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Endocrinology›Condition·Updated Jun 27, 2026·v1

Hyperthyroidism

Hyperthyroidism is a common endocrine disorder driven by excess thyroid hormone production, most often from autoimmune Graves disease. Diagnosis requires biochemical confirmation (suppressed TSH, elevated FT4/FT3) and etiologic testing (TRAb, scintigraphy). Methimazole is first-line therapy for Graves; definitive treatment with RAI or surgery is reserved for relapse, toxic nodular goiter, or pregnancy contraindications. Thyroid storm, a life-threatening emergency, demands immediate combination therapy with ATD, beta-blockade, and iodine. Even after treatment, patients require long-term surveillance for cardiovascular, skeletal, and neuropsychiatric sequelae.

High Evidence232 references·12,100 words·49 min read·v1
hyperthyroidismGraves diseasethyroid stormthyrotoxicosismethimazoleradioactive iodineTRAbthyroid noduleendocrine emergency

Quick Reference

RxDrug of choiceMethimazole 10-30 mg PO once daily for Graves disease; propranolol 20-40 mg PO q6h for symptom control.
AltAlternativesPropylthiouracil (PTU) 100-150 mg PO q8h for first trimester pregnancy or MMI intolerance; radioactive iodine (131I) 10-15 mCi as definitive therapy; total thyroidectomy when RAI contraindicated or GO active.
⊘AvoidRAI in pregnancy, breastfeeding, and active moderate-to-severe Graves orbitopathy; PTU in children (hepatotoxicity); methimazole in first trimester (aplasia cutis risk). Do NOT use digoxin for rate control in hyperthyroid AF.
DxTest of choiceSerum TSH as initial screening; if suppressed, measure FT4 and FT3. Confirm Graves disease with TRAb (second-generation assay: 97% sensitive, 99% specific). If TRAb negative, thyroid scintigraphy to distinguish toxic nodular goiter from thyroiditis.
ScKey scoreBurch-Wartofsky Point Scale (BWPS) for thyroid storm: ≥45 = imminent storm, 25-44 = impending storm.
→When to referEndocrinology for thyroid storm, pregnancy with Graves, pediatric hyperthyroidism, or active orbitopathy; ophthalmology for moderate-to-severe Graves orbitopathy; surgery for large goiter or compressive symptoms; cardiology for atrial fibrillation or heart failure.
Confirm hyperthyroidism with suppressed TSH + elevated FT4/FT3; identify Graves disease with TRAb; treat with methimazole (first-line) or definitive therapy (RAI/surgery); manage emergencies (storm, TPP, AF) with aggressive combination therapy; monitor lifelong for cardiovascular and skeletal sequelae.
Hyperthyroidism is a syndrome of thyroid hormone excess from sustained glandular overproduction, most commonly due to Graves disease, toxic nodular goiter, or thyroiditis. Untreated, it carries a 20-40% increase in all-cause mortality driven by atrial fibrillation, heart failure, and thromboembolic events. Diagnosis rests on suppressed TSH followed by free T4/T3 measurement and TRAb positivity to identify Graves disease. Management proceeds from antithyroid drugs (methimazole first-line) to definitive therapy with radioactive iodine or thyroidectomy, guided by etiology, orbitopathy activity, and pregnancy status. Even after biochemical cure, cardiovascular and skeletal risks persist, mandating lifelong surveillance.

Overview and Recommendations

Background

  • •Hyperthyroidism is a clinical syndrome of thyroid hormone excess resulting from sustained overproduction of triiodothyronine (T3) and thyroxine (T4) by the thyroid gland, most commonly due to Graves disease, toxic nodular goiter, or thyroiditis. It affects approximately 1.2% of the US population with a female-to-male ratio of 5:1, and its prevalence is rising in children.
  • •Graves disease accounts for ~70% of hyperthyroidism cases in iodine-sufficient regions and is driven by stimulatory TSH-receptor autoantibodies (TRAb) that constitutively activate the TSH receptor on thyrocytes, independent of pituitary TSH. TRAb is detectable in >95% of cases and is the disease's specific biomarker.
  • •Toxic nodular goiter (uninodular or multinodular) causes ~16% of cases, increasing with age and in iodine-deficient regions. Iodine supplementation in such populations can precipitate overt hyperthyroidism from pre-existing autonomous nodules via the Jod-Basedow phenomenon.
  • •Thyroiditis (subacute, silent, postpartum, drug-induced) accounts for ~3% of hyperthyroidism and represents destructive release of stored hormone rather than increased synthesis, as evidenced by low or absent uptake on scintigraphy. It is typically self-limited.
  • •Untreated hyperthyroidism increases the risk of atrial fibrillation (HR 1.42), hip fracture (HR 1.36), dementia (HR 1.39), and all-cause mortality (pooled RR 1.21). Even subclinical hyperthyroidism (suppressed TSH with normal T4/T3) carries significant long-term risks, including a 19% increase in cardiovascular mortality.
  • •The four pillars of GDMT for Graves disease, methimazole, radioactive iodine, thyroidectomy, and beta-blockade, each target different points in the physiology: hormone synthesis, follicular destruction, surgical removal, and adrenergic symptom control. The choice depends on etiology, patient preference, pregnancy plans, and the presence of active Graves orbitopathy.

Evaluation

  • •Suspect hyperthyroidism in any patient with weight loss despite increased appetite, palpitations, heat intolerance, and fatigue, the classic symptom triad. Symptoms typically develop over weeks to months in Graves disease, whereas thyroiditis often has a more abrupt onset over days.
  • •Ask about family history of thyroid disease (sibling OR 7.5 for Graves), smoking (OR 1.9-3.3 for Graves; 5.7 for orbitopathy), recent iodine exposure (contrast media, amiodarone), immune checkpoint inhibitor therapy, and pregnancy status. In women of reproductive age, inquire about pregnancy plans and last menstrual period.
  • •Examine for diffuse goiter (often with a bruit on auscultation in Graves), lid retraction, lid lag, proptosis, conjunctival injection, periorbital edema, tremor, hyperreflexia, and proximal muscle weakness. Auscultate the heart for irregular rhythm and assess for pretibial dermopathy or acropachy in Graves disease.
  • •Order serum TSH as the initial screening test, a suppressed TSH (<0.4 mIU/L) has >99% sensitivity for overt hyperthyroidism. If TSH is suppressed, measure free T4 (FT4) and free T3 (FT3). Overt hyperthyroidism: suppressed TSH with elevated FT4 and/or FT3. Subclinical: suppressed TSH with normal FT4 and FT3.
  • •Check for biotin interference, biotin, a common supplement, can cause falsely low TSH and falsely high FT4/FT3 on many immunoassay platforms. Patients should stop biotin for at least 3 days before testing.
  • •Order TSH-receptor antibodies (TRAb) as the cornerstone of noninvasive diagnosis for Graves disease. A positive TRAb (second- or third-generation assay) has 97% sensitivity and 99% specificity, confirming Graves disease without need for further imaging in most cases.
  • •If TRAb is negative, perform thyroid scintigraphy (technetium-99m pertechnetate or iodine-123) to distinguish toxic nodular goiter (focal/multifocal increased uptake) from thyroiditis (low or absent uptake). In pregnancy, scintigraphy is contraindicated; rely on clinical context and TRAb.
  • •Order thyroid ultrasound with color Doppler if scintigraphy is equivocal or to assess nodule characteristics. In Graves disease, findings include diffuse hypoechogenicity and increased vascularity (peak systolic velocity >40 cm/s in the inferior thyroid artery).
  • •Assess severity immediately: use the Burch-Wartofsky Point Scale (BWPS) for thyroid storm, score ≥45 indicates imminent storm, 25-44 impending storm. In thyroid storm, initiate therapy without waiting for lab confirmation if clinical suspicion is high.
  • •Also consider: ECG for atrial fibrillation (present in 10-25% of overt cases), complete blood count (baseline before starting antithyroid drugs), liver enzymes (baseline for methimazole/PTU), and serum potassium if weakness or paralysis is present (suspect thyrotoxic periodic paralysis when K+ <3.0 mmol/L).
  • •Diagnostic criteria for Graves disease: suppressed TSH, elevated FT4/FT3, positive TRAb, and diffuse goiter (often with orbitopathy). For toxic nodular goiter: suppressed TSH, elevated FT4/FT3, negative TRAb, and nodular goiter on imaging with focal uptake on scintigraphy.
  • •Special populations: in pregnancy, use trimester-specific TSH reference intervals; gestational transient thyrotoxicosis (GTT) is common in the first trimester and does not require antithyroid drugs. In the elderly, TSH may be less suppressed and FT4 may be normal despite overt hyperthyroidism (apathetic hyperthyroidism).
  • •Differential diagnosis includes factitious hyperthyroidism (exogenous thyroid hormone ingestion, low thyroglobulin, suppressed RAIU), TSH-secreting pituitary adenoma (elevated or inappropriately normal TSH, elevated alpha-subunit), and resistance to thyroid hormone (elevated T4/T3 with inappropriately normal/high TSH).

Management

  • •For symptomatic control in all patients, initiate a beta-blocker: propranolol 20-40 mg PO every 6 hours or atenolol 25-50 mg PO daily. Titrate to heart rate <90-100 bpm. Continue until euthyroidism is achieved.
  • •First-line antithyroid drug (ATD) for non-pregnant adults is methimazole (MMI) 10-30 mg PO once daily, depending on baseline FT4 elevation (10-15 mg for mild, 20-30 mg for moderate-to-severe). After achieving euthyroidism (typically 4-8 weeks), reduce to the lowest effective maintenance dose (5-10 mg daily).
  • •Propylthiouracil (PTU) is reserved for the first trimester of pregnancy (due to lower teratogenicity risk than MMI), for patients with minor adverse reactions to MMI, and for thyroid storm. Dose: 100-150 mg PO every 8 hours (300-450 mg/day).
  • •For Graves disease, offer ATD for 12-18 months; after withdrawal, remission occurs in 40-50% of patients. Higher remission rates are seen in those who become TRAb-negative and have small goiters. For relapse after a full course, offer definitive therapy (RAI or surgery) or long-term ATD (≥5 years).
  • •Radioactive iodine (RAI) as definitive therapy: administer 131I as a fixed dose of 10-15 mCi (370-555 MBq) or a calculated dose based on thyroid uptake and volume. Goal is to induce hypothyroidism, managed with levothyroxine. Contraindicated in pregnancy, breastfeeding, and active moderate-to-severe Graves orbitopathy.
  • •In patients with mild Graves orbitopathy or risk factors (smoking, high TRAb) undergoing RAI, administer prednisone prophylaxis: 0.2-0.5 mg/kg/day PO for 6-12 weeks, starting 1-3 days after RAI, to prevent progression of orbitopathy.
  • •Total thyroidectomy is indicated when RAI is contraindicated, when Graves orbitopathy is active, when a large goiter causes compressive symptoms, or when coexistent thyroid cancer is suspected. Achieves immediate cure but carries risks of permanent hypoparathyroidism (1-2%) and recurrent laryngeal nerve injury (1-2%) in high-volume centers.
  • •For thyroid storm (BWPS ≥25), initiate three drug classes simultaneously within the first hour: methimazole 20-30 mg PO or per NG tube, then 20 mg every 4-6 hours; propranolol 60-120 mg PO every 6 hours or 1-2 mg IV every 5-10 minutes; and iodine (SSKI 5 drops PO every 6 hours or Lugol's solution 8 drops every 6 hours) given 1 HOUR after the first ATD dose.
  • •For thyrotoxic periodic paralysis (TPP): administer IV potassium chloride (KCl) at 10 mmol/hour until weakness resolves (mean dose 63±32 mmol for full recovery). Give propranolol 40-80 mg PO immediately, then 40-80 mg every 6 hours. Correct underlying hyperthyroidism with methimazole 20-40 mg PO daily.
  • •For atrial fibrillation in hyperthyroidism: rate control with beta-blockers (propranolol or cardioselective agent if LVEF <40%); anticoagulate per CHA2DS2-VASc criteria until euthyroid for 4-6 weeks (DOACs preferred over warfarin unless valvular AF or hemodynamic instability). Defer electrical cardioversion until euthyroid unless hemodynamically unstable.
  • •Monitoring during ATD therapy: check TSH, FT4, FT3 every 4-6 weeks until euthyroid, then every 3-6 months. Goal is normal TSH (0.4-4.0 mIU/L). Warn patients about agranulocytosis (risk ~0.3%): instruct to stop drug and seek immediate attention if fever or sore throat develops.
  • •After RAI or thyroidectomy: start levothyroxine 1.6-1.8 mcg/kg/day when hypothyroidism develops. Check TSH 6-8 weeks after initiation, then annually once stable. Target TSH 0.5-2.5 mIU/L for most adults; higher target (1.0-4.0 mIU/L) may be appropriate for older patients or those with cardiac disease.
  • •For toxic nodular goiter: definitive therapy (RAI or surgery) is preferred because spontaneous remission is rare. ATDs are not curative. Choice between RAI and surgery depends on goiter size, compressive symptoms, and patient preference.
  • •What NOT to do: Do NOT administer iodine before an ATD in thyroid storm, iodine alone can worsen the storm. Do NOT use digoxin for rate control in hyperthyroid AF, it has reduced efficacy. Do NOT use block-and-replace ATD regimens, they increase drug exposure without improving remission. Do NOT perform electrical cardioversion for AF unless the patient remains in AF after 4-6 weeks of euthyroidism.
  • •Treatment failure: For ATD failure (persistent hyperthyroidism after 6-12 months of adequate dosing or relapse after withdrawal), offer RAI or surgery. For RAI failure (persistent hyperthyroidism at 6 months), repeat RAI or proceed to surgery. For thyroid storm not improving after 24-48 hours of maximal medical therapy, add iopanoic acid (1 g PO then 0.5 g every 6 hours), initiate therapeutic plasma exchange, or consider urgent thyroidectomy.
  • •When to refer: to endocrinology for complex cases (thyroid storm, pregnancy with Graves, pediatric hyperthyroidism, orbitopathy), to ophthalmology for moderate-to-severe Graves orbitopathy, to surgery for large goiter or compressive symptoms, and to cardiology for AF management or heart failure.
  • •Discharge criteria after thyroid storm: euthyroid state (or near-euthyroid), heart rate <90 bpm off IV beta-blockers, no signs of organ failure. Transition to definitive management plan.

Board Review — High Yield

  • •Burch-Wartofsky Point Scale (BWPS), A clinical scoring system (≥45 = thyroid storm) that guides emergency management; therapy should not wait for labs if suspicion is high.
  • •TRAb (TSH-receptor antibody), The specific biomarker for Graves disease, positive in >95% of cases; its titer correlates with disease severity and predicts relapse after ATD withdrawal.
  • •Methimazole embryopathy, Aplasia cutis and choanal atresia; avoid MMI in the first trimester; use PTU instead.
  • •Jod-Basedow phenomenon, Iodine-induced hyperthyroidism in patients with pre-existing nodular goiter, seen after iodinated contrast or amiodarone.
  • •Thyrotoxic periodic paralysis (TPP), Acute flaccid paralysis with hypokalemia (K+ <3.0 mmol/L), typically in young Asian men; treat with IV KCl 10 mmol/h and propranolol; correct underlying hyperthyroidism.
  • •Subclinical hyperthyroidism, Suppressed TSH with normal FT4/FT3; not benign, increases risk of atrial fibrillation (HR 1.42), hip fracture (HR 1.36), and dementia (HR 1.39).
  • •Graves orbitopathy, Smoking and RAI exacerbate it; steroid prophylaxis (prednisone 0.2-0.5 mg/kg/day for 6-12 weeks) is mandatory if RAI is used in patients with risk factors.
  • •Amiodarone-induced thyrotoxicosis (AIT), Type 1 (iodine-induced, high RAI uptake) responds to thionamides, type 2 (destructive, low uptake) responds to glucocorticoids; mixed forms common.
  • •Resistance to thyroid hormone (RTH), Elevated T4/T3 with inappropriately normal or high TSH; due to THRB mutation; treat with beta-blockers, not ATDs.
  • •Therapeutic plasma exchange (TPE), Rapidly reduces circulating T4/T3 by 60-80% per exchange; indicated for refractory thyroid storm as a bridge to thyroidectomy.

Deep Dive — Evidence Details

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