Medications and the Thyroid: Mechanisms and Management

This transcript has been edited for clarity.

Kaniksha Desai, MD: Welcome to the Thyroid Stimulating Podcast. This podcast was created in partnership with the American Thyroid Association to discuss up-to-date diagnosis and management of a wide array of thyroid diseases. I'm your host, Dr Kaniksha Desai.

Today we're going to be discussing medications and the thyroid gland. Medications are frequently and clinically significant contributors to thyroid dysfunction, yet their impact is often underrecognized in routine clinical practice.

A wide range of commonly prescribed medications, including cardiovascular medications, psychiatric medications, oncologic medications, and even endocrine therapies, as well as supplements, can alter the thyroid physiology, affect laboratory interpretation, or even change the dose of levothyroxine requirement.

In this episode, we'll review the mechanisms, clinical presentations, and management strategies for medication-associated thyroid effects, with an emphasis on practical evidence-based approaches that you can take in your own clinical practice. Our goal is to equip clinicians with tools to accurately recognize, monitor, and manage these interactions in everyday patient care.

I'm thrilled to welcome Dr Jacqueline Jonklaas, a nationally recognized leader in thyroid disease and clinical endocrinology. She's a professor in the Division of Endocrinology at Georgetown University, where her work spans patient care, research, and education, with a particular emphasis on hypothyroidism and optimizing thyroid hormone therapy.

Dr Jonklaas served as the co-author of the American Thyroid Association hypothyroidism treatment guidelines in 2014 and is currently an author of the upcoming updated guidelines in progress. She received the American Thyroid Association Distinguished Service Award in 2020 and most recently served as president of the American Thyroid Association, from 2024 to 2025.

Today she joins us to discuss the impact of medications on the thyroid gland, a topic with wide-reaching implications for clinicians and patients across many areas of medicine. Thank you so much for joining us today, Dr Jonklaas.

Jacqueline Jonklaas, MD, PhD: Thank you very much for the invitation. As you outlined, I think this is a critically important topic that affects everyone taking thyroid hormones.

Desai: Let's get started by defining drug-induced thyroid dysfunction for our audience.

Jonklaas: It's a complex topic. There's a large number of different drugs that can affect thyroid function, and they can do it at a number of different levels.

They can alter transport or metabolism of thyroid hormone, they can affect the synthesis or the release of thyroid hormone, or they can alter the secretion of TSH. They can also alter the absorption of thyroid hormone in someone who's actually being treated with thyroid hormone. And just to complicate the situation, some drugs can do more than one of these things.

Desai: We often look at a drug effect causing hypo- or hyperthyroidism, so, underactive or overactive thyroid. What do you think is most common with medications? Are they more likely to cause hypo- or hyperthyroidism?

Jonklaas: Generally, drug-induced hypothyroidism is more common than drug-induced hyperthyroidism. Also, luckily for us, I think drug-induced hypothyroidism is usually easier to treat than drug-induced hyperthyroidism.

Desai: We'll be talking about both of those — how to treat them and how to deal with the medication. The first medication I wanted to get started with is a cardiac medication, amiodarone. Many patients with cardiac disease maybe started on this medication. How does amiodarone alter thyroid physiology?

Jonklaas: Amiodarone is one of those very complex drugs that can affect thyroid levels without really causing thyroid dysfunction, or it can cause hypothyroidism or hyperthyroidism. For the effect, it has to affect thyroid function without actually usually causing clinical disturbance in thyroid function. It inhibits thyroid hormone entry into cells, inhibits type I and type II deiodinase, and decreases T3 binding to its receptor.

The net effect in someone who has normal thyroid function is that TSH increases, and then gradually over time, maybe about 6 months or so, returns to baseline. T3 levels tend to remain a little below baseline and T4 levels tend to remain elevated, but usually the patient is clinically euthyroid. I can also describe the hypo- and hyperthyroidism effects.

Desai: Let's go through each of them. This is a great medication because we get to go through abnormal thyroid function, both how it causes hypothyroidism and how it causes hyperthyroidism. We talked about the abnormal thyroid function test, which you mentioned was the higher free T4, lower T3, and a normal TSH.

Jonklaas: Right. Amiodarone can also have intrinsic drug effects through cytotoxicity to thyroid cells, resulting in destructive thyroiditis. That's a direct drug effect, but also it can have iodine-like induced effects. It can precipitate hypothyroidism in patients with underlying Hashimoto's disease through failure to escape from the Wolff-Chaikoff effect, or it can alternatively produce hyperthyroidism by fueling production of thyroid hormone in patients who have autonomous nodules or latent Graves disease. It’s very complex.

Desai: I think the question most clinicians have is whether this is reversible, and do you just stop the amiodarone or do we treat through it?

Jonklaas: In general, the hypothyroidism can be treated. You can place the patient on thyroid hormone and you don't necessarily need to stop the amiodarone, but I think the thyrotoxicosis is a little more problematic. It also depends on the type of thyrotoxicosis that has been induced.

For type 1 thyrotoxicosis, which is induced by the iodine component, this will cause thyrotoxicosis in someone who has preexisting thyroid disease. It can be diagnosed by thyroid scanning and color Doppler sonography. Generally with the type 1, you'll see low or normal uptake on the thyroid scan and uptake, and the color Doppler shows increased flow within the gland. That can be treated with thionamides. I think that's, on the whole, easier to treat.

For type 2 thyrotoxicosis in which there's typically no uptake on a thyroid scan and there's decreased flow within the gland by color flow Doppler, that would need prednisone as the best treatment.

In practice, it's not so easy sometimes to tell what you're dealing with, whether it's type 1 or type 2. Sometimes in practice, in the moment, you can't really distinguish between the two entities. Physicians may end up using both thionamides and prednisone as dual treatment until things are sorted out.

Desai: I think it's important to consult with cardiology also and make sure that the patient is appropriately treated for their cardiac disease. Short term, stopping the medicine isn't really going to reverse the damage.

Jonklaas: Exactly. There's a huge iodine load when you administer amiodarone, so just stopping the medication doesn't reverse the iodine load.

Desai: Our second medication, which I think is also commonly used, is lithium. Lithium also has a very interesting impact on the thyroid gland, as it can cause hypo- and hyperthyroidism as well. Can we start with how lithium causes hypothyroidism?

Jonklaas: You hit the nail on the head. Lithium's another one of those complex drugs with multiple actions on the thyroid. I think there are some analogies to the effect of amiodarone and iodine. Lithium can inhibit the synthesis and release of thyroid hormone from the thyroid gland. This can be accompanied by a compensatory increase in TSH and development of a goiter, which may occur in about 50% of patients who are being treated with lithium. Over time, in some of these patients, that can evolve into overt hypothyroidism, maybe 20% or so of patients, especially in those with underlying Hashimoto’s thyroiditis.

Because of this, thyroid function should be monitored, maybe annually, particularly in individuals who have positive thyroid peroxidase antibodies. Lithium-induced hypothyroidism is very amenable to treatment with levothyroxine. If the lithium is of benefit for the underlying psychiatric disease or depression, it doesn't need to be discontinued. Quite rarely or much more rarely, lithium can cause a destructive thyroiditis that's much more difficult to treat, but luckily, that's not very common.

Desai: For both these medications, amiodarone and lithium, you would recommend, ideally, baseline thyroid function tests prior to starting and maybe even some TPO antibodies or TSI antibodies prior to starting?

Jonklaas: Yes. I think both of those things are wise, and then monitoring as the drug continues and providing patient education about what to expect in terms of if new symptoms develop. The time course of many of these drugs is not always very predictable, so continued monitoring is important.

Desai: To switch to a third medication, I wanted to talk about some oncologic medications as well. I know we have a whole podcast episode on checkpoint inhibitors, but I was going to talk about medications and only briefly mention the checkpoint inhibitors. If you were on a checkpoint inhibitor for the management of your cancer, what are some of the common thyroid changes that you might see?

Jonklaas: Checkpoint inhibitors, particularly PD-L1/PD-1 and PD-L2/PD-1, can cause thyroid dysfunction, which can occur in maybe 20% of patients. It's usually a biphasic thyroid disorder with a thyroiditis and thyrotoxicosis, followed by evolution into hypothyroidism or, alternatively, that can be isolated hypothyroidism, and the mechanism seems to be a T cell-mediated immune response. Thyroid autoantibodies can be present at baseline or they may develop after the use of the checkpoint inhibitors.

The onset of the thyroid disease is usually early, within the first few weeks after therapy, but it can occur later, too. The preexisting thyroid autoimmunity is a risk factor. Again, like we mentioned for amiodarone and lithium, monitoring of thyroid function is important, and probably with these drugs, maybe monthly monitoring. I think this is where working with our oncology partners is important, as they would be key in monitoring for the development of thyroid dysfunction.

Desai: When we're talking about medications, another big group is tyrosine kinase inhibitors that are used for targeted chemotherapy for many different cancers, not only thyroid cancer. Do you recommend TSH screening for these patients on tyrosine kinase inhibitors?

Jonklaas: Definitely, because of the effects. If patients do develop hypothyroidism, you have a patient who's getting a fairly toxic therapy anyway, and they'll feel considerably worse if they develop thyroid disease. Yes, I would recommend monitoring, particularly because the spectrum of effects the tyrosine kinase inhibitors can have is very varied according to whether it's a multikinase inhibitor or one of the more selective RET inhibitors.

They can damage follicular cells by disrupting the vasculature of thyroid cells. They can also inhibit iodine uptake and they can increase thyroid hormone metabolism and result in increased TSH, decreased T4, and decreased T3, and a decreased T3 to T4 ratio. Because of all these actions, I completely agree there should be regular monitoring of thyroid function, potentially on a monthly basis or with every cycle of therapy, depending on what the particular therapy is.

Desai: Most of those can be treated with levothyroxine. Can you talk a bit about the RET inhibitors and why they're a little different?

Jonklaas: Some of the multikinase inhibitors, like vandetanib, block VEGF and may impair thyroid blood flow and cause capillary regression with thyroiditis, whereas the selective RET inhibitors — selpercatinib may be a good example — act primarily through impairing peripheral metabolism of thyroid hormones. It’s a different mechanism of action with those newer drugs.

Desai: Do you use different thyroid hormone replacements for RET inhibitors that you would not use for VEGF?

Jonklaas: Obviously, if someone develops hypothyroidism, our standard of care is levothyroxine. There is a school of thought that for the RET inhibitors, because they have a stronger action to decrease T3 more than T4, maybe this is a case where combination therapy may be particularly helpful because these patients do have a low T3. I'm not sure it's made it into any official guideline, but definitely the combination therapy would fit the profile of the decreases in thyroid hormone that you see with those particular drugs.

Desai: We can't not talk about biotin. That's the last medication that I have. There was a huge 5-year period where biotin was, and still may be, impacting thyroid function tests. Can you talk a little bit about biotin and what its role is in the thyroid?

Jonklaas: Biotin can interfere with a number of different lab tests, not just thyroid, so it's a very pervasive effect. The recommended daily allowance of biotin is in the microgram range, and some of the biotin supplements that are available over the counter have very large doses in milligrams.

These high doses of biotin can cause errors in assays that use a biotin-streptavidin signaling system. Biotin has a potential to cause a large amount of clinical confusion, as it can lead to a false-positive or a false-negative result, depending on whether the assay being used is a competitive assay or a sandwich assay.

As far as thyroid tests, biotin causes a false negative for the TSH assay, so TSH would be erroneously picked up as low, whereas it has a false-positive effect on free T4 and T3, so you have an erroneously high value. These large doses of biotin not only cause the low TSH, but they cause high thyroid hormone levels. Furthermore, they can cause falsely high measurements for the TSH-stimulating receptor antibodies.

All of that will combine to look like a diagnosis of Graves disease, when there is no such diagnosis. Luckily, all those laboratory abnormalities will resolve with discontinuation of the biotin. It can be withheld for 2-5 days before doing blood tests. The other option is to do the thyroid blood tests by an alternative assay method that doesn't use that biotin-streptavidin signaling system. There are ways to correctly measure the thyroid blood test.

Desai: Just to be clear, it's not actually causing anything to happen to the thyroid gland; it’s just causing the results of the lab tests.

Jonklaas: Yes. The patient is clinically euthyroid, but the lab tests look like the patient has hyperthyroidism. It's all in the lab or in the test tube. It's not in the patient.

Desai: Can you share some pearls on what would make you think to ask the patient? Sometimes patients aren't very forthcoming that they're taking supplements, so it can be a surprise.

Jonklaas: I think it's difficult, but if you have a patient who clinically just looks completely euthyroid and yet their numbers are kind of off the wall when you get them back from the lab, talk to the patient, share the thought that maybe something is being mismeasured in the labs, and ask them what they're taking.

I agree that sometimes patients don't necessarily even think about the biotin they’re taking for hair loss or whatever. The good thing about biotin is you don't have to stop it for too long to get your blood test, so it's not onerous to the patient. If they really want to take the biotin, they can go back on it once the blood test has been obtained.

Desai: For the second half, I want to talk a little bit about patients who are hypothyroid for whatever reason, such as a total thyroidectomy or Hashimoto's, and they are on levothyroxine, but now we add another medication for a different disease state. How do we manage thyroid hormone replacement when we're adding or subtracting other medications? This is a common issue that comes up, and oftentimes we forget about it or we don't necessarily think about it in the forefront. It's not a direct drug interaction, but medications sometimes need to be readjusted.

One of the most common things, especially because thyroid diseases are common in women and there's a huge push for hormone replacement therapy in postmenopausal women, is how does estrogen impact the thyroid hormone?

Jonklaas: Sex hormones can alter levothyroxine requirements in patients who are being treated for hypothyroidism, as you outlined, by affecting the thyroxine-binding globulin, or TBG, that transports thyroid hormone in the circulation. Estrogen therapy will increase the TBG such that circulating total thyroid hormone may increase, but with a decrease in free T4 and an increase in TSH.

When someone starts on estrogen or hormone replacement, the levothyroxine dose that the patient is taking may need to be increased to maintain the same serum TSH, and actually the opposite theoretically occurs with androgens, which decrease the TBG, can increase free T4, and potentially lead to a reduced requirement for levothyroxine.

Desai: Let's say that a patient is starting estrogen. Do you automatically increase the dose or do you wait and get labs?

Jonklaas: I don't usually make an adjustment upfront because the effect can be a little bit variable. Some patients may not really need much of a dose adjustment. I think it's better, if a patient is contemplating starting estrogen, to just alert them that we may need to change their dose of thyroid hormone, and perhaps schedule them for some blood tests after they've been on the estrogen for a few months to recheck and adjust. I wouldn't normally make a dose adjustment ahead of time just because it varies from patient to patient.

Desai: Since we're on the topic of hormones, and we already talked about estrogen and testosterone, what about growth hormone?

Jonklaas: Growth hormone seems to lower free T4 levels by increasing the conversion of T4 to T3. When you have someone who is growth hormone-deficient and they're started on growth hormone, their levothyroxine dose may need to be increased when the growth hormone is started.

Desai: It’s different with each of the medications. It's important, especially in the panhypopituitarism patients, that you're considering multiple hormone replacements and to keep a close eye on these patients in the beginning until they get well regulated on all their hormones together.

Jonklaas: Right, exactly.

Desai: Another big category of medications that is very commonly being used currently is GLP-1 receptor agonists. There's a big hype about these medicines. How do they affect thyroid function, directly or indirectly, and what can we do about that?

Jonklaas: Yes. There is a large amount of literature about these agents. They do affect thyroid gland volume and potentially affect TSH, but I don't really think it's well understood. I think the challenge we have is that there are data about thyroid cancer. Multiple large studies and meta-analyses have found no significant link between GLP-1 use and increased risk for differentiated thyroid cancer compared with other diabetes drugs. I think the early observational data suggested an increase in medullary thyroid cancer rates, but later analyses pointed more to detection bias, with more monitoring and people taking the GLP-1 agonists, or very low absolute numbers.

While the theoretical risk exists due to the animal data, more robust recent human studies have shown that these agonists generally don't increase thyroid cancer risk in most people, but with the FDA caution primarily existing for those with preexisting medullary thyroid cancer risk factors.

However, probably the effect of these agents that we're seeing more, perhaps in our practice, is the effect on thyroid hormone or levothyroxine requirement being mediated by the weight loss that patients may experience.

Desai: How much do you have to lose to get an adjustment?

Jonklaas: As a rule of thumb, weight changes of roughly more than 10% may affect levothyroxine dose requirements. If someone taking levothyroxine loses weight with a GLP-1 agonist, they are likely to need a reduction in their levothyroxine. Conversely, if someone stops a GLP-1 agonist and regains weight, they may require a dosage increase. The thing to remember is that levothyroxine requirement is more closely linked to lean body weight as opposed to actual body weight.

Sometimes the alterations in dose requirements may not be quite as large as we expect. Certainly, this is something we've all seen — that people suddenly become overreplaced on their thyroid hormone if they've lost substantial weight.

Desai: The other interesting part, and I don't know if you've seen this in your practice, is that the GLP-1 mechanism slows everything down. It increases the risk for gastroparesis. Is there any change in the absorption of thyroid hormone on these medications?

Jonklaas: I haven't seen robust data on that, but maybe as we get more information, that will be another component of the complexity that we will be faced with.

Desai: It's even more complicated in patients who have gastric sleeve or gastric bypass surgery because their absorption changes on top of the weight loss.

Jonklaas: Right. You have the two components. Exactly.

Desai: People don't necessarily think about antibiotics impacting thyroid hormone. I recently had a patient on rifampin for indolent tuberculosis that he tested positive for, and interestingly, I had to adjust his dose of thyroid hormone. Can you talk a little bit about how antibiotics, such as rifampin, affect the metabolism of thyroid hormone?

Jonklaas: I think some antibiotics, like fluoroquinolones, can decrease absorption of levothyroxine. The tetracycline type of antibiotics can interfere with thyroid uptake. In regard to antibiotics that interfere with thyroid hormone metabolism by inducing hepatic enzymes, obviously that can increase levothyroxine requirement.

The drug you mentioned, rifampin, is kind of a classic example in the literature. It can increase levothyroxine metabolism and dramatically increase thyroid dose requirement. Then, once that antibiotic has discontinued, the requirement would return to baseline. I think the best way to adjust levothyroxine dose in these types of circumstances is to make increases as necessary, based on the TSH level.

Again, patient education would be key as a patient gets started on these medications, and monitoring for potential impact.

Desai: Usually antibiotics are very short duration. I don't think people necessarily consider it, as it's like 7-10 days, so maybe that might not have the same impact. This interesting situation arose because for tuberculosis, you need to be on it for months and months.

Can you talk a little bit about proton pump inhibitors, or PPIs? This is a common medication that many people are on, and you can get it over the counter without a prescription these days. How does this impact levothyroxine absorption?

Jonklaas: An acidic environment in the stomach seems to optimize levothyroxine absorption in the small intestine. When PPIs are introduced, they're often associated with TSH levels increasing above the normal range. I think the issue is that many of these PPIs that we use these days are long-acting, so separating the time of intake of levothyroxine from the time of intake of the PPI doesn't generally fix the problem. I think the best approach is to increase the dose of levothyroxine to compensate for the reduced absorption and base the adjustment on normalizing the patient's TSH.

Some people do advocate — and it's not something I've tried routinely — switching to liquid levothyroxine preparations, as their absorption may be less affected by stomach acidity than the tablets. That might be another option.

Desai: It’s a different approach, right? You can change the dose or you can switch to liquid. That transitions us into supplements of iron and calcium. These medications are known to bind thyroid hormone significantly. Can you talk a little bit about the timing of taking medications?

Jonklaas: Iron and calcium are really among the most significant culprits in reducing levothyroxine absorption. It seems that the levothyroxine is adsorbed to the calcium and iron. It seems to make these kind of insoluble complexes with the levothyroxine in the stomach, leading to the 20%-50% decrease in absorption that you see.

The recommendation is to take these, the levothyroxine and the supplements, 4 hours apart. That's tough because if patients are taking their levothyroxine in the morning, they then have to remember to take their supplements around lunchtime or something. One option that I think may work better in some patients is to take the calcium and the iron in the evening. You definitely do need to separate those two.

Desai: It's hard on patients who have hypoparathyroidism. Do you sometimes just give a higher dose of thyroid medicine if it's needed?

Jonklaas: Yes, I think that's another approach. One thing you'd have to assess is that you want everything to remain as consistent as possible. If you have a patient who sometimes takes their calcium and iron but doesn't always, and you increase the dose, you may have some fluctuation. If a patient has a regular schedule, is always going to take the calcium and iron, it would be another approach to just increase the dose as needed.

Desai: I think they do that in pediatrics a little more than we consider doing in the adult world, just because it's harder. But it is an option, especially if, as you mentioned, there's consistency.

In general, when do you recommend checking thyroid hormone tests if you have a new medication that's added or if you stop a medication? Do you check it a week later? Do you check it 2 months later?

Jonklaas: If you're reassessing thyroid function, particularly if it's after a dose adjustment in the thyroid medication, you would need about 4-6 weeks to get to a new steady state because of the half-life of the levothyroxine. I think rechecking after about 6 weeks is reasonable. If you're rechecking because of a new medication, depending on what the medication is, maybe a month later or 2 months later. If you've adjusted the levothyroxine dose, about 6 weeks later is reasonable.

Desai: For our listeners, what are three takeaway points to remember about the impact of drugs on levothyroxine dosing?

Jonklaas: Educating patients because patients are their own best advocates. Educating patients about what they can potentially expect or what they should be alert for with new medications is important.

Also, closely working with our colleagues, whether it be primary care physicians, oncologists, or gastroenterologists. It's the oncologists, for example, who are monitoring for side effects of some of their therapies, and then they may refer to us when the patient develops a thyroid problem. We have to work hand in hand with those other specialists.

Another point is that it's very hard to give patients, or even ourselves, a rule of thumb about some of these medications because they have a very varying impact and the time course may be very different. Some people may develop thyroid dysfunction a few weeks after a particular drug, and for other patients, it's a much later effect. Just being alert for the need for continued monitoring is important. Also, if you've adjusted your thyroid hormone because of a medication, you have to also remember that, when the medication is discontinued, you may need to readjust.

The only other thing I would say is that it's generally reassuring that drug-induced hypothyroidism is more common than thyrotoxicosis because that's definitely easier for us to manage. I think the condition that is much harder, which luckily is less common, is drug-induced thyrotoxicosis.

Desai: Thank you for joining us today. I really appreciate you taking the time to come and talk with me about this.

For our listeners, medications can influence the thyroid in multiple ways, as Dr Jonklaas mentioned, including altering thyroid hormone production, triggering inflammation, or interfering with lab assays. Changing levothyroxine absorption or metabolism is also an issue for patients who are on thyroid hormone replacement for their hypothyroidism.

The important part is that recognizing these interactions early helps prevent misdiagnosis and unnecessary treatment changes. In summary, very clear communication, thoughtful monitoring, and patient education are key to optimizing thyroid care in these complex medical landscapes.

Stay tuned for our next episode, where we'll explore thyroid health and aging, and what clinicians need to know as patients move across their lifespan.

Cite this: Kaniksha Desai, Jacqueline Jonklaas. Medications and the Thyroid: Mechanisms and Management - Medscape - Mar 25, 2026.