Thyroiditis refers to inflammation of the thyroid gland. It can be caused by an infection, autoimmune response, radiation exposure, or medication side effects. Some types of thyroiditis are short-lived and resolve on their own, while others can lead to permanent hypothyroidism if not treated properly.
The SARS-CoV-2 virus that causes COVID-19 has been associated with various extrapulmonary manifestations, including effects on the endocrine system. Some studies have found that COVID-19 may trigger subacute thyroiditis, an inflammatory condition that causes neck pain and thyrotoxicosis (excess thyroid hormone production). However, the data so far is limited.
In this article, we will examine the current evidence on whether COVID-19 can trigger thyroiditis. We will cover:
- What is thyroiditis?
- Types of thyroiditis
- Mechanisms by which viruses may trigger thyroiditis
- Data on COVID-19 and subacute thyroiditis
- Case reports linking COVID-19 and thyroiditis
- Limitations of current studies
- Conclusions on the association between COVID-19 and thyroiditis
Understanding this relationship is important for managing thyroid-related complications in COVID-19 patients. Prompt diagnosis and treatment of thyroiditis can help improve outcomes.
What is Thyroiditis?
The thyroid gland is a small, butterfly-shaped organ located at the base of the neck. It produces thyroid hormones (triiodothyronine/T3 and thyroxine/T4) that regulate metabolism, growth, development, and other important functions.
Thyroiditis refers to inflammation of the thyroid gland, which disrupts normal thyroid hormone production. The inflammation impairs the thyroid follicles’ ability to make and store thyroid hormones. It may also damage thyroid cells and cause them to leak stored hormones into the bloodstream.
There are several potential causes of thyroiditis:
- Viral infections: Viruses are a common cause of subacute thyroiditis. The mumps virus is a frequent culprit, but others like influenza A and B, adenoviruses, echoviruses, and SARS-CoV-1 have also been implicated.
- Bacterial infections: Bacteria such as tuberculosis, syphilis, and borreliosis can, in rare cases, infect the thyroid and cause inflammation.
- Autoimmune response: Hashimoto’s thyroiditis results from an autoimmune attack on the thyroid.
- Radiation exposure: Radioactive iodine treatment or radiation therapy for cancers like lymphoma can damage the thyroid and cause inflammation.
- Medications: Certain medicines like interferon-alpha, interleukin-2, lithium, amiodarone, and checkpoint inhibitors may trigger thyroiditis.
- Infiltrative diseases: Amyloidosis, sarcoidosis, and hemochromatosis can cause thyroiditis when abnormal deposits build up in the gland.
The symptoms and clinical course of thyroiditis depend on the underlying cause. But common features include neck pain, thyroid gland swelling and tenderness, fatigue, weight changes, and signs of hyperthyroidism like rapid heartbeat, anxiety, tremors, sweating, and sensitivity to heat.
Types of Thyroiditis
There are several distinct types of thyroiditis with different mechanisms and clinical presentations:
Subacute Thyroiditis
Subacute thyroiditis, also called subacute granulomatous thyroiditis or de Quervain thyroiditis, is the type most commonly associated viral infections. It often follows an upper respiratory illness.
The usual course is 1-3 months of thyrotoxicosis, followed by 4-8 weeks of hypothyroidism before normal thyroid function returns. Neck pain is a prominent symptom. Low-grade fever and enlarged, tender thyroid gland may be present on exam. Sedimentation rate and thyroid hormone levels help confirm the diagnosis.
NSAIDs and steroids treat symptoms and shorten disease duration. Beta-blockers control hyperthyroid symptoms. It usually resolves spontaneously but can become chronic in some cases. Recurrences happen occasionally.
Silent Thyroiditis
Silent thyroiditis, or painless thyroiditis, also has viral triggers. It is similar to subacute thyroiditis but lacks inflammatory symptoms like neck pain and tenderness. Patients usually have mild hyperthyroidism for 1-3 months before developing temporary hypothyroidism. Diagnosis is made by lab tests and ultrasound or radionuclide scanning. Treatment involves symptom relief and monitoring thyroid function.
Postpartum Thyroiditis
Postpartum thyroiditis occurs in 5-9% of women within 12 months after giving birth. Symptoms are mild but 60% have long-term hypothyroidism. The cause is autoimmune and it is associated with positive anti-TPO antibodies. Treatment depends on the phase – thyroid hormone if hypothyroid or beta-blockers if hyperthyroid.
Drug-Induced Thyroiditis
Some medications can trigger thyroid inflammation and dysfunction, most commonly interferon and amiodarone. Onset occurs within the first 3-6 months of therapy. Restoring euthyroidism with thyroid hormone replacement may allow the drug to be continued under close monitoring. Stopping the drug leads to recovery in most cases.
Radiation Thyroiditis
Radiation treatment for cancers like Hodgkin’s lymphoma can damage the thyroid, causing inflammation and hypothyroidism. Onset is usually within the first year post-radiation. Thyroid hormone replacement is needed lifelong in most cases.
Acute Thyroiditis
Acute suppurative thyroiditis is very rare. It results from a bacterial infection of the thyroid gland, more commonly in children. Symptoms include fever, neck pain and swelling, and dysphagia. Intravenous antibiotics are used to treat the infection.
Hashimoto’s Thyroiditis
Hashimoto’s thyroiditis is an autoimmune disease and the most common cause of hypothyroidism in the US. It occurs when the immune system mistakenly attacks and slowly destroys the thyroid. Genetic factors make some people more prone. Symptoms are initially mild but worsen over time as thyroid damage accumulates. Levothyroxine replacement therapy is required lifelong.
Riedel’s Thyroiditis
Riedel’s thyroiditis is a very rare chronic fibrotic form of thyroiditis. It is not well understood but involves invasion of the thyroid by fibrous tissue, leading to a wooden, hard goiter. Hypothyroidism develops over time. Treatment is with tamoxifen or steroids to reduce fibrosis, along with thyroid hormone replacement.
Mechanisms by Which Viruses May Trigger Thyroiditis
Viruses are among the most common causes of subacute thyroiditis. Exactly how viral infections trigger thyroid gland inflammation is not fully known. Potential mechanisms include:
- Direct viral infection of the thyroid
- Inflammation from immune response against the virus
- Molecular mimicry – the virus shares epitopes with thyroid proteins, leading to autoimmune reaction
- Increased thyroid vascular permeability allows immune cell entry
- Virus-induced cytokine release mediates inflammatory changes
Several viruses have been found to directly infect thyroid cells in culture, including mumps, influenza, adenoviruses, respiratory syncytial virus (RSV), and echoviruses. However, evidence of viral presence in the thyroid gland of patients with subacute thyroiditis is lacking.
A vigorous immune response against a thyroid-tropic virus could trigger local inflammation through mechanisms like cytokine release and infiltration of immune cells like lymphocytes and macrophages.
Molecular mimicry may provoke Hashimoto’s flares but seems less applicable to subacute thyroiditis given the transient course.
Overall, no single mechanism has been proven. Multiple processes likely contribute in ways that still need clarification.
Data on COVID-19 and Subacute Thyroiditis
Given that viruses often precede subacute thyroiditis, it’s plausible that SARS-CoV-2 could trigger it. But so far, few studies have investigated this association in depth.
In Italy, a retrospective study looked at 491 COVID-19 patients hospitalized from March 1 to April 20, 2020. It found 10 patients developed subacute thyroiditis beginning 3-6 weeks after onset of COVID-19 symptoms. They had mild COVID-19 illness initially. All cases were detected because of neck pain prompting thyroid ultrasound. The estimated incidence was 2.0% among these hospitalized patients. Researchers concluded SARS-CoV-2 may cause subacute thyroiditis through direct infection or immune-mediated inflammation.
Another study from Milan, Italy reported 3 cases of subacute thyroiditis 2-6 weeks after onset of mild COVID-19 illness in young women. Two had transient hyperthyroidism followed by normalization of thyroid function. The third developed permanent hypothyroidism requiring long-term treatment.
Additionally, a literature review described 19 cases of subacute thyroiditis associated with mild COVID-19 illness across Europe and the United States. 68% had thyroid hormone elevations consistent with hyperthyroidism initially, often followed by hypothyroid phase.
These initial reports suggest SARS-CoV-2 may trigger subacute thyroiditis in a small portion of patients. However, larger prospective studies are needed to firmly establish the relationship and determine the incidence rate.
Case Reports Linking COVID-19 and Thyroiditis
Beyond these small case series, there are numerous individual case reports of various types of thyroiditis developing after COVID-19:
- A 42-year-old woman in New York developed neck pain and thyrotoxicosis 2 weeks after COVID-19 diagnosis. She was diagnosed with subacute thyroiditis.
- A middle-aged nurse in Mexico City had severe COVID-19 pneumonia. Two months into recovery, he developed clinical thyrotoxicosis and biopsy-confirmed subacute thyroiditis.
- A 36-year-old pregnant physician in California noticed thyroid gland pain and neck fullness 5 weeks after mild COVID-19 illness. She had hyperthyroid lab results consistent with subacute thyroiditis.
- A 44-year-old man in India developed fever and neck swelling 2 weeks after recovering from severe COVID-19 pneumonia. He was diagnosed with suppurative thyroiditis from a bacterial superinfection.
- A teenage girl in Italy developed Graves’ disease (autoimmune hyperthyroidism) 2 months after asymptomatic COVID-19 infection.
- A 47-year-old woman in Brooklyn had asymptomatic COVID-19 but 3 months later developed clinical hypothyroidism and was found to have Hashimoto’s thyroiditis.
These cases reveal a temporal relationship between COVID-19 and subsequent thyroiditis. While they provide supporting evidence, cumulative data from large studies is still needed.
Limitations of Current Studies
Despite these reported links, there are important limitations to consider regarding the current data:
- Published studies are small case series or case reports. Larger cohort studies are needed.
- Proving causality is difficult – viral triggers often precede thyroiditis so the relationship may be coincidental.
- Under-recognition and under-reporting are likely, skewing incidence rates.
- Subacute thyroiditis may be subclinical in many patients and overlooked.
- Long-term follow up is lacking; unclear if associated thyroiditis persists.
- Possible roles of medications (steroids, anti-virals) are unknown.
- Mechanisms behind a potential causal link are still speculative.
Research into this topic is still in the early, observational stage. Determining if COVID-19 triggers thyroiditis requires formal epidemiological investigation through analysis of large, controlled populations over time.
Conclusions on the Association Between COVID-19 and Thyroiditis
Based on the evidence so far, there appears to be an association between COVID-19 and subsequent thyroiditis, especially subacute thyroiditis. However, large cohort studies are needed to truly define incidence rates and establish causality.
While rare, thyroiditis should be considered as a possible extrapulmonary manifestation in patients recovering from COVID-19. Presence of symptoms like neck pain, thyroid gland swelling, palpitations, weight changes, and heat intolerance warrant checking thyroid function tests and antibody levels.
For now, clinicians should be aware of this potential link and monitor thyroid status in COVID-19 patients, particularly those with suggestive symptoms in the post-infection period. Early detection of thyroiditis allows for appropriate treatment to prevent complications of thyroid dysfunction.
Further research is still required to understand the mechanisms behind this relationship and define the characteristics that predispose certain patients to develop thyroiditis after COVID-19 illness. This includes determining risks based on COVID-19 severity, age, gender, medications used, and presence of thyroid antibodies.
In summary, COVID-19 does appear capable of triggering thyroiditis in some patients. However, larger studies are needed to corroborate the association and provide definitive evidence that SARS-CoV-2 directly causes inflammation of the thyroid gland.
| Type of Thyroiditis | Key Features |
|---|---|
| Subacute thyroiditis | Most common type; Often follows viral infection. Neck pain common. Transient hyperthyroid phase then hypothyroid. |
| Silent thyroiditis | Similar to subacute but painless. Mild hyperthyroidism then hypothyroid. |
| Postpartum thyroiditis | Within 12 months after giving birth. Mild symptoms but often leads to permanent hypothyroidism. |
| Drug-induced | Triggered by medications like interferon, amiodarone. Resolves with drug withdrawal. |
| Radiation thyroiditis | After radiation therapy to neck/chest. Leads to hypothyroidism. |
| Acute (suppurative) thyroiditis | Rare. Bacterial infection of thyroid gland. |
| Hashimoto’s thyroiditis | Most common cause of hypothyroidism. Autoimmune destruction of thyroid. |
| Riedel’s thyroiditis | Very rare. Fibrosis invading thyroid gland. |
| Mechanism | Evidence |
|---|---|
| Direct viral infection | Some viruses infect thyroid cells in vitro but unproven in vivo |
| Immune response | Plausible; needs confirmation |
| Molecular mimicry | Could trigger Hashimoto’s but unlikely in subacute thyroiditis |
| Increased permeability | Allows immune cell infiltration; possible factor |
| Cytokine release | Mediates inflammation; likely involved |
| Limitation of Current Studies |
|---|
| Small sample sizes, lack of large cohorts |
| Difficult to prove causality |
| Under-recognition and under-reporting |
| Many subclinical cases likely missed |
| Limited long-term follow up data |
| Role of medications unclear |
| Mechanisms speculative |