What medications can cause hyperthyroidism? An in-depth pharmacological review

October 6, 2025 •

4 min read

Affecting approximately 1% of the population, hyperthyroidism can be triggered by various factors, including certain medical treatments. For both patients and healthcare providers, it is crucial to understand what medications can cause hyperthyroidism and the diverse mechanisms that lead to this adverse effect.

Quick Summary

Certain medications such as amiodarone, immune checkpoint inhibitors, lithium, and iodine-based substances can induce hyperthyroidism through various physiological pathways.

Key Points

Amiodarone: A heart medication rich in iodine, it can cause hyperthyroidism either through excessive iodine content (Type 1 AIT) or via a destructive process (Type 2 AIT).
Immune Checkpoint Inhibitors: Used in cancer therapy, these drugs can trigger an autoimmune thyroiditis, leading to a thyrotoxic phase often followed by permanent hypothyroidism.
Levothyroxine Overdose: Taking too high a dose of thyroid hormone replacement is a common cause of iatrogenic hyperthyroidism, diagnosed by monitoring TSH levels.
Iodinated Contrast Media: Large iodine loads from contrast agents used in radiology can cause the Jod-Basedow effect in susceptible patients, such as those with pre-existing thyroid nodules.
Lithium: This mood stabilizer can, in rare cases, induce hyperthyroidism, either through thyroiditis or by triggering Graves' disease.
Management Depends on Mechanism: Treatment for drug-induced hyperthyroidism varies; it may include stopping the drug, using beta-blockers for symptoms, or targeted therapies based on the cause.

While hyperthyroidism is commonly associated with autoimmune conditions like Graves' disease, a number of prescription and over-the-counter drugs can also disrupt thyroid function. Drug-induced thyrotoxicosis can arise from several distinct mechanisms, including excessive iodine exposure, direct damage to the thyroid gland, or the induction of autoimmunity. Recognizing the link between specific medications and this condition is essential for accurate diagnosis and effective management.

Amiodarone: The High-Iodine Antiarrhythmic

Amiodarone, a medication used to treat heart rhythm disorders, is one of the most well-known causes of drug-induced thyroid dysfunction. The drug contains a massive amount of iodine—a single 200 mg tablet provides a daily iodine intake that is up to 100 times higher than recommended. This excess iodine can disrupt thyroid hormone production in two primary ways, leading to two different types of amiodarone-induced thyrotoxicosis (AIT):

Type 1 Amiodarone-Induced Thyrotoxicosis

This form occurs in individuals with pre-existing thyroid conditions, such as latent Graves' disease or a multinodular goiter. In these susceptible patients, the excess iodine from amiodarone acts as a substrate, triggering an overproduction of thyroid hormones. This mechanism is an example of the Jod-Basedow effect.

Type 2 Amiodarone-Induced Thyrotoxicosis

This is a destructive thyroiditis caused by the direct toxic effect of the amiodarone molecule itself on the thyroid gland. The drug damages the follicular cells, leading to a release of pre-formed thyroid hormones into the bloodstream. This type of AIT is more common in iodine-sufficient regions. Because the mechanisms differ, distinguishing between Type 1 and Type 2 is critical for appropriate treatment, which may involve anti-thyroid drugs or corticosteroids.

Immune Checkpoint Inhibitors (ICIs): Unmasking Autoimmunity

Immune checkpoint inhibitors, a class of cancer immunotherapy drugs, have revolutionized oncology but can also cause immune-related adverse events (irAEs), including thyroid dysfunction. These drugs, which include PD-1 inhibitors like nivolumab and pembrolizumab, trigger an autoimmune reaction that can lead to thyroiditis. The typical progression involves a brief period of hyperthyroidism, or thyrotoxicosis, followed by permanent hypothyroidism as the gland is destroyed. Another ICI, alemtuzumab, is specifically known to cause Graves' disease through the stimulation of autoimmunity.

Overmedication with Thyroid Hormone

One of the most frequent causes of hyperthyroidism is simply taking too much thyroid hormone replacement medication, typically levothyroxine. This can occur for two reasons:

Iatrogenic Hyperthyroidism: The patient's prescribed dose of levothyroxine is too high and has not been adjusted based on regular monitoring.
Factitious Hyperthyroidism: An individual intentionally takes excessive amounts of thyroid hormone. This is a rarer cause and may be linked to certain psychological conditions.

Lithium: A Mood Stabilizer with Endocrine Effects

While more commonly associated with hypothyroidism, lithium can rarely cause hyperthyroidism, sometimes by inducing Graves' disease or thyroiditis. Lithium concentrates in the thyroid gland and can disrupt hormone release and metabolism. Therefore, regular thyroid function monitoring is recommended for patients on long-term lithium therapy.

Iodinated Contrast Media: A Radiological Risk

Iodinated contrast media (ICM), used for CT scans and other radiological procedures, contain a large iodine load that can trigger hyperthyroidism in susceptible individuals. Patients with pre-existing thyroid disorders, such as a toxic multinodular goiter, are particularly at risk of developing iodine-induced hyperthyroidism (Jod-Basedow effect).

Other Medications and Supplements

Interferon-alpha: This medication, used for conditions like chronic hepatitis C and some cancers, is known to cause thyroid dysfunction, including a thyrotoxic phase.
High-Dose Iodine Supplements: Over-the-counter supplements like kelp tablets, which are high in iodine, can also trigger hyperthyroidism in vulnerable individuals.

Comparison of Hyperthyroidism-Inducing Medications


Medication/Class	Primary Mechanism	Typical Onset	Monitoring Recommendations	Risk Factors
Amiodarone	Type 1: Iodine excess (Jod-Basedow); Type 2: Destructive thyroiditis	Months to years	TSH/fT4 at baseline, every 6 months	Pre-existing thyroid nodules/Graves' disease (Type 1); Iodine-sufficient areas (Type 2)
ICIs (e.g., Nivolumab, Pembrolizumab)	Autoimmune-mediated thyroiditis	Weeks to months	TSH/fT4 at baseline, periodically during treatment	Underlying autoimmune predisposition
Lithium	Inhibition of hormone release, potentially inducing autoimmunity	Typically within the first 2 years	TSH at baseline, every 6-12 months	Female sex, higher risk in younger women
Iodinated Contrast Media	Iodine excess (Jod-Basedow effect)	2-12 weeks after exposure	Clinical observation, thyroid function tests if symptoms arise	Pre-existing thyroid nodules or goiter
Levothyroxine (Overdose)	Excessive exogenous hormone	Varies; depends on dosage change	Regular TSH monitoring to ensure correct dose	Pre-existing hypothyroidism

Symptoms and Diagnosis

Drug-induced hyperthyroidism can present with symptoms similar to other forms of hyperthyroidism, but their onset may be masked by the patient's underlying condition. Symptoms can include:

Cardiovascular: Rapid or irregular heartbeat (palpitations), atrial fibrillation.
Nervous System: Tremors, anxiety, irritability, restlessness.
Metabolic: Unexplained weight loss, increased appetite.
Other: Sweating, fatigue, muscle weakness, frequent bowel movements.

Diagnosis requires a comprehensive review of the patient's medication history and is confirmed by blood tests showing suppressed thyroid-stimulating hormone (TSH) and elevated free thyroxine (fT4) or triiodothyronine (fT3). A detailed history is crucial, as is regular monitoring for high-risk medications.

Management and Conclusion

Managing drug-induced hyperthyroidism typically involves a multidisciplinary approach. The first step, if possible, is to discontinue or adjust the dosage of the offending medication. However, this is not always feasible, especially with essential drugs like amiodarone for severe cardiac conditions. Treatment strategies vary based on the underlying mechanism:

Symptom Control: Beta-blockers can effectively manage symptoms like tremors and palpitations.
Excess Hormone Synthesis (e.g., AIT Type 1, Jod-Basedow): Thionamides like methimazole are used to block the production of new thyroid hormone.
Destructive Thyroiditis (e.g., AIT Type 2): Since hormone is released from a damaged gland rather than overproduced, corticosteroids may be the primary treatment.

Many cases are transient, resolving after the drug is stopped, but some may require ongoing management or result in permanent hypothyroidism. Careful screening and consistent monitoring are the best strategies for preventing or promptly addressing drug-induced hyperthyroidism. Patients should always inform their healthcare providers about all medications and supplements they are taking.

For more detailed information, consult authoritative medical resources, such as the Merck Manuals on Hyperthyroidism.

Frequently Asked Questions

Yes, taking too much thyroid hormone replacement medication, such as levothyroxine, is a common cause of hyperthyroidism, sometimes called iatrogenic hyperthyroidism. It's crucial to follow your doctor's dosage instructions and attend regular monitoring appointments.

Amiodarone contains a very high concentration of iodine and can cause hyperthyroidism through two different mechanisms: inducing excessive hormone production (Type 1) or damaging the thyroid gland (Type 2). Regular monitoring of thyroid function is essential for patients on this drug.

Immune checkpoint inhibitors used in cancer treatment can cause an autoimmune thyroiditis. This process often begins with a hyperthyroid phase due to the release of stored hormones, followed by a hypothyroid phase as the gland is damaged.

The Jod-Basedow effect refers to iodine-induced hyperthyroidism. It occurs when an excess amount of iodine, from sources like iodinated contrast media or high-dose supplements, triggers hormone overproduction in individuals with pre-existing thyroid conditions, such as a goiter.

Yes, lithium use requires monitoring for thyroid dysfunction. While hypothyroidism is more common, lithium can also rarely cause hyperthyroidism, sometimes by inducing Graves' disease or thyroiditis. Your doctor will typically check your thyroid function periodically.

No. While iodine is necessary for thyroid function, excess intake, such as from kelp supplements, can trigger hyperthyroidism in susceptible individuals. It's advisable to speak with a doctor before taking any iodine-rich supplements.

Treatment depends on the underlying cause. It may involve discontinuing the causative drug, using beta-blockers for symptom control, anti-thyroid drugs for excess hormone synthesis, or corticosteroids for destructive thyroiditis. Close medical supervision is required.