Hyperthyroidism

Symptoms

• Nervousness, anxiety, irritability, and mood swings
• Difficulty sleeping (insomnia)
• Unintentional weight loss despite an increased appetite
• Feeling hot and increased sweating (heat intolerance)
• Heart palpitations (feeling your heart race) or a rapid heart rate (tachycardia)
• Frequent bowel movements or diarrhea
• Muscle weakness, especially in the upper arms and thighs
• Fatigue
• Fine tremor, particularly in the hands
• Thinning skin and fine, brittle hair
• Changes in menstrual patterns, such as lighter periods
• An enlarged thyroid gland (goiter)
• Bulging eyes (proptosis/exophthalmos), gritty sensation, pressure or pain in the eyes, puffy or retracted eyelids, light sensitivity, double vision, or impaired vision (Graves' ophthalmopathy, specific to Graves' disease)
• Red, swollen skin with an 'orange peel' texture, usually on the shins and tops of the feet (Graves' dermopathy, rare and specific to Graves' disease)
• Clubbing of the fingers and toes and swelling of the hands and feet (thyroid acropachy, very rare)
• Enlargement of breast tissue in men (gynecomastia)
• In older adults, symptoms may be subtle or absent, presenting as depression, apathy, weight loss (anorexia), or cardiovascular issues like atrial fibrillation or heart failure (apathetic hyperthyroidism)
• High fever (often above 103°F or 39.4°C), severe rapid heart rate, heart failure, agitation, delirium, psychosis, coma, nausea, vomiting, diarrhea, or jaundice (signs of thyroid storm, a medical emergency)

Causes & Risk Factors

• Graves' disease: An autoimmune disorder where antibodies stimulate the thyroid gland to overproduce hormones, accounting for 60-80% of cases.
• Toxic nodular or multinodular goiter (Plummer's disease): Autonomous nodules in the thyroid gland produce excess hormone, more common in older adults.
• Toxic adenoma: A single, autonomous nodule in the thyroid gland producing excess hormone.
• Thyroiditis: Inflammation of the thyroid gland causing a temporary release of stored hormones. This includes subacute (de Quervain's) thyroiditis, postpartum thyroiditis (after childbirth), and silent (painless) thyroiditis.
• Excessive iodine intake: Can induce hyperthyroidism in susceptible individuals, including from medications like amiodarone or radiographic contrast agents.
• Medication-induced: Amiodarone, interferon-alpha, interleukin-2, and certain checkpoint inhibitors can cause hyperthyroidism or thyroiditis.
• Exogenous thyroid hormone: Over-treatment for hypothyroidism or intentional/unintentional ingestion of thyroid hormone.
• TSH-secreting pituitary adenoma: A rare benign tumor in the pituitary gland that produces excess TSH, overstimulating the thyroid.
• Struma ovarii: A rare ovarian tumor containing thyroid tissue that produces excess thyroid hormone.
• Trophoblastic tumors / Hydatidiform mole: Produce high levels of human chorionic gonadotropin (hCG), which can weakly stimulate the TSH receptor.
• Female sex: Graves' disease is 7-8 times more common in women than men.
• Age: Most common in people aged 20 to 40, but toxic nodular goiter is more common in older adults.
• Personal or family history of thyroid disease or autoimmune diseases (e.g., type 1 diabetes, pernicious anemia, primary adrenal insufficiency).
• Genetic predisposition: Specific HLA haplotypes are associated with Graves' disease.
• Recent high iodine intake, including from medications (e.g., amiodarone) or radiographic contrast agents, especially in individuals with pre-existing thyroid nodules.
• Smoking: A significant risk factor for developing and worsening Graves' disease and Graves' ophthalmopathy.
• Major emotional or physical stress (possible trigger for Graves' disease in genetically susceptible individuals, but evidence is not definitive).
• Postpartum period: A known trigger for autoimmune thyroid disease, including postpartum thyroiditis and Graves' disease.
• Infections (some have been postulated to trigger autoimmune thyroid disease, but a causal link is not firmly established).

Diagnosis

• Review of your symptoms, including weight loss, palpitations, and heat intolerance.
• Discussion of your personal and family history of thyroid or autoimmune diseases.
• Review of your medication history, including iodine supplements or contrast media.
• Inquiry about recent pregnancy and smoking history.
• Physical examination to assess for signs of anxiety, hyperactivity, and weight loss.
• Palpation of your neck to check the size, symmetry, and consistency of your thyroid gland, and for any nodules. Your doctor may listen for a thyroid bruit (a vascular sound) over the gland.
• Assessment of your heart rate and rhythm for tachycardia or atrial fibrillation.
• Neurological examination to check for fine tremor and hyperreflexia.
• Eye examination for signs of Graves' ophthalmopathy, such as lid lag, lid retraction, or bulging eyes.
• Skin assessment for warmth, moisture, or pretibial myxedema.
• Thyroid-Stimulating Hormone (TSH) blood test: This is the initial and most sensitive test. In primary hyperthyroidism, TSH will be suppressed (low).
• Free Thyroxine (FT4) and Free or Total Triiodothyronine (T3) blood tests: These hormone levels are usually elevated. T3 may be disproportionately elevated in Graves' disease or toxic nodular goiter.
• TSH Receptor Antibodies (TRAb) blood test: Recommended if the cause is not clear. High levels are highly specific for Graves' disease.
• Thyroid Peroxidase (TPO) Antibodies blood test: Often positive in Graves' disease and Hashimoto's thyroiditis.
• Erythrocyte sedimentation rate (ESR) blood test: May be elevated in subacute thyroiditis.
• Radioactive Iodine Uptake (RAIU) and Scan: Measures how much iodine your thyroid gland takes up and its pattern. High/diffuse uptake suggests Graves' disease. High uptake in one or more nodules suggests toxic adenoma or toxic multinodular goiter. Low/near-absent uptake suggests thyroiditis, exogenous hormone intake, or iodine-induced thyrotoxicosis.
• Thyroid Ultrasound: Used to evaluate the size, structure, and presence of nodules in your thyroid. Doppler flow can show increased vascularity in Graves' disease. It helps assess structure but not function.
• Overt Primary Hyperthyroidism is diagnosed by suppressed TSH with elevated FT4 and/or T3.
• Subclinical Hyperthyroidism is diagnosed by suppressed TSH with normal FT4 and T3.
• The cause is determined by clinical features, TRAb levels, and/or RAIU scan results.
• Your doctor will consider other conditions with similar symptoms, such as anxiety disorders, pheochromocytoma, malignancy, chronic infections, or substance abuse.

Treatment Options

• Smoking cessation: Strongly advised, especially for patients with Graves' disease, to reduce the risk and severity of eye problems.
• Diet: No specific diet is recommended, but ensuring adequate calcium and vitamin D intake is important due to the increased risk of osteoporosis.
• Avoidance of high iodine supplements, unless specifically directed by a physician.
• Beta-blockers (e.g., Propranolol, Atenolol): Used to relieve symptoms like palpitations, tremor, and anxiety by controlling the effects of excess thyroid hormones on your body. They do not treat the underlying cause.
• Antithyroid Drugs (ATDs) / Thionamides: These medications inhibit the synthesis of thyroid hormones.
• Methimazole (MMI) or Carbimazole (CBZ): Generally preferred due to a better side-effect profile, except during the first trimester of pregnancy.
• Propylthiouracil (PTU): Reserved for the first trimester of pregnancy, thyroid storm, or for patients who cannot tolerate MMI. It carries a black box warning for severe liver injury.
• Radioactive Iodine (RAI) Therapy (I-131): A common treatment where radioactive iodine is taken up by the thyroid gland, gradually destroying the overactive cells. This often leads to permanent hypothyroidism, requiring lifelong thyroid hormone replacement.
• Thyroidectomy (total or near-total): Surgical removal of the thyroid gland. This is a definitive treatment recommended for very large goiters, suspected malignancy, coexisting hyperparathyroidism, or when other treatments are not suitable or desired. It results in permanent hypothyroidism.
• Watchful waiting: May be an option for mild, subclinical hyperthyroidism, especially in older adults, with regular monitoring of thyroid function.
• Emergency treatment for Thyroid Storm: Requires immediate hospitalization in an intensive care unit. Management includes supportive care (IV fluids, cooling blankets), high-dose PTU or MMI to block hormone synthesis, beta-blockers for symptom control, inorganic iodide (given at least one hour after ATDs) to block hormone release, and glucocorticoids to reduce T4-to-T3 conversion and treat potential adrenal insufficiency.
• Follow-up during ATD therapy: Thyroid function tests (TFTs) are monitored every 4-6 weeks initially, then less frequently once thyroid hormone levels are normal. Monitoring for rare side effects like agranulocytosis or liver damage is also important.
• Follow-up after RAI therapy: TFTs are monitored at 1-2 months post-treatment and then every 4-6 weeks for 6 months to check for hypothyroidism. Lifelong annual monitoring is recommended.
• Follow-up after surgery: Calcium levels are monitored post-operatively. Lifelong thyroid hormone replacement therapy is started, and TFTs are monitored.

Frequently Asked Questions