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Most of us would like to forget COVID-19! But, even though the COVID-19 pandemic is no longer the worldwide emergency it was in the last few years, you can still contract it, even with proper precautions. In a subset of people who were, are, or will be infected with COVID-19, the virus appears to trigger other conditions, including autoimmune thyroid disease. In this article, we’ll examine the connection between COVID-19 and Hashimoto’s thyroiditis, an autoimmune disease affecting the thyroid gland.
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The immune system’s job is to guard and defend against bacteria, viruses, and toxins. A healthy individual’s immune system can easily distinguish between these “foreign” cells and the cells of our bodies. In an autoimmune disease, your immune system mistakenly attacks your organs, glands, tissues, and cells. The immune system identifies parts of your body, like joints or organs, as foreign and produces autoantibodies, whose job is to attack and destroy the foreign “invaders.”
Over time, this attack can lead to various symptoms depending on what part of the body the immune system is attacking.
Hashimoto’s thyroiditis
Hashimoto’s thyroiditis is one such autoimmune disease. In the case of Hashimoto’s, antibodies attack healthy thyroid tissue, causing thyroid inflammation. Hashimoto’s attacks the thyroid to the point that, in many cases, the gland can no longer produce enough thyroid hormone. When this occurs, you develop low thyroid hormone levels, known as hypothyroidism. In fact, Hashimoto’s is the number one cause of hypothyroidism in the United States.
Experts don’t know the exact causes of autoimmune diseases. It’s theorized that a combination of factors may determine one’s likelihood of developing an autoimmune disorder. These factors include:
- Family history and genetics
- Environmental triggers such as infection and toxic exposures
- Hormonal imbalances
- Immune system dysregulation
Understanding Hashimoto's Thyroiditis
This guide will teach you about Hashimoto's Thyroiditis, its anatomy, how to diagnose it, and treatment options.
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It’s well known that many viruses are capable of triggering autoimmune diseases, including:
- Parvovirus B19
- Epstein-Barr-virus (EBV)
- Cytomegalovirus (CMV)
- Herpes virus-6 (HHV-6)
- Hepatitis A and C
- Rubella virus
Experts believe these viruses trigger chronic and cascading inflammation -- a factor in autoimmunity -- and eventually develop into an autoimmune condition such as Hashimoto’s and many more. There are a few explanations for how viruses can induce autoimmunity,
Molecular mimicry
Every cell in your body has markers called antigens. These markers help your immune system recognize your cells and tissues as part of your body. Since your immune system knows these antigens and recognizes that they’re normal and meant to be there, it does not attack them.
Traditional research suggests that viruses carry antigens. Sometimes, the virus’ antigens look like the antigens on your cells. This can confuse your immune system. Your immune system attacks the virus first, and while doing so, it may encounter antigens that closely resemble normal antigens. But since it’s in attack mode, the immune system also attacks healthy cells, and that attack can continue even when the virus is no longer present in your body.
Bystander activation
Sometimes, your immune system can become overactive and release self-antigens (your body’s antigens). Immune system cells detect these self-antigens, which activate extra lymphocytes. Lymphocytes are essential because they help control the immune response by attacking cells marked as foreign. As a result, tissue destruction ensues.
Remember, your healthy cells are tagged as foreign in an autoimmune disorder. So, activation of lymphocytes can damage your healthy cells and cause inflammation.
Epitope spreading
An epitope refers to an antibody’s specific target -- the antigen --. Epitope spreading describes a situation where the immune system expands its attacks beyond a particular antigen and begins to recognize and expand its attack to other antigens ordinarily present in the body.
In autoimmune conditions, the immune system mistakenly targets normal self-antigens, which leads to chronic inflammation and damage to cells, tissues, and organs. Epitope spreading can exacerbate these autoimmune responses by expanding the immune reaction to target other self-antigens, fueling the autoimmune process.
While research is still underway, there’s growing evidence that COVID-19 patients face a higher risk of new-onset Hashimoto’s thyroiditis. Most of the current data comes from recent case reports. Here are some theories behind the connection between Hashimoto’s thyroid autoimmunity and COVID-19.
Autoimmune predisposition
Some people may be genetically predisposed to autoimmune disorders, including Hashimoto’s disease. When they contract COVID-19, the virus’s impact on the immune system could trigger or worsen an existing autoimmune response.
Viral infection of the target cells
COVID-19 can trigger the production of pro-inflammatory cytokines. Cytokines are part of your immune system that helps regulate the immune response and inflammation associated with an infection.
In this case, the release of too many pro-inflammatory cytokines causes excess inflammation. Furthermore, antibodies against COVID-19 may react with the thyroid tissues. Antibodies are made by your immune system against a virus or bacteria. They allow for the detection and destruction of a virus or bacteria. However, if COVID-19 antibodies mistakenly react with the thyroid tissues, this may trigger a new autoimmune disorder, in this case, Hashimoto’s.
Abnormal immune regulation
COVID-19 can cause changes in thyroid function through several different immune-mediated ways.
Some people with COVID-19 develop non-thyroidal illness syndrome. In a non-thyroidal illness, your thyroid gland is working as it should. But, for unclear reasons, the amount of thyroid hormone released decreases. Often, these decreases are temporary and return to normal once the underlying infection has resolved.
Studies have shown lower thyroid hormone levels in people who have severe or critical cases of COVID-19. The resulting thyroid dysfunction can vary in severity. There have been reports of people developing thyrotoxicosis (an overactive thyroid) after COVID-19 infection, as well as other thyroid issues, including subacute thyroiditis. Subacute thyroiditis is a temporary inflammatory disease of the thyroid gland, often resembling hyperthyroidism.
Some people may develop Hashimoto’s thyroiditis after having COVID-19. The time from contracting COVID-19 to Hashimoto’s can vary from a few days to months after the infection has cleared. Based on case reports, the majority of people who developed Hashimoto’s after COVID-19 didn’t have any pre-existing thyroid problems.
LDN: Treatment For Hypothyroidism And Hashimoto's
Learn how LDN can be implemented as part of your treatment plan to support your thyroid.
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Frequently, individuals with COVID-19-induced thyroid disorders don’t present with typical signs of thyroid disorders for unclear reasons. General signs and symptoms of hypothyroidism include:
- Anterior neck tenderness or pain
- Fatigue
- Weight changes
- Constipation
You should also be aware of symptoms of subacute thyroiditis. These symptoms are the opposite of those seen in hypothyroidism. While neck pain and tenderness, fatigue, and weight changes are symptoms seen in both disorders, other symptoms that may indicate subacute thyroiditis include:
- Nervousness
- Heat intolerance
- Sweating
- Diarrhea
- Tremor
- Heart palpitations
Fever and cough were the most common symptoms observed in those who developed subacute thyroiditis after a COVID-19 infection.
After the initial assessment, your practitioner will typically order blood tests to check your thyroid function. This includes measuring levels of thyroid-stimulating hormone (TSH), free thyroxine (T4), and free triiodothyronine (T3).
Another crucial blood test to diagnose Hashimoto’s is testing for thyroid antibodies. Thyroid peroxidase antibodies (TPO antibodies) are a marker that is typically elevated in people with Hashimoto’s. These antibodies attack the thyroid gland, causing inflammation and interfering with hormone production.
In some cases, a thyroid ultrasound may be performed to visualize the thyroid gland and assess for any abnormalities, such as nodules or enlargement.
Elevated antibodies can help a practitioner make a diagnosis of Hashimoto’s. If thyroid levels are still within the reference range, treatment may not be required. In Hashimoto’s, TSH levels are often elevated, indicating that the thyroid gland has become underactive. In that situation, treatment for hypothyroidism typically involves thyroid hormone replacement medication to help restore thyroid levels and alleviate symptoms. Levothyroxine is the most common one prescribed, but others are discussed here.
Most individuals mentioned in the case reports discussed earlier reported relief in their symptoms after starting thyroid medication.
If you have been diagnosed with COVID-19 within the last couple of months and you have noticed symptoms of hypothyroidism or any other unusual changes in your health, talk to your provider. These could be signs of thyroid issues or other COVID-19 complications.
Your provider may recommend that you have thyroid function tests, as mentioned above. While many people have blood drawn at the doctor’s office or a lab, you can easily test your thyroid hormone function from home. Paloma’s at-home thyroid testing kit requires a painless finger prick blood sample to measure your thyroid biomarkers and detect the presence of TPO antibodies. If your test results show a thyroid disorder, your provider will talk to you about your treatment options. You also have the option of working with a knowledgeable Paloma provider about optimal treatment for an underactive thyroid.
Even if you didn’t have COVID-19 within the last couple of months but have symptoms of hypothyroidism that we mentioned above, call your healthcare provider. Diagnosing a thyroid disorder early on can help prevent thyroid complications and allow for better management.
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