Hyperthyroidism is a condition of excess thyroid hormone. It may be caused by intrinsic thyroid dysfunction or, rarely, by excessive stimulation of the thyroid gland by an autonomous source of thyroid-stimulating hormone (TSH). The prevalence of hyperthyroidism in the US is about 1.2%. Approximately 70% of cases result from Graves’ disease, in which autoantibodies to the TSH receptor continually stimulate the thyroid gland to overproduce thyroid hormone. Other common causes include toxic multinodular thyroid, toxic adenoma, and thyroiditis.[1] Hyperthyroidism may also be caused by excessive ingestion of exogenous thyroid hormone or iodine. Rarely, hyperthyroidism may be caused by a TSH-secreting anterior pituitary adenoma or struma ovarii. Symptoms may also result when physiologically high doses of levothyroxine are used during treatment for thyroid malignancy in order to suppress TSH.

Clinical manifestations of hyperthyroidism vary significantly from patient to patient, with symptom severity often correlating with circulating thyroid hormone concentrations. Common signs and symptoms include tachycardia, palpitations, heat intolerance, weight loss, menstrual irregularities, nausea, vomiting, restlessness, anxiety, tremor, and atrial fibrillation. Further signs and symptoms depend on the etiology and severity of hyperthyroidism. In Graves’ disease, for example, typical symptoms include a diffuse, symmetric goiter; ophthalmopathy (including lid lag and irreversible exophthalmos); and dermopathy (including pretibial myxedema, a thickening and redness of the pretibial skin). Graves’ hyperthyroidism may be associated with other autoimmune diseases, including Addison disease and type 1 diabetes mellitus.

The most severe form of hyperthyroidism is thyroid storm, which can be precipitated by thyroidectomy, acute stress (e.g., infection, trauma, nonthyroid surgery), or an acute iodine load. One of the most common inciting factors is noncompliance with anti-thyroid medication. Presentation may include hyperpyrexia (up to 104ºF-106ºF), severe nausea, vomiting, jaundice, rigidity, and altered mental status, including agitation, delirium, or stupor. These symptoms may progress to seizures, coma, tachycardia or atrial fibrillation, congestive heart failure, shock, and death. Thyroid storm may be the first sign of thyrotoxicosis.[2]

Risk Factors

Gender. Hyperthyroidism is more common in females.

Genetics. Certain HLA-D subtypes increase risk for Graves’ disease, and the disease tends to run in families

Iodine. Excess dietary iodine intake and iodine-rich medication (amiodarone) use may cause hyperthyroidism. Amiodarone may also cause thyroiditis.


Physical findings may include a rapid heart rate and an enlarged thyroid. TSH is the most cost-effective assay for hyperthyroidism and should be the initial screening test. TSH is decreased in all types of hyperthyroidism, except when pituitary tumors produce TSH or the thyroid hormone feedback loop malfunctions.

Free T 4 concentration is increased; the magnitude of T4 elevation is correlated with the degree of biochemical disease. If TSH and T3 are elevated but T4 is normal, Graves’ disease or thyroid adenoma are likely causes. A total T3:T4 ratio greater than 20 is common in Graves’ disease.

Once hyperthyroidism has been diagnosed, further testing can determine the underlying etiology. Thyroid stimulating immunoglobulins, antithyroglobin, and antithyroid peroxidase levels are often elevated in Graves’ disease—high titers can help establish the etiology of hyperthyroidism. A 24-hour radioactive iodine uptake scan is often necessary for diagnosis of Graves’ disease and exclusion of other disorders. Uptake is increased in Graves’ disease, toxic adenoma, and multinodular goiter and is decreased in thyroiditis, excessive iodine consumption, and overmedication with thyroid hormone supplementation.

Radioimaging can define the shape and size of the thyroid and determine where “hot” nodules are distributed (iodine will concentrate in “hot” nodules). Functional nodules may represent toxic adenoma or multinodular goiter. Diffuse uptake is seen in Graves’ disease. Absence of uptake strongly suggests thyroiditis, exogenous thyroid hormone ingestion, or, rarely, struma ovarii.


Initial therapy often uses a beta-blocker to oppose the adrenergic effects of thyroid hormone.

Antithyroid drugs (e.g.,propylthiouracil, methimazole) interfere with thyroid hormone production. Although antithyroid drugs must generally be continued for at least 1-2 years, they may be a useful temporizing measure in anticipation of spontaneous remission of hyperthyroidism, which occurs in about 30% of patients with Graves’ disease over 1-2 years.[1]

Radioactive iodine (I131) to ablate thyroid tissue is a definitive treatment with excellent success rates; it is the most commonly used treatment in the US It cannot, however, be used in pregnancy, and breast-feeding mothers must pump and dispose of their milk for about 5 days after treatment. Radioiodine treatment can cause or worsen Graves’ ophthalmopathy.[3] Complete destruction of the thyroid gland typically occurs within 8-10 weeks, at which point thyroid hormone replacement is necessary to reestablish a euthyroid state.

Surgical removal of the thyroid (thyroidectomy) is also an effective treatment. It is often indicated in hyperthyroid patients who have an obstructive goiter.

Lifelong thyroid hormone supplementation will be necessary after ablation or thyroidectomy due to resultant hypothyroidism.

Thyroid storm treatment is generally similar to that for hyperthyroidism but with closer monitoring and higher medication doses. Treatment with glucocorticoids or potassium iodine may be indicated (excess iodine reduces release of stored thyroid hormone into the circulation). Intensive care unit observation is essential.

Nutritional Considerations

Iodine-induced hyperthyroidism has been reported in patients after treatment for previous thyroid diseases. Specifically, patients treated with antithyroid drugs for Graves’ disease are prone to develop iodine-induced hyperthyroidism.[4] ,[5] ,[6] Excess iodine exposure may occur through drugs, antiseptics, food preservatives, and contrast media, where iodine amounts can be several thousand times higher than what is recommended.[1],[7] Cow’s milk is a primary source of dietary iodine in the United States.[8] Certain breads and milk contained up to 587 µg and 110 µg iodine per serving, respectively,[4] which would provide a large excess when compared with the Recommended Dietary Allowance for adults of 150 µg.

Patients with celiac disease have an increased prevalence of autoimmune disease, including Graves’ disease.[9] It is unclear whether the association is due to a common genetic basis for the two conditions[10] or to an as-yet unidentified cause-and-effect relationship. Limited evidence indicates that antithyroid antibody production abates in celiac patients after 3-6 months on a gluten-free diet.[11]


See Basic Diet Orders Chapter

Nutrition consultation to assist patient in planning appropriate iodine intake.

What to Tell the Family

Hyperthyroidism is common and generally responds well to medical therapy. In some cases, the disease spontaneously remits. In others, radioactive iodine therapy, antithyroid drugs, or surgery are indicated to remove or destroy overactive thyroid cells, which may necessitate lifelong thyroid hormone replacement to maintain a normal hormone level. Patients with mild to moderate disease could attempt a trial period of avoiding foods that contain high concentrations of iodine (including dairy products, bread made with iodate dough conditioners, iodized salt, sea salt, fish and shellfish, and eggs) and foods that contain iodides, iodate, algin, alginates, carrageen, agar, and red dye number 3.


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