Graves’ disease is an autoimmune condition where the immune system mistakenly targets the thyroid gland, leading to an overproduction of thyroid hormones (hyperthyroidism). This disorder is the most frequent cause of hyperthyroidism in the United States, accounting for 50% to 80% of all cases. While it is chronic, the elevated hormone levels and associated symptoms are manageable with medical intervention. It is significantly more common in women than in men.
Understanding the Autoimmune Cause
Graves’ disease involves the immune system producing autoantibodies, primarily Thyroid Stimulating Immunoglobulins (TSI), that bind to the thyroid-stimulating hormone (TSH) receptor. These TSI antibodies mimic the action of TSH, constantly activating the thyroid gland.
This perpetual stimulation causes the thyroid follicular cells to increase the synthesis and release of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). The excess T3 and T4 accelerate the body’s metabolism, causing hyperthyroidism symptoms. This overproduction triggers a negative feedback loop, suppressing the pituitary gland’s release of TSH, resulting in a very low TSH level in the blood.
The immune system’s attack is not limited to the thyroid, as the TSH receptors targeted by TSI antibodies are also present on tissues around the eyes. This shared target explains the development of Graves’ ophthalmopathy. Genetic factors contribute to the risk, though environmental triggers like stress, infection, or pregnancy may initiate the onset.
Identifying the Physical Signs
The symptoms of Graves’ disease stem from the body’s accelerated metabolism. Patients often experience weight loss despite an increased appetite because the body rapidly burns calories. Other common symptoms include heat intolerance, increased sweating, and skin that feels warm and moist.
The cardiovascular system is frequently affected, leading to a rapid or irregular heartbeat, commonly described as palpitations. Neurological symptoms include nervousness, anxiety, irritability, and a fine tremor, typically noticeable in the hands or fingers. Patients may also report difficulties with sleeping and muscle weakness.
Signs specific to Graves’ disease include Graves’ ophthalmopathy, or thyroid eye disease, which affects 25% to 40% of patients. Symptoms involve a gritty sensation, light sensitivity, and bulging eyes. This is caused by the accumulation of fluid and tissue swelling behind the eyeballs. Less commonly, Graves’ dermopathy can occur, presenting as a reddish, thickened skin patch, usually on the shins or feet.
Confirming the Diagnosis
Diagnosis begins with a physical examination and a review of symptoms. Blood tests measure hormone levels, starting with the thyroid-stimulating hormone (TSH). In Graves’ disease, the TSH level is typically suppressed or very low because the pituitary gland detects high circulating thyroid hormones and attempts to stop thyroid activity.
Following a suppressed TSH result, free T3 and free T4 levels are measured and are generally found to be elevated. The definitive step for confirming Graves’ disease is testing for the presence of Thyroid Stimulating Immunoglobulins (TSI) or TSH receptor antibodies (TRAb). Finding these autoantibodies distinguishes Graves’ disease from other causes of hyperthyroidism.
A radioactive iodine uptake (RAIU) scan may be performed, where a small amount of radioiodine is swallowed. The thyroid gland naturally absorbs iodine, and in Graves’ disease, the scan shows an increased and diffuse uptake across the entire gland, confirming hyperactivity. This imaging test is useful for differentiating Graves’ disease from other forms of thyroid inflammation.
Managing Graves’ Disease
Management focuses on reducing the production and effects of thyroid hormones. Antithyroid medications, such as methimazole, are typically the initial therapy. These drugs work directly to block the thyroid gland from synthesizing T3 and T4 hormones.
Antithyroid drugs can be used long-term to achieve disease remission, though hyperthyroidism may recur in about half of patients after the medication is stopped. Methimazole is favored due to a lower risk profile compared to propylthiouracil (PTU). PTU is usually reserved for the first trimester of pregnancy or cases where methimazole is not tolerated.
Radioactive iodine (RAI) therapy involves swallowing a capsule containing iodine-131. The radioactive substance is absorbed by the thyroid cells, where its localized radiation gradually destroys the overactive tissue. This process typically takes several weeks to months to fully resolve the hyperthyroidism.
The intended result of RAI therapy is the destruction of enough thyroid tissue to cause hypothyroidism. Patients who become hypothyroid require lifelong daily hormone replacement medication. RAI may not be suitable for patients with moderate to severe Graves’ ophthalmopathy, as it can temporarily worsen eye symptoms.
Surgery involves the complete removal of the thyroid gland (total thyroidectomy). This option is chosen for patients with very large goiters, those who cannot tolerate antithyroid medication, or those who prefer a single, permanent treatment. Like RAI, surgery results in permanent hypothyroidism, necessitating lifelong thyroid hormone replacement therapy.