In this series, I’m discussing my approach to diagnosis, treatment, and management of thyroid conditions. In the final part of this series, we’ll focus on hyperthyroidism and Graves’ disease.
Welcome back to my series on thyroid conditions. I frequently treat hypothyroidism, hyperthyroidism, and autoimmune thyroiditis in my practice. While hyperthyroidism is less common than hypothyroidism, patients suffering from overactive thyroid often are left feeling poorly despite conventional treatment. This is my approach to diagnosing and managing hyperthyroidism and Graves’. To learn more about hypothyroidism, see Part 2.
Hypothyroidism & Graves’
In case you missed Part 1 of this series, let’s review some common symptoms associated with overactive thyroid status, or hyperthyroidism:
Symptoms of hyperthyroidism:
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insomnia
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rapid or irregular heartbeat (tachycardia, palpitations)
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unexplained weight loss
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anxiety or irritability
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heat intolerance
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increased perspiration
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diarrhea, loose stool, or more frequent bowel movements
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trembling of the hands
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shorter, lighter menstrual periods
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fatigue
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muscle weakness
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hair loss
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increased appetite
Symptoms of Graves’:
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protrusion of eyes or puffy eyes (exophthalmos) – only seen in about 30% of Graves’ patients
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gritty feeling or irritated eyes
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light sensitivity (photophobia)
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enlargement of the thyroid, aka: goiter (typically painless)
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hyperthyroid symptoms listed above
Hyperthyroidism occurs when the thyroid gland produces too much thyroid hormone. The two main thyroid hormones produced are thyroxine (T4) and triiodothyronine (T3).
An overactive thyroid can occur for variety of a reasons. The most common cause of hyperthyroidism in the US is due to an autoimmune condition called Graves’. Other causes of hyperthyroidism include: multinodular goiter, inflammation of the thyroid gland due to infection, postpartum, certain medications, or radiation, issues with the pituitary gland, excess iodine ingestion, or overmedication from thyroid hormone replacement. Graves disease occurs when the body inappropriately produces autoantibodies against the thyroid receptor for TSH (thyroid stimulating hormone). These autoantibodies are referred to as TRAb. TRAb is a stimulatory autoantibody and results in continuous secretion of excess T4 and T3.
If you’re experiencing the symptoms listed above, talk to your health care provider.
Diagnosis
Diagnosis starts with a thorough medical intake to fully understand the patient’s symptoms. I always perform a physical examination as there are further clues of the underlying cause of patient’s symptoms that may be observable. The next step in diagnosis is ordering comprehensive labs and/or imaging.
Hyperthyroidism is diagnosed when the thyroid stimulating hormone (TSH), made by the pituitary gland in the brain, is suppressed (too low) and T4 and/or T3 are too high.
Subclinical hyperthyroidism is an earlier presentation. It is diagnosed when T4 and T3 are still within range, but the TSH is starting to become suppressed. Typically these patients are either asymptomatic or mildly symptomatic. It is much more rare than subclinical hypothyroidism.
In rare cases, a patient may have normal or high TSH with high T4 and T3 resulting in hyperthyroidism. This is typically caused by an issue with the pituitary gland.
Biotin supplementation can interfere with laboratory assays and cause results that (falsely) look like hyperthyroidism. Biotin is a common ingredient in many multivitamins, B complex products, and hair, skin, and nail supplements. I always instruct patients to discontinue biotin supplementation for 72-hours before having labs drawn.
Diagnosis of Graves’ disease is characterized by hyperthyroidism due to autoantibodies. Thyroid-stimulating immunoglobulins (TSI) and occasionally thyroid peroxidase (TPO) or thyroglobulin antibodies will be elevated in Graves’. I routinely check for these antibodies when I suspect hyperthyroidism is the cause of a patient’s symptoms.
If physical examination reveals an enlarged or nodular thyroid gland, or if the patient reports symptoms such as difficulty swallowing, a lump in the throat sensation, or hoarse voice, I will often recommend a thyroid ultrasound. If labs reveal Graves’ disease, I also recommend that patients get a baseline ultrasound so we can better assess how damaged the thyroid gland is. Graves’ can cause enlargement of the thyroid gland and ultrasound is useful in this evaluation. Thyroid nodules can also occur in Graves’ and it’s important to monitor these through ultrasound, especially because there is an increased risk of thyroid cancer in these patients.
Occasionally a special test called a radioactive iodine uptake is necessary to confirm the diagnosis. If further evaluation and workup is needed, I will refer patients to an endocrinologist.
Labs – Looking Beyond TSH & T4
While every case is unique, in general, the labs I look at to assess for hyperthyroidism are: TSH, free and total T4, free and total T3, TSI, TPO, and thyroglobulin antibodies. I typically evaluate adrenal status via AM cortisol and DHEA-S for these patients too because of the close relationship between thyroid hormones and adrenal function. I also check serum iron levels, ferritin, iodine, a complete blood count (CBC), and comprehensive metabolic panel (CMP) for most of my hyperthyroid patients. Since patients with hyperthyroidism are at an increased risk of developing osteoporosis and heart arrhythmia, Vitamin D status and comprehensive cardiovascular risk markers can also be helpful.
Comprehensive labs are helpful for making an accurate diagnosis, along with identifying additional problems that hyperthyroidism and Graves’ are associated with.