Propylthiouracil 50 mg

agranulocytosis (see Warnings and Precautions), aplastic anemia, granulocytopenia, hemolytic anemia, hyperglobulinemia, hypoprothrombinemia, leukopenia, myeloblastic leukemia and thrombocytopenia.

drug fever, lupus-like syndrome (e.g., splenomegaly, skin ulcers, pericarditis), lymphadenopathy and polyarteritis.

The mechanism of propylthiouracil-induced, anti-neutrophil cytoplasmic autoantibody (ANCA)-positive vasculitis is unknown. The renal, musculoskeletal and dermatologic systems are affected. Characterized by inflammation and destruction of the blood vessels, clinical presentation is variable and may include fever, fatigue, skin ulcerations, pulmonary edema, nephritis and/or complications involving other organs. Time to develop vasculitis varies from months to years. Patients are at an increased risk if they are Asian or if they are receiving therapy for an extended duration. Discontinue propylthiouracil if this occurs.

hair loss, depigmentation, erythema nodosum, vesicular eruption in newborns.

neuritis, paresthesia.

sialadenopathy (enlargement of salivary glands). Hypothyroidism may develop with excessive dosage. Dose should be reduced or therapy temporarily discontinued. (See Warnings and Precautions, General.)

dizziness, drowsiness, depression.

edema.

Long-term propylthiouracil treatment can be used in children and adolescents with hyperthyroidism to achieve and maintain a euthyroid state in an attempt to delay the need for ablative therapy with RAI. Neonatal hyperthyroidism can also be treated with propylthiouracil; once a euthyroid state is achieved, the dose should be gradually tapered to the lowest effective maintenance dose. It has been recommended that propylthiouracil use in children be avoided if possible because of concerns that propylthiouracil may induce liver failure in some children [N Engl J Med 2009;360(15):1574-5]. Methimazole should be the preferred alternative in children.

Signs of hypothyroidism such as increased vascularity and size of the thyroid gland may manifest with antithyroid therapy. This is indicative of overtreatment and the dose of propylthiouracil should be reduced or temporarily discontinued.

Propylthiouracil readily crosses the placenta. Maternal therapy can cause fetal goiter and hypothyroidism. The effects on fetal thyroid, however, are often mild. Follow-up studies of children exposed in utero have shown normal intellectual and physiological development. Pregnant women should receive the lowest dose of propylthiouracil needed to control symptoms and to achieve and maintain serum free thyroxine (FT₄) in the upper half of the normal range. As pregnancy progresses, especially in the 3^rd trimester, it is common for those with Graves’ disease to experience a significant improvement in their condition, and the dose may need to be significantly reduced or the drug discontinued. Frequent monitoring of thyroid function (FT₄ levels) is important for detecting any changes in the mother’s condition so dosing can be adjusted accordingly. Do not administer thyroxine concurrently with propylthiouracil. Thyroxine does not cross the placenta in sufficient amounts to reverse the effects of fetal hypothyroidism and can necessitate the need for higher maternal doses of propylthiouracil, further increasing the risk to the fetus.

Propylthiouracil is classified as compatible with breastfeeding by the American Academy of Pediatrics and is considered to be the preferred antithyroid therapy during breastfeeding. Ionized at physiologic pH and highly protein bound, propylthiouracil transfer into breast milk is minimal. Infant exposure through breastfeeding has not shown any adverse effects on thyroid function. Follow-up studies have demonstrated no subsequent impairment in intellectual development. Monitor the infant’s serum T₄ and thyroid stimulating hormone (TSH) levels every 2-4 weeks.

Obtain baseline FT₄ and TSH levels prior to initiating propylthiouracil treatment. Monitor thyroid function every 4-6 weeks until a euthyroid state is achieved, then monitor thyroid function every 2-3 months for 6 months and then every 4-6 months for the duration of therapy. For all patients who enter remission, the risk of spontaneously redeveloping hyperthyroidism years after discontinuing therapy requires that lifelong thyroid assessment be routinely performed.

A baseline CBC count with differential is recommended at the start of propylthiouracil treatment. Hyperthyroid-induced leukopenia can be differentiated from leukopenia and/or agranulocytosis that may develop as a result of propylthiouracil therapy. Baseline serum transaminases may be useful in identifying the development of drug-induced hepatotoxicity.

Propylthiouracil is widely distributed throughout the body. It crosses the placenta and is minimally distributed into milk. In serum, propylthiouracil is 75% to 80% protein-bound.

Following oral administration, approximately 75% of the dose is rapidly absorbed from the gastrointestinal tract. Absorption is unaffected by concomitant food intake.

Propylthiouracil reduces plasma concentrations of thyroid hormones (T₃, T₄). The drug is actively transported into the thyroid gland. Propylthiouracil depletes preformed thyroid hormone stores and inhibits synthesis of thyroid hormones. It inhibits thyroid hormone synthesis by interfering with the coupling of iodotyrosine and the incorporation of iodine onto tyrosine residues in thyroglobulin. Propylthiouracil is suspected of inhibiting thyroid peroxidase thereby preventing the oxidation of iodide ions and iodotyrosyl groups required for the production of active thyroid hormone. Before a euthyroid state is achieved, a lag time of 3-4 weeks may occur, as it takes time for T₄ to be depleted.

Propylthiouracil inhibits the peripheral conversion of T₄ (produced solely by the thyroid gland) to T₃ (which is metabolically more active than T₄) by inhibiting 5’-monodeiodinase in a rapid dose-related manner.

Propylthiouracil does not inhibit the pharmacologic effect on thyroid hormone already formed and present in the thyroid gland or circulation nor will it interfere with the effect of exogenously administered thyroid hormone.

Approximately 35% of the drug and its metabolites are excreted in the urine within 24 hours.

The liver rapidly metabolizes propylthiouracil to a glucuronide conjugate and other minor metabolites.

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