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There are over 80 autoimmune disorders affecting more than 20 million Americans. Autoimmune thyroid diseases -- specifically Hashimoto’s and Graves’ disease -- are among the most common autoimmune conditions. Hashimoto’s causes an underactive thyroid -- hypothyroidism -- while Graves’ disease causes an overactive thyroid, known as hyperthyroidism.
This article examines a unique situation: when Hashimoto’s and Graves’ disease coexist in a patient. To better understand how this happens, it’s helpful to review the basics of thyroid hormone regulation first.
Your Guide To The Genetics Of Thyroid Function
Knowing your risk for thyroid disease can help you stay in front of complications. Learn in this guide how genes impact your risk for hypothyroidism.
A complex feedback loop regulates how much thyroid hormone your thyroid gland makes and releases. There are three hormones you need to know about:
- Thyrotropin-releasing hormone (TRH). Your hypothalamus releases TRH in response to low thyroid hormone levels. It travels to your pituitary gland, where it binds to TRH receptors. When a hormone binds to its receptor, it tells the cell to either start or stop a specific action.
- Thyroid stimulating hormone (TSH): When TRH binds to TRH receptors in your pituitary gland, it tells it to release TSH. TSH then enters your bloodstream and travels to your thyroid gland.
- Thyroid hormone: TSH binds to TSH receptors in your thyroid gland, causing a release of thyroid hormone. Thyroid hormone then travels to its target cells in your body, where it helps your cells effectively use oxygen and energy.
A breakdown or change in any part of the loop can affect your thyroid hormone levels. For instance, in those with an underactive thyroid (hypothyroidism), the thyroid gland can’t make enough thyroid hormone. Because of this, the pituitary gland keeps producing TSH, resulting in a high TSH level, as it tries to increase the production of more thyroid hormone. Hashimoto’s is the most common cause of primary hypothyroidism.
In contrast, Graves’ disease commonly causes hyperthyroidism. Patients with Graves’ disease and hyperthyroidism tend to have low TSH and high thyroid hormone levels. When your thyroid is overproducing thyroid hormone, there is no signal to the pituitary gland to release TSH, resulting in low levels.
Since Hashimoto’s and Graves’ disease are both autoimmune disorders, let’s review what an autoimmune disorder is.
Your immune system keeps you healthy by preventing or fighting off infections. It attacks “invaders” like viruses, bacteria, and toxins when they enter your body. After attacking them, your immune system develops antibodies against them, which helps your body remember them. Then, when you are exposed again, your immune system quickly recognizes and destroys them before they can cause an infection or reaction.
Sometimes, and not always for clear reasons, your immune system mistakenly attacks the body’s own cells and tissues as if they were foreign substances. You then develop antibodies against your own healthy cells, organs, and tissues, resulting in inflammation, damage, and a wide range of symptoms depending on which part of the body is affected. The exact causes of autoimmune diseases are not fully understood, but they are believed to result from a combination of genetic and environmental factors.
Autoimmune diseases can affect any part of the body. There are over 80 known autoimmune diseases, including rheumatoid arthritis, lupus, multiple sclerosis, type 1 diabetes, psoriasis, and inflammatory bowel disease. Two of the most common are Hashimoto’s thyroiditis and Graves’ disease, autoimmune diseases that affect your thyroid gland.
Hashimoto’s thyroiditis, also known as chronic lymphocytic thyroiditis, is an autoimmune disorder that affects your thyroid gland. In this condition, antibodies attack your thyroid gland, causing inflammation and damage to the thyroid cells, making the gland unable to produce enough thyroid hormone -- a condition known as hypothyroidism.
Symptoms of Hashimoto’s and hypothyroidism can vary widely from person to person and may include fatigue, weight gain, sensitivity to cold, dry skin, hair loss, constipation, depression, brittle hair and nails, memory impairment and brain fog, muscle aches and weakness, joint pain and stiffness, heavy or irregular menstrual periods, and infertility.
Graves’ disease is an autoimmune disorder that causes hyperthyroidism, an overactive thyroid gland. In this condition, the immune system produces antibodies that bind to the thyroid gland and cause it to make too much thyroid hormone.
The symptoms of Graves’ disease can be mild or severe and develop slowly over time. Common symptoms of hyperthyroidism experienced by people with Graves’ disease include anxiety, irritability, weight loss, increased appetite, diarrhea, tremors, difficulty sleeping, heat intolerance, sweating, palpitations, and an enlarged thyroid gland (goiter). Some people may also develop eye problems, such as bulging eyes, eye pain, and double vision.
Several types of thyroid antibodies are measured via blood tests to diagnose and monitor autoimmune thyroid disorders. These include:
Thyroid peroxidase (TPO) antibodies (TPOAb): These antibodies target an enzyme called thyroid peroxidase, which is necessary to produce thyroid hormones. TPOAb are often elevated in Hashimoto’s thyroiditis and can also be seen in some cases of Graves’ disease.
Thyroglobulin antibodies (TgAb): These antibodies target thyroglobulin, a protein that helps produce thyroid hormones. TgAb can be elevated in Hashimoto’s thyroiditis but may also be present in Graves’ disease and other thyroid disorders.
Thyroid-stimulating hormone receptor antibodies (TRAb): These antibodies stimulate the thyroid gland to produce more thyroid hormones and are typically elevated in Graves’ disease. TRAb can be further classified as stimulating (TSAb), blocking (TBAb), or neutral (TNAb), depending on their effect on the thyroid gland.
Thyroid-stimulating immunoglobulins (TSI): These antibodies target the TSH receptor on thyroid cells and stimulate the thyroid gland to produce more thyroid hormones, leading to hyperthyroidism. TSI are most commonly associated with Graves’ disease. TSI levels can be elevated in conditions other than Graves’ disease, such as subacute thyroiditis.
Thyroid-binding inhibitory immunoglobulins (TBII): These antibodies block the binding of thyroid hormones to proteins in the blood and are typically elevated in Graves’ disease.
TSH receptor blocking antibodies (TSHR-BAb): These antibodies inhibit the action of thyroid-stimulating hormone (TSH), which usually stimulates the thyroid gland to produce more thyroid hormones. TSHR-BAb are typically elevated in autoimmune hypothyroidism.
Thyroid-stimulating immunoglobulins (TSI): These antibodies target the TSH receptor on thyroid cells and stimulate the thyroid gland to produce more thyroid hormones, leading to hyperthyroidism. TSI are most commonly associated with Graves’ disease. TSI levels can be elevated in conditions other than Graves’ disease, such as subacute thyroiditis.
TPOAb and TgAb tests are the most commonly used antibody tests to diagnose Hashimoto’s. Because these antibodies prevent your thyroid gland from releasing thyroid hormone, they are referred to as thyroid-stimulating blocking antibodies.
To diagnose Graves’ disease, TRAb and TSI are usually tested. These antibodies are referred to as thyroid-stimulating antibodies. In addition, imaging tests and scans are often used to help confirm a diagnosis.
In summary, Hashimoto’s is known for blocking antibodies, while Graves’ disease has stimulating antibodies.
Despite having opposite effects on your thyroid, it’s possible to have both Hashimoto’s thyroiditis and Graves’ disease at the same time.
The Conversion/Shift Phenomenon: In some cases, as the autoimmune process progresses and the thyroid gland becomes damaged, a person with Graves’ disease can develop Hashimoto’s thyroiditis. While symptoms can shift back and forth, it’s more common for one clinical presentation will overshadow the other. For instance, in the most common presentation of this situation, there are more thyroid-blocking antibodies than stimulating antibodies, typically causing symptoms of hypothyroidism.
Hypothyroid Graves’ Disease: This condition is a subtype of Graves’ disease where individuals with Hashimoto’s present with Graves’ eye disease and elevated blood levels of stimulating antibodies. In 2010 four case reports illustrated this subtype of Graves’ disease. While the exact reason this occurs is unknown, researchers believe TSH receptors and antibodies are the links. As the concentration of thyroid stimulating and blocking antibodies changes, so does the clinical presentation of thyroid dysfunction.
Graves’ Disease to Hashimoto’s: Moving from a hypothyroid to a hyperthyroid state is also possible, as discussed in a 2022 case report. Changing blood levels of thyroid stimulating and blocking antibodies are the driving force in moving from a hypothyroid state to a hyperthyroid one. You could conceivably go from Hashimoto’s to Graves’ disease as the concentration of thyroid-stimulating antibodies increases and blocking antibodies decrease. This situation is rare, however, because TPO antibodies and prolonged exposure to thyroid-stimulating blocking antibodies can cause irreversible damage to your thyroid cells. So even if thyroid stimulating antibodies increased, your thyroid might not fully respond to them.
Concurrent Hashimoto’s and Graves’ Disease: It is also possible for a person to have both conditions concurrently. In this case, the immune system produces both stimulating and blocking antibodies, leading to fluctuating thyroid hormone levels and variable symptoms that shift between hypothyroid and hyperthyroid. When both conditions are present, it’s still more likely that one condition will dominate in terms of the symptoms. For example, in a 2014 case report, the authors theorized that some individuals have concurrent Hashimoto’s and Graves’. Part of the thyroid is overactive, and other parts are underactive. In this case, the patient still presented with overt signs of Graves’ disease, despite also having Hashimoto’s.
The coexistence of Hashimoto’s and Graves’ disease is rare but possible. One of the first steps in determining if you have one or both thyroid autoimmune diseases is checking your thyroid function. Paloma Health’s convenient, at-home testing kit measures your TSH, thyroid hormone levels, and TPO antibodies. All it requires is an easy, at-home finger-prick blood sample.
Once you have your results, schedule an appointment with one of Paloma Health’s thyroid specialists. They can help you understand your results and determine the next steps.
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