Propylthiouracil changes thyroid status and the balance of vitamin K-dependent factors, unpredictably altering the effect of warfarin, with a bleeding risk or anticoagulant failure.
Mechanism overlapping that of carbimazole: thionamide-induced normalisation of thyroid function alters the synthesis/catabolism of vitamin K-dependent factors and warfarin sensitivity, with a variable net effect (INR up or down); PTU-related agranulocytosis fever or hepatotoxic jaundice may also mask or confuse bleeding signs.
Frequent INR, TSH and free T4, full blood count with neutrophils, transaminases, bleeding signs.
Bleeding, fever with sore throat (agranulocytosis), jaundice, abdominal pain (hepatotoxicity).
Measure INR before starting and every 1–2 weeks while adjusting thyroid function; adjust warfarin in small steps; in the setting of fever or jaundice, exclude PTU agranulocytosis and hepatotoxicity before attributing the change to INR.
Drugs.com professional monograph Methimazole/Warfarin — anticoagulant effect "increased or decreased" with antithyroid drugs; Howard-Thompson A. et al. (PMC4065757): https://pmc.ncbi.nlm.nih.gov/articles/PMC4065757/; INFARMED Prontuário Terapêutico (11th ed., 2012), 8.3 — Propylthiouracil entry (dose adjustments with inducers; reduction in renal impairment).
Povidone-iodine provides a systemically absorbed iodine load that may affect the thyroid and destabilise propylthiouracil therapy, besides interfering with thyroid function tests.
As with carbimazole, absorbed iodine alters thyroid response and may counteract or confuse the antithyroid effect; the Prontuário (Povidone-iodine 13.1.1) documents this absorption and the interference with thyroid tests.
TSH, free T4, T3, signs of hypo- or hyperthyroidism.
Worsening hyperthyroidism or developing hypothyroidism, goitre.
Avoid application to extensive or mucosal areas during antithyroid therapy; prefer chlorhexidine; reassess TSH and free T4 after exposure.
INFARMED Prontuário Terapêutico (11th ed., 2012), Povidone-iodine 13.1.1 — systemic absorption affecting the thyroid, and 8.3 Thyroid hormones and antithyroid drugs (Propylthiouracil entry).
Foods very rich in iodine (seaweed, kelp) can destabilise hyperthyroidism control during PTU treatment.
Avoid seaweed and iodine supplements.
Prontuário Terapêutico INFARMED, 8.3 (PTU — same class mechanism as carbimazole).
Propylthiouracil causes severe hepatotoxicity (fulminant hepatic failure reported, mainly in adults) — avoid in active liver disease.
Prefer carbimazole if pre-existing liver disease; monitor transaminases during PTU therapy.
Prontuário Terapêutico INFARMED, 8.3 — PTU: idiosyncratic hepatotoxicity; EMC-UK PTU SmPC 4.4 (hepatic failure warning).
Like the other thionamides, it crosses the placenta and can cause fetal goitre, fetal/neonatal hypothyroidism and neonatal aplasia cutis. Historically it is the preferred thionamide in the 1st trimester, because carbimazole/thiamazole is associated with a specific pattern of congenital malformations (aplasia cutis, choanal atresia, abdominal defects).
Preferred in the 1st trimester at the lowest effective dose; consider switching to carbimazole in the 2nd–3rd trimesters because of the risk of serious maternal propylthiouracil hepatotoxicity. Monitor maternal and fetal thyroid function.
Propylthiouracil is excreted into milk in smaller amounts and with less risk of neonatal hypothyroidism than thiamazole; some authors consider it the preferred thionamide if breastfeeding — always at the minimum dose and monitoring infant thyroid function.
Prontuário Terapêutico INFARMED — 8.5 (Antithyroid agents); Annex 1 (See Thionamides); EMC-UK (MHRA) — Propylthiouracil SmPC: https://www.medicines.org.uk/emc/product/6472/smpc (section 4.6).
Clinical and educational support tool. The information does not replace a medical prescription or the opinion of a qualified healthcare professional.
Fast T3 reduction (↓ thyroid synthesis + ↓ peripheral T4→T3 conversion); useful in thyroid storm.
Inhibition of thyroid peroxidase (TPO) and of peripheral type-1 deiodinase (blocks T4 → T3 conversion).
Oral: rapid absorption; peak 1–2 h; requires divided doses due to short half-life.
Hepatic glucuronidation; renal excretion; less protein binding than methimazole (more crosses placenta in 2nd–3rd trimester).
~ 1–2 h.
Medicines from the same therapeutic group (ATC classification) or the same pharmacological class.
