Drugs For Hyperthyroidism

Written by Megan Boucher

Last updated 29th January 2026
5 Revisions

The thyroid gland is a major endocrine organ that produces thyroxine (T4), triiodothyronine (T3), and calcitonin, with T3 and T4 playing a central role in regulating metabolic rate. For more information on the thyroid gland, please see the related article The thyroid gland.

Thyrotoxicosis describes the hypermetabolic state caused by elevated circulating free T3 and T4. Symptoms include tachycardia, diarrhoea, anxiety, muscle weakness and sweating.

Hyperthyroidism refers specifically to hyperfunction of the thyroid gland and is classified as primary or secondary.

Primary hyperthyroidism

Caused by intrinsic thyroid pathology:

  • Graves’ disease (diffuse thyroid hyperplasia)
  • Toxic multinodular goitre
  • Toxic adenoma
  • Hyperfunctioning thyroid carcinoma
  • Iodine‑induced hyperthyroidism

Secondary hyperthyroidism

Caused by pathology external to the thyroid gland:

  • TSH‑secreting pituitary tumour

This article outlines the pharmacology, therapeutics and key prescribing points for drugs used in the management of hyperthyroidism.

Treatment options

Treatment involves symptomatic management (e.g. beta‑blockers) and pharmacological or surgical suppression of thyroid hormone production. Common pharmacological treatments include radioiodine therapy, thioureylenes and iodide.

 

Fig 1: Mechanism Of Action Of Drugs For Hyperthyroidism

Radioiodine Therapy

Radioiodine uses the radioactive isotope iodine‑131 (¹³¹I) to selectively damage thyroid follicular cells and reduce thyroid hormone production.

Mechanism of action

¹³¹I is taken up by follicular cells via iodide transporters and incorporated into thyroglobulin. It emits both beta and gamma radiation. Gamma radiation passes through tissue with minimal effect, whereas beta particles are absorbed locally, causing follicular cell destruction and reduced hormone synthesis.

Therapeutic considerations

  • Administered orally as a single dose, typically 400–800 MBq
  • Radioactive effects persist for ~2 months (half‑life ≈8 days)
  • Clinical effect begins after 1–2 months, with maximal effect after a further 2 months
  • >50% of patients develop hypothyroidism and require lifelong thyroid hormone replacement
  • Contraindicated in pregnancy, breastfeeding and children
  • Patients should:
    • Avoid pregnancy for 6 months after treatment
    • Avoid fathering children for 4 months after treatment
  • No increased incidence of thyroid cancer has been demonstrated following therapeutic use

Thioureylenes

Thioureylenes contain a thiocarbamide (S–C–N) group and include carbimazole, methimazole and propylthiouracil (PTU).

Their mechanism is not fully understood, but they inhibit iodination of thyroglobulin, reducing synthesis of T3 and T4. Propylthiouracil additionally inhibits peripheral conversion of T4 to T3.

Although iodination is reduced by ~90% within 12 hours, clinical improvement takes several weeks due to large intrathyroidal hormone stores and the long half‑life of T4.

Pharmacokinetic Properties

Parameter Carbimazole Propylthiouracil
Absorption Peak plasma thiamazole levels within 1–2 hours Rapid GI absorption; bioavailability 50–75%
Distribution Vd ≈0.5 L/kg; concentrated in thyroid; moderate protein binding; crosses placenta and enters breast milk Concentrated in thyroid; ~80% protein bound; crosses placenta and enters breast milk
Metabolism Rapidly metabolised to active thiamazole Rapid first‑pass hepatic metabolism to glucuronide
Elimination >90% renal excretion; ~10% enterohepatic circulation Renal excretion of glucuronide; minimal faecal excretion
Half‑life 5.3–5.4 hours (shorter in hyperthyroidism; prolonged in renal/hepatic impairment) 1–2 hours (prolonged in renal/hepatic impairment)

Pregnancy and Breastfeeding

Treatment should only be initiated on specialist advice.

  • Methimazole and propylthiouracil cross the placenta and enter breast mil
  • PTU has a lower risk of severe congenital malformations than methimazole
  • Choice of agent is based on individual risk–benefit assessmen
  • Use the lowest effective dose to avoid fetal goitre and hypothyroidism
  • Block‑and‑replace therapy is contraindicated in pregnancy

Adverse Effects

Carbimazole adverse effects usually occur within the first 8 weeks and include nausea, headache and skin rash. Propylthiouracil may cause alopecia, oedema, nausea and vomiting.

Rare but serious effects (0.1–1.2%) for both agents include bone marrow suppression (neutropenia, agranulocytosis, eosinophilia, leucopenia).

Patients should stop treatment and seek urgent medical advice if they develop:

  • Sore throat
  • Fever
  • Mouth ulcers
  • Bruising or bleeding
  • Malaise

Other serious adverse effects:

  • Acute pancreatitis (carbimazole)
  • Hepatotoxicity (both agents)
  • Systemic vasculitis (propylthiouracil)

Contraindications

Carbimazole:

  • Severe hepatic impairment
  • Previous carbimazole‑induced pancreatitis
  • Serious pre‑existing haematological disorders

Drug Interactions

  • Caution with drugs that cause agranulocytosis
  • Carbimazole may increase the effect of vitamin K antagonists (e.g. warfarin)
  • Digoxin and theophylline doses may require reduction as thyroid function normalises

Iodine / Iodide

Iodine is converted to iodide (I⁻), causing a temporary reduction in thyroid hormone release. High‑dose iodide improves symptoms within 1–2 days.

Indications

  • Pre‑operative preparation for thyroid surgery
  • Post‑exposure prophylaxis following radioactive iodine exposure

Iodide reduces iodination of thyroglobulin and decreases thyroid gland vascularity.

Therapeutic considerations

  • Maximal effect seen within 10–15 days
  • Adverse effects include allergic reactions, lacrimation, conjunctivitis and salivary gland pain

Key prescribing point

Iodide is used as a short‑term adjunct, and long‑term use should be avoided due to loss of antithyroid efficacy.

References

  1. Hall J, Guyton A. Guyton and Hall textbook of medical physiology. 13th ed. Philadelphia, PA: Elsevier; 2016.
  2. Radioiodine for thyrotoxicosis – The Christie NHS Foundation Trust [Internet].  Available from: 146-radioiodine-treatment-for-thyrotoxicosis-nm-march-2020.pdf
  3. Kumar V, Abbas A, Aster J, Robbins S. Robbins and Cotran pathologic basis of disease. 7th ed. 2005.
  4. Rang H, Dale M, Flower R, Henderson G. Rang and Dale’s pharmacology. 8th ed. 2016.
  5. Hyperthyroidism | Health topics A to Z | CKS | NICE Accessed 5/1/2026
  6. Hyperthyroid and Pregnant – Thyroid UK Accessed 5/1/2026
  7. 2017 Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Disease During Pregnancy and the Postpartum | Thyroid® Accessed 5/1/2026
  8. Carbimazole 5 mg Tablets – Summary of Product Characteristics (SmPC) – (emc) | 13015 Accessed 5/1/2026
  9. Propylthiouracil Tablets BP 50mg – Summary of Product Characteristics (SmPC) – (emc) | 9177 Access 5/1/2026
  10. Aqueous Iodine Oral Solution BP – Summary of Product Characteristics (SmPC) – (emc) | 4828 accessed 5/1/2026

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