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.109 (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.109 (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.109 (See Fetal/Neonatal Morbidity and also see Pregnancy under Cautions.)
REMS:
FDA approved a REMS for propylthiouracil (ptu) to ensure that the benefits of a drug outweigh the risks. However, FDA later rescinded REMS requirements. See the FDA REMS page () or the ASHP REMS Resource Center ().
Introduction
Antithyroid agent;109 b thiourea-derivative.b
Uses for Propylthiouracil
Hyperthyroidism
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.109
Amelioration of symptoms of hyperthyroidism in preparation for thyroidectomy or radioactive iodine therapy in patients who are intolerant of methimazole.109
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.100 112 100 103 107 109 112 (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.100 103 106 109 112 (See Pediatric Use under Cautions.)
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.100 103 107 108 109 112 For second and third trimesters, may be preferable to switch from propylthiouracil to methimazole because of the risk of maternal adverse effects associated with propylthiouracil (e.g., hepatotoxicity).109 (See Fetal/Neonatal Morbidity and also see Pregnancy under Cautions.)
Therapy with thioamide antithyroid agents maintains patient in euthyroid state for a period of several (generally 1–2) years until spontaneous remission occurs;b c however, spontaneous remission does not occur in all patients, and most eventually require ablative therapy (i.e., surgery, radioactive iodine).b Because thioamide antithyroid agents do not affect underlying cause of hyperthyroidism, generally avoid long-term use; minimum duration of therapy necessary before assessing whether spontaneous remission has occurred not clearly established.b
Therapy with propylthiouracil returns hyperthyroid patient to a normal metabolic state prior to thyroidectomy and controls the thyrotoxic crisis that may accompany thyroidectomy.b
Therapy with propylthiouracil controls the symptoms of hyperthyroidism before and during radioactive iodine therapy until the ablative effects of iodine occur.b However, pretreatment with thioamides may lower the cure rate and increase the need for subsequent doses of radioactive iodine.c
Thyrotoxic Crisis
May be used for management of thyrotoxic crisis;103 109 b c preferred over methimazole due to more rapid onset of effect (i.e., by inhibiting peripheral deiodination of thyroxine [T4] to triiodothyronine [T3], a dominant source of the hormone).103 c d Usually initiated before iodide (e.g., potassium iodide, strong iodine solution) therapy.b c d
Alcoholic Liver Disease
Has been studied in patients with alcoholic liver disease†.116
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.116
Propylthiouracil Dosage and Administration
General
Concomitant Therapy
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).b c
REMS Program
FDA has approved a Risk Evaluation and Mitigation Strategy (REMS) for propylthiouracil.112 114
The program consists of a medication guide that must be dispensed with every propylthiouracil prescription.112 113 114
The goal of the program is to inform patients about the serious risks (e.g., hepatotoxicity) associated with the use of propylthiouracil (see Cautions).114
Administration
Administer orally.109 b c May administer rectally† as extemporaneously prepared suppositories or enemas.c d o
Oral Administration
Administer total daily dosage orally in 3 equally divided doses at approximately 8-hour intervals.109 b c More frequent administration (e.g., at 4- or 6-hour intervals) may be necessary in some cases.b c
Dosage
Pediatric Patients
Hyperthyroidism
Oral
Generally not recommended for use in pediatric patients except in rare instances in which alternative therapies are not appropriate options.109 (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.109
Severe liver injury reported with dosages as low as 50 mg daily, but most cases were associated with dosages of ≥300 mg daily.109 (See Hepatotoxicity under Cautions.)
Adults
Hyperthyroidism
Graves’ Disease with Hyperthyroidism or Toxic Multinodular Goiter
Oral
Initially, 300 mg daily.109 For patients with severe hyperthyroidism and/or very large goiters, initial dosage may be increased to 400 mg daily;109 occasionally, an initial dosage of 600–900 mg daily may be required.109
Continue therapy at initial dosage for about 4–8 weeks until symptoms resolve and euthyroidism is achieved.b c d j Then, gradually taper to a dosage that maintains euthyroidism.c d j
Usual maintenance dosage: Manufacturer recommends 100–150 mg daily.109
Most data support duration of 12–18 months.c l
Preparation for Thyroidectomy
Oral
Initially, 300 mg daily.109 For patients with severe hyperthyroidism and/or very large goiters, initial dosage may be increased to 400 mg daily;109 occasionally, an initial dosage of 600–900 mg daily may be required.109
Some clinicians recommend continuing therapy at initial dosage for about 6–8 weeks until euthyroidism is achieved; then add iodide therapy for 10–14 days (to decrease vascularity of thyroid gland) before surgery.j
Preparation for Radioactive Iodine Therapy
Oral
Initially, 300 mg daily.109 For patients with severe hyperthyroidism and/or very large goiters, usual initial dosage may be increased to 400 mg daily;109 occasionally, an initial dosage of 600–900 mg daily may be required.109
Some clinicians recommend continuing therapy at initial dosage for about 6–8 weeks until euthyroidism is achieved; then discontinue propylthiouracil ≥7 days before radioactive iodine therapy.c May reinstitute propylthiouracil 4 days after radioactive iodine therapy as needed (e.g., in patients with cardiac disease).c j
Thyrotoxic Crisis
Oral
Usually, 200 mg every 4–6 hours on the first day.b Once full control of symptoms is achieved, reduce dosage gradually to usual maintenance dosage.b
Special Populations
Hepatic Impairment
No specific dosage recommendations at this time.109
Renal Impairment
No specific dosage recommendations at this time.109
Geriatric Patients
No specific dosage recommendations at this time.109
Pregnancy
If used during pregnancy for the management of hyperthyroidism, a sufficient, but not excessive, dosage is necessary.109 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.109 (See Pregnancy under Cautions and also see Hepatotoxicity under Cautions.)
Cautions for Propylthiouracil
Contraindications
Known hypersensitivity to propylthiouracil or any ingredient in the formulation.109 b
Warnings/Precautions
Warnings
Hepatotoxicity
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.100 101 102 103 104 106 107 109 112 (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.112
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.109 (See Pediatric Use under Cautions.)
Cases of liver injury, including liver failure and death, reported in women receiving propylthiouracil during pregnancy.109 Two cases of in utero exposure with liver failure and death of a newborn also reported.109 Use of an alternative antithyroid drug (e.g., methimazole) may be advisable after the first trimester of pregnancy.109 (See Fetal/Neonatal Morbidity and also see Pregnancy under Cautions.)
Extent of propylthiouracil-induced hepatitis and true incidence of severe liver injury not known.104 107
Propylthiouracil-induced liver failure may occur at any time during therapy with a sudden onset, rapid progression, and a low chance of reversibility;103 104 liver failure has been observed after 6–450 days of propylthiouracil therapy (median: 120 days).107
Effect of dosage on risk of hepatotoxicity not clearly elucidated;104 however, reported average daily dosage associated with liver failure was approximately 300 mg in both children and adults.107
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.100 109 112 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.100 109 Some clinicians state that in patients with thioamide-induced hepatitis, rechallenge with alternative thioamide is not recommended because death has been reported.c
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.103 104 107 109
Hematologic Effects
Risk of agranulocytosis;109 b c d f usually occurs within first 3 months of therapy,109 but rarely may occur after 4 months of therapy.b Increased risk in patients >40 years of age;b d use with caution in such patients.b n
Leukopenia, thrombocytopenia, and aplastic anemia (pancytopenia) also may occur.109 b Hypoprothrombinemia and bleeding reported rarely with thioamides.c j (See Laboratory Monitoring under Cautions.)
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.b c d If fever, sore throat, or other signs or symptoms of illness occur, determine leukocyte and differential counts to assess whether agranulocytosis has developed.109 b d f 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.109 b
If agranulocytosis, aplastic anemia (pancytopenia), or fever is suspected, discontinue propylthiouracil and initiate appropriate supportive and symptomatic therapy.109 b c Obtain bone marrow indices.109
Hypothyroidism
May cause hypothyroidism necessitating routine monitoring of TSH and free T4 concentrations with dosage adjustments to maintain a euthyroid state.109
May cause fetal goiter and cretinism when administered to a pregnant woman, because the drug readily crosses the placenta.109 (See Fetal/Neonatal Morbidity and also see Pregnancy under Cautions.)
Fetal/Neonatal Morbidity
May cause fetal harm (i.e., induction of goiter, hypothyroidism, or cretinism).109 113 b
Congenital malformations reported approximately 3 times more often with prenatal exposure to methimazole compared with propylthiouracil.112 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).112 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.112 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.112 (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.104 106 109 (See Hepatotoxicity under Cautions.)
Sensitivity Reactions
Cross-Sensitivity
Cross-sensitivity between thioamides likely to occurc f (i.e., in approximately 50% of patients switched from one thioamide agent to the other).d j
General Precautions
Laboratory Monitoring
Before initiating thioamide therapy, some clinicians recommend obtaining baseline T4 and TSH concentrations.c Baseline WBC with differential also may be useful in evaluating thioamide-induced adverse effects (e.g., leukopenia and/or agranulocytosis).c 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.103 104 107 109 (See Hepatotoxicity under Cautions.)
Monitor thyroid function periodically109 b (e.g., 4–6 weeks after initiation of therapy and after any dosage adjustmentsc ); decrease dosage if TSH is elevated.109 b Once euthyroidism is achieved, monitor thyroid function every 3–6 months.c
Determine leukocyte and differential counts in patients who develop any signs or symptoms of illness (e.g., fever, sore throat) during therapy.b f
Consider monitoring PT during therapy, particularly before surgical procedures, because of possible risk of hypoprothrombinemia and bleeding.109 b
Dermatologic Effects
Exfoliative dermatitis reported.109 If exfoliative dermatitis is suspected, discontinue propylthiouracil and initiate appropriate supportive and symptomatic therapy.109 b
Immunologic Effects
Vasculitic syndrome associated with the presence of antineutrophil cytoplasmic antibody (ANCA) reported.109 d Manifestations of ANCA-positive vasculitis may include rapidly progressive glomerulonephritis (crescentic and pauci-immune necrotizing glomerulonephritis) sometimes leading to acute renal failure, fever, pulmonary infiltrates or alveolar hemorrhage, arthritis, skin ulcers, and leukocytoclastic vasculitis.109 d If ANCA-positive vasculitis is suspected, discontinue propylthiouracil promptly.109 d
Pulmonary Effects
Interstitial pneumonitis reported.109 b If interstitial pneumonitis is suspected, discontinue propylthiouracil.109
Specific Populations
Pregnancy
Category D.109 h (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.108 d e Since methimazole may be associated with the rare development of fetal abnormalities (e.g., aplasia cutis, choanal atresia), propylthiouracil may be preferred when an antithyroid drug is indicated during organogenesis, in the first trimester of pregnancy, or just prior to the first trimester of pregnancy.100 103 106 107 108 109 (See Boxed Warning and also see Fetal/Neonatal Morbidity under Cautions.) May be preferable to switch from propylthiouracil to methimazole for the second and third trimesters, because of potential maternal adverse effects of propylthiouracil (e.g., hepatotoxicity).109 (See Hepatotoxicity under Cautions.) Not known if risk of methimazole-induced aplasia cutis or embryopathy outweighs risk of propylthiouracil-induced hepatotoxicity.104
When used in pregnancy, administer lowest effective dosage to maintain T4 concentrations at high end of normal range.108 c d e f As thyroid dysfunction improves during course of pregnancy, may reduce propylthiouracil dosage; in some patients, may discontinue propylthiouracil several weeks or months before delivery.109 b
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.104 106 109
Lactation
Distributed into milk to a small extent and, therefore, likely does not result in clinically important doses to the nursing infant.109 110 d h 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.109 110 AAP and other clinicians consider propylthiouracil compatible with breast-feeding.108 d f h i
Adult Use
Patients >40 years of age: Use with caution because of increased risk of agranulocytosis.b n (See Hematologic Effects under Cautions.)
Pediatric Use
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.109 117 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.100 103 106 109 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.105 106
When propylthiouracil is used in children, inform parents and patients of risk of liver failure.109 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.109 (See Hepatotoxicity under Cautions.)
Common Adverse Effects
Rash,109 b d f j l urticaria,109 b d pruritus,109 b abnormal hair loss,109 b skin pigmentation,109 b edema,109 b nausea,109 b f l vomiting,109 b l epigastric distress,109 b anorexia,f loss of taste109 b f or smell,f taste perversion,109 arthritis,f arthralgia,109 b d j myalgia,109 b paresthesia,109 b fever,f j l headache,109 b drowsiness,109 b neuritis,109 b vertigo,109 b jaundice,109 b sialadenopathy,109 b lymphadenopathy.109 b
Interactions for Propylthiouracil
Drugs Known to be Associated with Agranulocytosis
Use concomitantly with extreme caution.109 b
Specific Drugs
Drug | Interaction | Comments |
|---|---|---|
Anticoagulants, oral (e.g., warfarin) | Activity of oral anticoagulants (e.g., warfarin) may be increased because of the potential inhibition of vitamin K activity by propylthiouracil;109 however, increased and decreased PT/INR responses reported with concomitant use of propylthiouracil and warfarin115 | Consider additional monitoring of PT/INR, particularly prior to surgery109 |
β-Adrenergic blocking agents (e.g., propranolol) | Possible increased clearance of β-adrenergic blocking agents with a high extraction ratio during hyperthyroid state109 | Reduction of β-blocker dosage may be needed when patient becomes euthyroid109 |
Digitalis glycosides (e.g., digoxin) | Possible increased serum digitalis concentrations when hyperthyroid patients receiving a stable digitalis glycoside regimen become euthyroid109 | Reduction of digitalis glycoside dosage may be needed when patient becomes euthyroid109 |
Theophylline | Possible decreased theophylline clearance when hyperthyroid patients on a stable theophylline regimen become euthyroid109 | Reduction of theophylline dosage may be needed when patient becomes euthyroid109 |
Propylthiouracil Pharmacokinetics
Absorption
Bioavailability
Rapidly and readily absorbed from the GI tract following oral administration.109 b d j Peak plasma concentrations attained within 1–2 hours;b d j however, plasma concentrations do not appear to correlate with therapeutic effects.b
Bioavailability is approximately 75%.b
Onset
Slow onset because thioamides block synthesis (rather than release) of thyroid hormones; some symptomatic improvement should be noted 2–3 weeks after initiation of therapy.c
Duration
12–24 hours.d
Distribution
Extent
Distribution into human body tissues and fluids not fully characterized; however, drug appears to be concentrated in the thyroid gland.b
Readily crosses the placenta.109 b d e f h (See Fetal/Neonatal Morbidity and also Pregnancy under Cautions.)
Distributed into milk to a small extent;109 b h extent of distribution is about 0.007–0.077% of a single orally administered dose.109 110 111 b (See Lactation under Cautions.)
Plasma Protein Binding
Approximately 80–90%.d h
Elimination
Metabolism
Extensively metabolized to its glucuronide conjugate and other minor metabolites.109 b
Elimination Route
35% of dose excreted in urine as unchanged drug and metabolites within 24 hours.109 b
Half-life
Approximately 1–2 hours.b c d
Stability
Storage
Oral
Tablets
15–30°C.109
Actions
Inhibits the synthesis of thyroid hormones109 d f h l by interfering with the incorporation of iodine into tyrosyl residues of thyroglobulin;b j also inhibits the coupling of these iodotyrosyl residues to form iodothyronine. b
Exact mechanism(s) not fully elucidated; however, propylthiouracil may interfere with the oxidation of iodide ion and iodotyrosyl groups.b
Limited evidence suggests that coupling reaction is more sensitive to antithyroid agents than the iodination reaction.b
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.109 b 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.b
Inhibits peripheral deiodination of T4 to T3.109 b c f h j
Advice to Patients
Under terms of FDA-approved REMS program, a medication guide must be dispensed with every propylthiouracil prescription.112 113 114 Importance of patient reading the manufacturer’s medication guide prior to initiating therapy with the drug and each time the prescription is refilled.112 113
Risk of liver failure.100 103 109 112 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.100 103 109 112 (See Hepatotoxicity under Cautions.)
Importance of informing a clinician immediately if signs or symptoms of illness (e.g., sore throat, skin eruptions, fever, chills, headache, general malaise) occur.109 b c j (See Hematologic Effects under Cautions.)
Importance of patient not discontinuing propylthiouracil therapy unless instructed by their clinician.112
Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as any concomitant illnesses.109
Importance of women immediately informing clinicians if they are or plan to become pregnant or plan to breast-feed.109 112 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.104 106 109 (See Fetal/Neonatal Morbidity and also see Hepatotoxicity under Cautions.)
Importance of informing patients of other important precautionary information.109 (See Cautions.)
Preparations
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | Tablets | 50 mg* | Propylthiouracil Tablets |
Comparative Pricing
This pricing information is subject to change at the sole discretion of DS Pharmacy. This pricing information was updated 10/2011. Actual costs to patients will vary depending on the use of specific retail or mail-order locations and health insurance copays.
Propylthiouracil 50MG Tablets (WEST-WARD): 90/$20.99 or 180/$34.97
Disclaimer
This report on medications is for your information only, and is not considered individual patient advice. Because of the changing nature of drug information, please consult your physician or pharmacist about specific clinical use.
The American Society of Health-System Pharmacists, Inc. and Drugs.com represent that the information provided hereunder was formulated with a reasonable standard of care, and in conformity with professional standards in the field. The American Society of Health-System Pharmacists, Inc. and Drugs.com make no representations or warranties, express or implied, including, but not limited to, any implied warranty of merchantability and/or fitness for a particular purpose, with respect to such information and specifically disclaims all such warranties. Users are advised that decisions regarding drug therapy are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and the information is provided for informational purposes only. The entire monograph for a drug should be reviewed for a thorough understanding of the drug's actions, uses and side effects. The American Society of Health-System Pharmacists, Inc. and Drugs.com do not endorse or recommend the use of any drug. The information is not a substitute for medical care.
AHFS Drug Information. © Copyright, 1959-2011, Selected Revisions October 27, 2011. American Society of Health-System Pharmacists, Inc., 7272 Wisconsin Avenue, Bethesda, Maryland 20814.
† Use is not currently included in the labeling approved by the US Food and Drug Administration.
References
100. Food and Drug Administration. FDA Alert: Propylthiouracil-induced liver failure. Rockville, MD; 2009 Jun 4. From FDA website. Accessed 2009 Oct 28.
101. Food and Drug Administration. FDA News Release: FDA warns about serious liver injury associated with anti-thyroid drug. Rockville, MD; 2009 Jun 3. From FDA website. Accessed 2009 Oct 30.
102. Russo MW, Galanko JA, Shrestha R et al. Liver transplantation for acute liver failure from drug induced liver injury in the United States. Liver Transpl. 2004; 10:1018-23. [PubMed 15390328]
103. Bahn RS, Burch HS, Cooper DS et al. The Role of Propylthiouracil in the Management of Graves' Disease in Adults: report of a meeting jointly sponsored by the American Thyroid Association and the Food and Drug Administration. Thyroid. 2009; 19:673-4. [PubMed 19583480]
104. Eunice Kennedy Shriver National Institute of Child Health and Human Development. Hepatic toxicity following treatment for pediatric Graves’ disease meeting: October 28, 2008. Conference proceeding. Available from website. Accessed 2009 Oct 30.
105. Rivkees SA, Mattison DR. Ending propylthiouracil-induced liver failure in children. N Engl J Med. 2009; 360:1574-5. [PubMed 19357418]
106. Rivkees SA, Mattison DR. Propylthiouracil (PTU) hepatotoxicity in children and recommendations for discontinuation of use. Int J Pediatr Endocrinol. 2009. Article ID 132041. DOI:10.1155/2009/132041.
107. Cooper DS, Rivkees SA. Putting propylthiouracil in perspective. J Clin Endocrinol Metab. 2009; 94:1881-2. [PubMed 19401361]
108. Abalovich M, Amino N, Barbour LA et al. Management of thyroid dysfunction during pregnancy and postpartum: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2007; 92:S1-47. [PubMed 17948378]
109. Dava Pharmaceuticals, Inc. Propylthiouracil tablets prescribing information. Fort Lee, NJ; 2010 Jan.
110. Kampmann JP, Johansen K, Hansen JM et al. Propylthiouracil in human milk. Revision of a dogma. Lancet. 1980; 1:736-7. [PubMed 6103158]
111. Low LC, Lang J, Alexander WD. Excretion of carbimazole and propylthiouracil in breast milk. Lancet. 1979; 2:1011. [PubMed 91730]
112. Food and Drug Administration. FDA drug safety communication: New boxed warning on severe liver injury with propylthiouracil. Rockville, MD; 2010 Apr 21. Available from FDA website (). Accessed 2010 Sep 8.
113. Dava Pharmaceuticals, Inc. Propylthiouracil tablets medication guide. Fort Lee, NJ; 2010 Mar.
114. Dava Pharmaceuticals, Inc. Propylthiouracil risk evaluation and mitigation strategy (REMS). Fort Lee, NJ; 2010 Mar 24. Available from FDA website (). Accessed 2010 Sep 8.
115. Bristol-Myers Squibb. Coumadin (warfarin sodium) tablets crystalline and Coumadin (warfarin sodium) for injection prescribing information. Princeton, NJ; 2010 Jan.
116. Rambaldi A, Gluud C. Propylthiouracil for alcoholic liver disease. Cochrane Database Syst Rev. 2005; :CD002800. [PubMed 16235302]
117. Rivkees SA, Szarfman A. Dissimilar hepatotoxicity profiles of propylthiouracil and methimazole in children. J Clin Endocrinol Metab. 2010; 95:3260-7. [PubMed 20427502]
b. AHFS drug information 2011. McEvoy GK, ed. Propylthiouracil. Bethesda, MD: American Society of Health-System Pharmacists; 2011.
c. Dong BJ. Endocrine Disorders. In: Koda-Kimble MA, Young LY, Kradjan WA et al, eds. Applied therapeutics: the clinical use of drugs. 8th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005.
d. Anon. Drugs for hypothyroidism and hyperthyroidism. Treat Guidel Med Lett. 2006; 4:17-24.
e. American Association of Clinical Endocrinologists. Medical
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