Last Updated on April 26, 2026
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In early 2020, the COVID-19 pandemic hit and reshaped daily life across the world. Over half a decade later, we’re still learning what it left behind.
For people with or without pre-existing thyroid conditions, it’s important to understand how COVID-19 can affect thyroid health, both during the acute infection and in the months that follow.
In this article, we will learn about long COVID, but from a thyroid perspective.
First, what do we mean by “long COVID”?
You’ve probably heard the term “long COVID” and wondered what it really means. In simple terms, it refers to ongoing or returning symptoms that last well beyond the initial infection.
According to the National Academies (NASEM) and the Center for Disease Control (CDC), long COVID is defined as a chronic condition that persists for three or more months after SARS-CoV-2 infection, with symptoms that can fluctuate or remain constant over time. SARS-CoV-2 is the name of the virus that causes the coronavirus 2019 disease (also known as COVID-19, or more colloquially as just COVID).
Also known as post-acute sequelae of SARS-CoV-2 infection (PASC), long COVID can involve a wide range of symptoms: from fatigue, shortness of breath, and heart palpitations to brain fog, muscle or joint pain, mood changes, and sleep problems. Importantly, a positive test isn’t required for diagnosing long COVID.
Because the thyroid regulates metabolism, energy, and heart rate, any thyroid dysfunction can worsen or mimic many of these same complaints. Interestingly, this overlap is especially pronounced in cases of hypothyroidism (including Hashimoto’s disease), where fatigue, weight changes, and brain fog already occur.
So, in case you are wondering if COVID-19 can affect the thyroid, the short answer is yes (and in more ways than one).
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Download ThyForLife for FreeHow can COVID‑19 affect the thyroid?
There are several ways in which the SARS‑CoV‑2 and the body’s response to it can influence the thyroid gland and thyroid hormone system.
Here are the some major mechanisms identified so far:
1. Direct viral effects on thyroid cells
Current and past research (including a study published in the Journal of Endocrinological Investigation in 2020) have shown that the thyroid gland contains the same entry points that SARS-CoV-2 uses to invade cells: the ACE2 receptor and the TMPRSS2 enzyme. This means the virus may be able to directly infect or injure thyroid follicular cells, leading to inflammation of the gland (known as thyroiditis). Such inflammation can temporarily disrupt hormone production.
2. Inflammation and cytokine storm
In more severe COVID-19, the immune system can release high levels of inflammatory molecules (cytokines such as IL-6 and TNF-α). This hyperinflammation can disrupt the hypothalamic–pituitary–thyroid (HPT) axis (which regulates thyroid hormone production) and change the activity of deiodinase enzymes that process thyroid hormones. The usual effect is less conversion of T4 (a less-potent precursor) into active T3 and more conversion into inactive forms (rT3). The result may be temporary changes in thyroid hormone levels, even when the thyroid gland itself isn’t directly infected.
3. Medication and treatment effects
Some of the medications used during COVID-19 (such as corticosteroids, antivirals, and immune-modulating drugs) can temporarily influence how the thyroid works or how thyroid hormones are processed in the body. Corticosteroids, for instance, can lower TSH levels and reduce the conversion of T4 to the more active T3, while certain antivirals and immune therapies may indirectly affect hormone metabolism. Severe illness itself can also temporarily change thyroid-binding proteins and deiodinase enzyme activity, causing mild lab abnormalities even when the thyroid gland is normal.
Post-COVID thyroid dysfunction has also been extensively documented worldwide
Research and systematic reviews show that people recovering from COVID-19 can develop subacute thyroiditis, autoimmune thyroid disease, or non-thyroidal illness syndrome. Most of these thyroid changes appear to be temporary, though some cases, particularly autoimmune forms, may persist and require ongoing monitoring.
1. Subacute thyroiditis (SAT)
Subacute thyroiditis is a painful, inflammatory thyroid condition often following viral illness. It tends to follow a three-phase course that comprises the following:
- A hyperthyroid phase of 1–6 weeks. Symptoms include anxiety, tremor, palpitations, and heat intolerance.
- A hypothyroid phase that occurs weeks to months later. Symptoms include fatigue, weight gain, and cold intolerance.
- A recovery phase where most people return to euthyroid within months, but some develop persistent hypothyroidism.
In recent years, especially since 2023, several medical reviews have reported cases of SAT after COVID-19 infection (and rarely after vaccination). In many cases, typical signs of SAT following COVID include neck pain, fever, and fatigue. Doctors often find signs of inflammation in blood tests and may see mild swelling or darker (“hypoechoic”) spots on thyroid ultrasound. Fortunately, most people recover fully with rest, anti-inflammatory medication, or short courses of steroids for pain or severe inflammation.
2. Autoimmune thyroid disease (AITD)
After SARS-CoV-2 infection, autoimmune changes can occasionally unmask new Graves’ disease or exacerbate pre-existing AITD. Case reports include patients long stable with Hashimoto’s who developed post-COVID Graves’ hyperthyroidism. This pattern seems consistent with infection-related immune dysregulation; some proposed mechanisms underlying this include molecular mimicry and bystander activation. Simply put, scientists think this may happen through processes like the virus “mimicking” thyroid tissue and by over-activating immune cells. Most reported post-COVID Graves’ cases respond to standard therapy (such as methimazole) similar to usual care.
3. Non-thyroidal illness syndrome (NTIS)
Sometimes called “euthyroid sick syndrome,” NTIS refers to temporary thyroid hormone changes that happen during or after serious illness, including COVID-19. In moderate to severe cases, levels of free T3 (FT3) often fall, while TSH may be low, normal, or slightly high, and free T4 (FT4) tends to stay in the normal or low-normal range.
These changes don’t mean the thyroid gland is failing; instead, they instead reflect how the body adapts to severe stress and inflammation by reducing energy use during illness. As patients recover, thyroid hormone levels typically return to normal on their own. Because these abnormalities are usually transient, routine thyroid testing during hospitalization isn’t recommended unless symptoms strongly suggest true thyroid disease.
An overview of findings and insights from the research research on thyroid issues during and after COVID
Research findings from studies on the acute phase of COVID
- A 2020 study of 287 hospitalized COVID‑19 patients in Italy found that about 20% had lab tests consistent with hyperthyroidism (low TSH) and about 5% with hypothyroidism (high TSH) during acute infection.
- A systematic review published in the BMC Endocrine Disorders journal in 2024 found a prevalence of about 26% of NTIS and about10% of thyrotoxicosis among COVID‑19 patients.
- Research has also shown that thyroid hormone abnormalities are more likely with more severe COVID‑19 illness.
Research findings from studies on the post-COVID phase
- A 2024 Cureus review titled “Long-Term Impacts of COVID-19 on Thyroid Health” reports that while much dysfunction appears transient, there is evidence of longer‑term thyroid abnormalities, including persistent hypothyroidism and exacerbation of pre‑existing autoimmune thyroid disease.
- In a large cohort study from China, among patients with pre‑existing autoimmune thyroid disease (AITD) and COVID‑19, thyroid hormone levels (FT3 and FT4) were lower initially and TSH/thyroid antibodies increased over the following 3–6 months.
- There is also evidence suggesting that the incidence of new autoimmune thyroid disease may have increased post COVID. For instance, a single-center, prospective study in Italy found about double the rate of autoimmune thyroid disease in COVID survivors versus expected.
- However, some recent large population‑based studies found little evidence for persistent thyroid dysfunction attributable to COVID in the long term. For example, one population‑based cohort in Hong Kong reported that COVID‑19 was unlikely to be associated with persistent thyroid function changes.
What do these findings mean?
Overall, the available research suggests that many thyroid abnormalities seen in acute COVID are transient. For instance, as mentioned earlier, thyroiditis triggered by SARS-CoV-2 can cause a temporary thyrotoxic (high hormone) phase, followed by a hypothyroid phase, and then recovery. Some survivors may have persistent or new onset thyroid disease. These cases, however, appear uncommon and typically occur in people with genetic or autoimmune susceptibility or more severe infection. For many people with long COVID, the thyroid may not be the main cause of symptoms, but testing can be helpful when symptoms (such as fatigue, palpitations, and brain fog) overlap.
Practical advice for thyroid patients after COVID
- Ensuring good nutrition (including anti-inflammatory foods), adequate sleep, managing stress, and gentle graded exercise (as tolerated) can support your overall recovery and thyroid health.
- If you develop new neck pain or swelling after COVID, new palpitations, tremors, weight loss (symptoms suggestive of thyrotoxicosis), or new cold intolerance, weight gain, constipation (symptoms suggestive of hypothyroidism), these patterns merit evaluation by your doctor.
- If your doctor finds mild thyroid abnormalities (such as low T3 or slightly low TSH) in the post‑COVID period, this may be part of the “recovery from ill‑health” pattern rather than permanent thyroid disease. So, it’s best to avoid jumping into conclusions without talking to your doctor about your health status.
- Track symptoms over time to notice patterns. You can do this by keeping a simple log of symptoms (fatigue level, heart rate, weight, cold/heat intolerance, mood, neck discomfort). This can help your doctor decide whether thyroid testing or treatment is needed.
Download the ThyForLife app today to track your symptoms easily.
FAQs
Yes. Post-COVID thyroiditis and hypothyroidism have been reported even in previously healthy individuals.
It can unmask or trigger autoimmune thyroid disease in a minority of people, or leave a temporary hypothyroid phase after SAT. Most cases normalize, but some need ongoing levothyroxine.
No. Long COVID remains a clinical diagnosis, and no single biomarker reliably confirms it. Thyroid testing helps rule in/out thyroid causes of overlapping symptoms.
