From the Guidelines
Graves' disease is an autoimmune disorder that causes the thyroid gland to produce too much thyroid hormone (hyperthyroidism), and its treatment typically involves anti-thyroid medications, beta-blockers, and long-term management with radioactive iodine therapy or surgical removal of the thyroid. According to the most recent evidence from 1, propranolol is the most widely studied nonselective beta-blocker to treat the increased heart rate and tremor associated with thyrotoxicosis, hyperthyroidism, thyroiditis, and Graves' disease. The symptoms of Graves' disease include:
- Weight loss
- Rapid heartbeat
- Anxiety
- Tremors
- Heat sensitivity
- Bulging eyes (Graves' ophthalmopathy)
- Enlarged thyroid gland (goiter) Treatment options for Graves' disease include:
- Anti-thyroid medications like methimazole (10-30 mg daily) or propylthiouracil (100-300 mg daily in divided doses)
- Beta-blockers such as propranolol (10-40 mg, 3-4 times daily) to manage symptoms like rapid heart rate and tremors
- Radioactive iodine therapy to destroy thyroid tissue
- Surgical removal of the thyroid (thyroidectomy) It is essential to note that most patients require lifelong monitoring of thyroid function, and those who undergo radioactive iodine treatment or surgery typically need thyroid hormone replacement therapy afterward. Graves' disease affects women more frequently than men and often has a genetic component, with environmental factors potentially triggering its onset in susceptible individuals, as mentioned in 1.
From the Research
Definition and Characteristics of Graves' Disease
- Graves' disease (GD) is an autoimmune disorder involving the thyroid gland, characterized by the presence of circulating autoantibodies that bind to and stimulate the thyroid hormone receptor (TSHR), resulting in hyperthyroidism and goiter 2.
- The disease can affect organs other than the thyroid, leading to extrathyroidal manifestations, including Graves' ophthalmopathy, dermopathy, and acropachy 2.
- The exact etiology of GD remains unclear, but it is believed to result from a complex interaction between genetic susceptibility and environmental factors 2.
Clinical Characteristics and Diagnosis
- Clinically, GD is characterized by the manifestations of thyrotoxicosis, as well as its extrathyroidal features when present 2.
- The diagnosis is generally based on the association of hyperthyroidism and usually diffuse goiter confirmed with serum anti-TSHR autoantibodies (TRAbs) 2.
- The presence of extrathyroidal manifestations, such as Graves' ophthalmopathy, can make the diagnosis almost unmistakable 2.
Treatment Options
- Treatment of GD relies on antithyroid drugs (ATDs), radioactive iodine (RAI), and thyroidectomy 3.
- ATDs are the first-line treatment worldwide and are usually given for 18-24 months, with long-term treatment potentially decreasing relapses 3.
- RAI is safe, although associated with a low risk of GO progression, particularly in smokers 3.
- Thyroidectomy requires skilled and high-volume surgeons and is associated with a risk of permanent hypothyroidism 3, 4.
- The choice of treatment depends on the patient's preferences and situation, including a woman's desire to conceive, size of the goitre, the degree of hyperthyroidism, and the presence of ophthalmopathy 4.