroid gland.
Readily crosses the placenta. (See Fetal/Neonatal Morbidity and also Pregnancy under Cautions.)
Distributed into milk to a small extent; extent of distribution is about 0.007–0.077% of a single orally administered dose. (See Lactation under Cautions.)
Extensively metabolized to its glucuronide conjugate and other minor metabolites.
35% of dose excreted in urine as unchanged drug and metabolites within 24 hours.
Approximately 1–2 hours.
25°C (may be exposed to 15–30°C).
Inhibits the synthesis of thyroid hormones by interfering with the incorporation of iodine into tyrosyl residues of thyroglobulin; also inhibits the coupling of these iodotyrosyl residues to form iodothyronine.
Exact mechanism(s) not fully elucidated; however, propylthiouracil may interfere with the oxidation of iodide ion and iodotyrosyl groups.
Limited evidence suggests that coupling reaction is more sensitive to antithyroid agents than the iodination reaction.
Does not inhibit the action of thyroid hormones already formed and present in the thyroid gland or circulation; also does not interfere with the effectiveness of exogenously administered thyroid hormones. Patients whose thyroid gland contains relatively high concentration of iodine (e.g., from prior ingestion or from administration during diagnostic radiologic procedures) may respond relatively slowly to antithyroid agents.
Inhibits peripheral deiodination of T4 to T3.
Advice to Patients
Importance of patient reading the manufacturer’s medication guide prior to initiating therapy with the drug and each time the prescription is refilled.
Risk of liver failure. Importance of immediately discontinuing the drug and promptly contacting clinicians if signs and symptoms of liver injury or hepatic dysfunction (e.g., fatigue, weakness, vague abdominal pain, right upper quadrant pain, loss of appetite, itching, easy bruising, yellowing of the eyes or skin, pruritic rash, light-colored stool, dark urine, joint pain, bloating, nausea) occur, particularly in the first 6 months of therapy. (See Hepatotoxicity under Cautions.)
Importance of informing clinicians immediately if signs or symptoms of illness (e.g., sore throat, skin eruptions, fever, chills, headache, general malaise) occur. Importance of immediately discontinuing the drug and contacting clinicians if signs or symptoms suggestive of agranulocytosis (e.g., fever, sore throat) occur. (See Hematologic Effects under Cautions.)
Importance of patient not discontinuing propylthiouracil therapy unless instructed by their clinician.
Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as any concomitant illnesses.
Importance of women immediately informing clinicians if they are or plan to become pregnant or plan to breast-feed. Necessity for clinicians to advise women of rare potential hazard to the mother and fetus of propylthiouracil-associated liver toxicity, as well as risks of methimazole-associated fetal malformations when considering antithyroid drug use during pregnancy. (See Fetal/Neonatal Morbidity and also see Hepatotoxicity under Cautions.)
Importance of informing patients of other important precautionary information. (See Cautions.)
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
AHFS DI Essentials™. © Copyright 2022, Selected Revisions November 27, 2013. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.
Frequently asked questions
More about propylthiouracil
- Side effects
- Drug interactions
- Dosage information
- During pregnancy or Breastfeeding
- Reviews (4)
- Drug images
- Pricing & coupons
- En español
- Drug class: antithyroid agents