Goiter

A goiter is any visible or palpable enlargement of the thyroid gland — the butterfly-shaped gland that sits at the base of the neck and produces the hormones that regulate your metabolism, energy, and body temperature. Despite the alarming appearance of a swollen neck, a goiter does not tell you whether the thyroid is working normally, overactively, or underactively. Most goiters are benign, and the majority of people with even large goiters have normal thyroid hormone levels. Understanding what type of goiter you have — and what is causing it — is the key to knowing whether you need treatment at all, and what kind.

Table of Contents

  1. What Is a Goiter — Types and Global Burden
  2. Causes — Iodine Deficiency and Nutritional Factors
  3. Causes — Autoimmune and Drug-Related
  4. Symptoms and Physical Findings
  5. Diagnosis — Imaging and Lab Testing
  6. Toxic Multinodular Goiter (Plummer's Disease)
  7. Substernal Goiter and Compressive Symptoms
  8. Treatment — Medical and Lifestyle
  9. Treatment — Surgery and Radioiodine
  10. Surveillance and Long-Term Monitoring
  11. Key Research Papers
  12. Connections
  13. Featured Videos

What Is a Goiter — Types and Global Burden

The word "goiter" comes from the Latin guttur, meaning throat. It refers to any enlargement of the thyroid gland large enough to be seen or felt — but it says nothing about why the gland grew or whether it is making too much, too little, or the right amount of thyroid hormone. This distinction matters enormously: a person can have a dramatic-looking goiter with a completely normal metabolism.

Clinicians classify goiters along two overlapping axes.

By structure:

By thyroid function:

Globally, goiter remains one of the most common endocrine conditions. The World Health Organization estimates that approximately 800 million people live in iodine-deficient regions, making nutritional goiter the dominant form worldwide — though in iodine-sufficient countries like the United States, autoimmune thyroid disease and sporadic nodular goiter account for most cases. Women develop goiter two to four times more often than men, and risk rises with age.

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Causes — Iodine Deficiency and Nutritional Factors

The single most common cause of goiter worldwide is iodine deficiency. Iodine is an essential mineral — your body cannot make it — and the thyroid gland requires it as the raw material for building thyroid hormones T3 (triiodothyronine) and T4 (thyroxine). When dietary iodine falls too low, the gland cannot manufacture enough hormone. The pituitary gland senses the shortage and responds by secreting more TSH (thyroid-stimulating hormone). This TSH surge drives the thyroid cells to divide and multiply — the gland hyperplasias and hypertrophies in a compensatory attempt to capture every available iodine atom. The result is a goiter.

Iodine deficiency remains endemic in parts of Sub-Saharan Africa, South and Southeast Asia, and mountainous regions (the Alps, Andes, and Himalayas) where iodine has been leached from the soil by glaciation and flooding. Universal salt iodization — adding 20–40 micrograms of iodine per gram of salt — has dramatically reduced endemic goiter in most developed countries over the past century. The recommended daily intake for adults is 150 micrograms; pregnant and breastfeeding women need 220–290 micrograms because the fetus depends entirely on maternal iodine for brain development.

Iodine excess can paradoxically also cause goiter through the Wolff-Chaikoff effect: when iodine levels spike very high, the thyroid temporarily shuts down hormone synthesis as a protective mechanism. The resulting brief drop in thyroid hormone triggers a compensatory TSH rise and transient thyroid enlargement. This usually resolves within days as the gland escapes the block — but in people with underlying thyroid disease, the suppression can persist. Sources of excess iodine include iodinated intravenous contrast dyes used in CT scans, the cardiac drug amiodarone (which is 37% iodine by weight), and high-dose kelp or seaweed supplements. Patients with known multinodular goiter should be counseled about iodine load risk before contrast procedures (see the Jod-Basedow risk under Surveillance).

Dietary goitrogens are compounds in food that interfere with thyroid hormone synthesis. The most discussed are glucosinolates found in raw cruciferous vegetables — broccoli, cabbage, kale, Brussels sprouts, and cauliflower. When these vegetables are chopped or chewed, glucosinolates are converted to isothiocyanates, which can competitively block the enzyme thyroid peroxidase and inhibit iodide organification. In practice, cooking largely inactivates glucosinolates, and clinical goiter from cruciferous vegetables is seen almost exclusively in people who already have iodine deficiency and consume very large quantities of raw brassicas. For iodine-sufficient people eating ordinary portions of cooked vegetables, the thyroid effect is negligible. Cassava (manioc), a staple crop across much of sub-Saharan Africa, contains linamarin, which is metabolized to thiocyanate — a genuine goitrogen that worsens iodine-deficiency goiter in populations dependent on cassava as their primary calorie source.

Pregnancy is a physiological goitrogen. Human chorionic gonadotropin (hCG), produced by the placenta in large quantities during the first trimester, has weak TSH-like activity and stimulates thyroid growth. Additionally, the increased glomerular filtration rate of pregnancy increases urinary iodine loss, raising dietary iodine requirements substantially. In iodine-sufficient women, thyroid volume increases 10–15% during pregnancy. In iodine-deficient regions, pregnancy-associated goiter enlargement can reach 20–40%, and the fetal brain — which depends on maternal thyroid hormone during the first 12 weeks before the fetal thyroid is functional — is at significant risk.

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Causes — Autoimmune and Drug-Related

Graves' disease is the most common cause of diffuse toxic goiter. The immune system produces antibodies (TSH receptor antibodies, or TSI) that bind to and continuously activate the TSH receptor on thyroid cells — mimicking a permanent TSH signal. The gland grows and produces excess T3 and T4. The goiter is typically smooth, diffuse, and often accompanied by a bruit (a rushing sound heard with a stethoscope caused by the increased blood flow through the hypervascular gland). Graves' disease is discussed in detail on the Graves' Disease page; the key point here is that the goiter is a consequence of the antibody-driven hyperstimulation.

Hashimoto's thyroiditis causes a more complex goiter pattern over time. In the early phase, lymphocytic infiltration of the thyroid and the inflammatory effects of thyroid peroxidase antibodies (anti-TPO) and thyroglobulin antibodies can cause transient gland enlargement and even temporary hyperthyroidism ("Hashitoxicosis"). As Hashimoto's progresses, the immune attack destroys functional thyroid tissue, and the gland may first enlarge then eventually atrophy. The classic Hashimoto's goiter is a moderately enlarged, firm, rubbery gland with an irregular or "bosselated" (bumpy) surface. Most Hashimoto's patients eventually develop hypothyroidism as gland mass is progressively lost to fibrosis.

Lithium is the drug most commonly associated with goiter — studies report thyroid enlargement in up to 50% of patients on long-term lithium therapy. Lithium concentrates in the thyroid at levels several times higher than in plasma and blocks the release of stored thyroid hormones from thyroglobulin. The resulting mild TSH elevation drives gland growth. Lithium can also impair iodide organification. For patients who require lithium for bipolar disorder and cannot be switched to alternative mood stabilizers, the approach is to monitor TSH annually and add levothyroxine replacement if frank hypothyroidism develops. The goiter itself often persists even with TSH normalization.

Antithyroid drugs (propylthiouracil and methimazole/carbimazole) deliberately suppress thyroid hormone synthesis — this is their therapeutic goal in hyperthyroidism. But by lowering circulating T4 and T3, they raise TSH, which drives thyroid enlargement as a side effect. Clinicians using these drugs for Graves' disease often add low-dose levothyroxine ("block-and-replace" therapy) to prevent goiter enlargement during treatment.

Thyroid hormone resistance is a rare genetic condition (mutations in the thyroid hormone receptor beta gene, THRB) in which target tissues fail to respond normally to thyroid hormone. The pituitary senses inadequate hormone action and keeps TSH elevated despite high or high-normal circulating T4 and T3 levels. The result is a goiter driven by persistently elevated TSH in the face of elevated — not deficient — hormone levels. This condition is frequently misdiagnosed as hyperthyroidism because the T4/T3 levels are elevated; the key clue is that TSH is normal or elevated rather than suppressed.

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Symptoms and Physical Findings

Many goiters — particularly small ones — cause no symptoms at all and are discovered incidentally during a physical exam, on an imaging scan done for another reason, or when a person notices the swelling in a mirror. Symptoms depend on the size of the goiter, whether it is causing compression, and whether thyroid hormone levels are abnormal.

The goiter itself: The cardinal finding is a visible or palpable mass in the front of the neck, just below the Adam's apple. The single most important clinical sign is that the mass moves upward when the patient swallows. This happens because the thyroid gland is anchored to the larynx and trachea by the pretracheal fascia — so as the larynx rises with swallowing, the thyroid rises with it. A neck mass that does not move with swallowing is unlikely to be thyroid in origin. The gland may feel smooth and soft (typical of iodine-deficiency or Graves' goiters) or firm and nodular (typical of multinodular goiter or Hashimoto's).

Compressive symptoms arise when a goiter becomes large enough to push against surrounding structures:

Symptoms of associated thyroid dysfunction: If the goiter is accompanied by hypothyroidism (as in Hashimoto's), patients may experience weight gain, fatigue, cold intolerance, constipation, slow heart rate, dry skin, hair thinning, and brain fog. If the goiter is accompanied by hyperthyroidism (as in Graves' disease or toxic multinodular goiter), symptoms include unintended weight loss, palpitations or racing heart, heat intolerance, tremor, anxiety, loose stools, and increased sweating. Exophthalmos (bulging eyes) and pretibial myxedema (orange-peel thickening of the skin over the shins) are features specific to Graves' disease — they do not occur with other causes of goiter or hyperthyroidism.

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Diagnosis — Imaging and Lab Testing

Evaluating a goiter requires answering two questions simultaneously: What is the structural nature of the gland? (diffuse vs. nodular; size; presence of suspicious features in any nodule) and What is the functional state of the gland? (TSH level). These two tracks run in parallel and inform each other.

Thyroid function tests: TSH is the most sensitive first-line test. A normal TSH essentially rules out clinically significant hyperthyroidism or hypothyroidism. If TSH is elevated, add free T4 to confirm hypothyroidism and check thyroid peroxidase antibody (anti-TPO) and thyroglobulin antibody (anti-Tg) to evaluate for Hashimoto's thyroiditis. If TSH is suppressed (below the lower limit of normal), check free T4 and free T3 to confirm and quantify hyperthyroidism, and add TSH receptor antibody (TRAb or TSI) to screen for Graves' disease.

Thyroid ultrasound is the cornerstone of structural evaluation and should be performed for every patient with a palpable goiter. Ultrasound can precisely measure gland volume, characterize the echotexture (the "graininess" of the tissue), assess vascularity, and identify and map individual nodules. It is far more sensitive than physical exam — nodules smaller than 1 cm are routinely detected that would never be palpated. Any nodule identified on ultrasound should be assessed using the ACR TI-RADS (Thyroid Imaging Reporting and Data System) criteria, which scores five ultrasound features: composition, echogenicity, shape, margin, and the presence of echogenic foci. Higher TI-RADS scores indicate greater cancer risk and lower thresholds for proceeding to biopsy.

Fine needle aspiration biopsy (FNA) is the procedure for evaluating individual thyroid nodules. A thin needle is passed into the nodule — usually under ultrasound guidance — to sample cells for cytologic analysis. FNA is generally recommended for solid nodules larger than 1 cm with any concerning ultrasound features, or for nodules larger than 1.5–2 cm even without suspicious features. Results are reported using the Bethesda System:

Radioiodine uptake and scan (using I-123, a low-dose isotope) maps the functional activity of the thyroid and its nodules. This test is most useful when TSH is suppressed — it distinguishes Graves' disease (diffuse, uniformly increased uptake throughout the gland) from toxic multinodular goiter (multiple discrete "hot" nodules with suppressed uptake in the surrounding background tissue). A "cold" nodule — one that takes up little or no radioiodine — has a slightly higher risk of malignancy than a hot nodule, though the majority of cold nodules are benign. A radioiodine scan is not routinely recommended when TSH is normal; in that situation, ultrasound and FNA provide the key structural information without radiation exposure.

CT or MRI of the neck and chest is indicated when substernal extension is suspected on clinical exam (Pemberton's sign, respiratory symptoms, chest X-ray showing mediastinal widening or tracheal deviation). CT provides excellent delineation of the goiter's relationship to the trachea, esophagus, and great vessels, and is essential surgical planning information. Important caution: if the patient is being considered for radioiodine treatment (I-131), avoid iodinated contrast CT for at least 6–8 weeks beforehand, as the large iodine load from contrast will competitively block I-131 uptake by the thyroid and reduce treatment efficacy.

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Toxic Multinodular Goiter (Plummer's Disease)

Toxic multinodular goiter — also called Plummer's disease after the American physician Henry Stanley Plummer, who first distinguished it from Graves' disease in 1913 — is the most common cause of hyperthyroidism in adults over 60, and the second most common cause of hyperthyroidism overall after Graves' disease. It arises from a longtime nontoxic multinodular goiter in which individual nodules acquire somatic mutations (acquired mutations in thyroid cells, not inherited) that make them functionally autonomous — meaning they produce thyroid hormone on their own, independent of TSH stimulation. These autonomous nodules suppress TSH as they secrete hormone, and over years, the cumulative autonomous production tips the patient into overt hyperthyroidism.

The transition from nontoxic to toxic MNG is gradual. The average age of diagnosis is over 60 years, and many patients have had their multinodular goiter for decades without symptoms of hyperthyroidism. When hyperthyroidism does emerge, its presentation can be subtler and more cardiovascular-dominant in older patients than the classic sweating-trembling picture seen in young Graves' disease patients. Atrial fibrillation is the presenting sign in a significant minority of older patients with toxic MNG — the persistent catecholamine-sensitizing effect of excess T3 on cardiac tissue lowers the threshold for arrhythmia. Any new-onset atrial fibrillation in an older patient warrants checking a TSH.

On radioiodine scan, toxic MNG shows a characteristic "moth-eaten" pattern: multiple discrete hot nodules with high iodine uptake scattered throughout a larger gland, while the intervening non-autonomous tissue is suppressed and takes up little isotope. This pattern distinguishes it clearly from Graves' disease (diffuse uniform uptake) and from a solitary toxic adenoma (a single hot spot with full suppression of the rest of the gland).

Unlike Graves' disease, toxic MNG will not go into remission with antithyroid drugs — the autonomous nodules do not depend on TSH receptor signaling, so blocking hormone synthesis with propylthiouracil or methimazole only controls hyperthyroidism temporarily. Antithyroid drugs are used as a bridge to definitive treatment, not as a cure. The two definitive options are:

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Substernal Goiter and Compressive Symptoms

A substernal goiter — also called retrosternal or intrathoracic goiter — is one in which thyroid tissue extends below the sternal notch (the top of the breastbone) into the superior mediastinum, the space inside the chest between the lungs. Substernal extension occurs in approximately 10–15% of goiters that require surgery. It arises when a growing thyroid nodule or lobe follows the path of least resistance downward into the chest, drawn by negative intrathoracic pressure during breathing.

The danger of substernal goiters is compression. The thoracic inlet — the bony ring formed by the first thoracic vertebra, the first pair of ribs, and the top of the sternum — is a fixed, non-expandable space. As the thyroid mass grows within it, it can compress the trachea, esophagus, and the great veins (superior vena cava and internal jugular veins). Tracheal compression is the most concerning complication: the normal tracheal diameter is roughly 2 cm, and symptomatic compromise typically begins when the lumen narrows below 1 cm. Severe tracheal compromise can cause positional stridor (the patient may sleep sitting up), exercise intolerance, or acute respiratory distress.

Venous compression causes a distinct syndrome: head, face, and arm swelling from venous congestion, accentuated when the patient raises their arms (Pemberton's sign). Superior vena cava syndrome from thyroid compression is uncommon but well-documented. Esophageal compression causes dysphagia, most pronounced for solid food.

Chest radiography often provides the first clue — deviation of the trachea to one side, widening of the superior mediastinal silhouette, or a visible mass. CT of the neck and chest provides definitive anatomic mapping and is essential for surgical planning, delineating exactly how far the goiter descends and its relationships to vital structures. The vast majority of substernal goiters — over 95% — can be removed via a standard transcervical incision (a "thyroidectomy" through a neck incision) without requiring a sternotomy, because the goiter's blood supply arises from neck vessels, and the mass can be delivered upward through the neck incision even when it has descended considerably into the chest.

Asymptomatic substernal goiters in poor surgical candidates can sometimes be observed, but the surgical risk threshold is generally lower for substernal goiters than for purely cervical ones — the potential for acute respiratory decompensation from even modest additional growth justifies earlier intervention, and elective surgery in a stable patient is far safer than emergency airway management in the context of acute compression.

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Treatment — Medical and Lifestyle

Not every goiter requires treatment. For many patients — particularly those with small, nontoxic, nonnodular goiters and no compressive symptoms — watchful waiting with periodic monitoring is the most appropriate management. The goal of treatment when it is needed is to address the underlying cause, relieve compressive symptoms, normalize thyroid function, and — for any suspicious nodule — exclude or confirm malignancy.

Iodine deficiency goiter responds to iodine repletion. The mainstay of prevention and treatment is iodized salt (approximately 20–40 micrograms per gram of salt) and adequate dietary iodine intake (150 micrograms per day for nonpregnant adults; 220 micrograms in pregnancy; 290 micrograms while breastfeeding). Seafood and dairy products are the richest dietary iodine sources in iodine-sufficient countries. When deficiency is confirmed by low urinary iodine excretion, supplementation can partially reduce goiter size — though a multinodular goiter that has been present for many years generally will not fully regress even with complete iodine repletion, because the structural nodular changes have become established.

Drug-induced goiter management begins with identifying and, where possible, discontinuing the offending agent. For patients on lithium who cannot safely switch medications, the practical approach is to monitor TSH every 6–12 months and prescribe levothyroxine replacement if the patient becomes hypothyroid. Goiter regression after lithium discontinuation is variable and often incomplete.

Levothyroxine suppression therapy — prescribing levothyroxine to suppress TSH below normal and thereby reduce the growth-stimulating signal to the thyroid — was widely used for decades to try to shrink euthyroid goiters. Current evidence and guidelines no longer recommend this approach routinely. The potential benefit (modest and inconsistent goiter size reduction) is outweighed by the risks of chronic subclinical hyperthyroidism: accelerated bone loss leading to osteoporosis, and increased risk of atrial fibrillation, particularly in older adults. Suppression therapy may be appropriate in select younger patients in iodine-deficient regions, but only when the benefits clearly outweigh the risks and with close monitoring.

Goitrogen reduction: For patients with iodine deficiency, minimizing dietary goitrogens — particularly high intake of raw cruciferous vegetables and cassava — may offer a small benefit. For iodine-sufficient patients eating normal diets, there is no evidence that avoiding kale or broccoli affects thyroid size. Cooking brassica vegetables largely inactivates their glucosinolate content. Advising patients to stop eating vegetables that are otherwise nutritionally beneficial, based on theoretical thyroid effects that only materialize with deficiency and extremely high intake, is not supported by evidence and is not recommended.

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Treatment — Surgery and Radioiodine

Definitive intervention is warranted when goiter causes compressive symptoms, when the thyroid is overactive (toxic goiter), when a nodule carries significant concern for malignancy, or when the patient has cosmetic distress from a visibly large neck mass. The two main interventional options are surgery and radioiodine ablation (I-131).

Thyroidectomy (surgical removal of all or part of the thyroid) provides immediate, permanent reduction of the gland. The scope of surgery depends on the indication:

Thyroid surgery carries specific risks that patients should understand: temporary or permanent hypoparathyroidism (the parathyroid glands, which regulate calcium, sit adjacent to the thyroid and can be inadvertently damaged or removed, causing low calcium levels requiring supplementation) and recurrent laryngeal nerve injury (causing hoarseness or, if both nerves are damaged, breathing difficulty). In experienced hands at high-volume thyroid centers, the rates of permanent hypoparathyroidism and permanent nerve injury are each under 2%, but they are real risks that factor into the decision for or against surgery.

Radioiodine (I-131) is a targeted radiation therapy: the patient swallows a capsule or solution containing radioactive iodine-131, which is selectively absorbed by thyroid tissue (the only tissue in the body that concentrates iodine). Radiation from the I-131 destroys thyroid cells over weeks to months. I-131 is most effective in hyperthyroid goiters (Graves' disease, toxic MNG, solitary toxic adenoma) where uptake is high, and less effective for large nontoxic goiters with normal or low radioiodine uptake.

I-131 is contraindicated in pregnancy and breastfeeding. Women of childbearing age should have a pregnancy test before treatment and avoid pregnancy for 6 months after I-131 therapy. I-131 should also not be used when there is concern for thyroid malignancy in any nodule, as radiation from I-131 would not adequately treat cancer and would complicate subsequent diagnostic workup.

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Surveillance and Long-Term Monitoring

Goiter management is a long-term commitment. Even after successful treatment, patients require ongoing monitoring because thyroid disease can evolve over time — a nontoxic MNG can develop autonomous function and become toxic; Hashimoto's thyroiditis can progress from a goiter phase to atrophic hypothyroidism; and new nodules can appear within a previously evaluated gland.

Nodule surveillance: For patients managed with observation rather than intervention, the American Thyroid Association recommends repeat ultrasound at 6–12 months after the initial evaluation for higher-risk nodules (Bethesda III or any suspicious features), and every 1–2 years for stable benign nodules (Bethesda II). A nodule that grows more than 20% in two dimensions (or more than 2 mm in the smallest diameter) is considered to have grown significantly and warrants repeat FNA evaluation even if the prior biopsy was benign. Nodules that remain stable for 5 years without suspicious features can be discharged from active ultrasound surveillance in most cases.

TSH monitoring: Annual TSH measurement is appropriate for patients with multinodular goiter who remain in observation, because autonomous function can develop gradually. A falling TSH — even still within the normal range — over several years of observation signals emerging autonomous hormone production and warrants closer monitoring. Patients with Hashimoto's thyroiditis and a currently euthyroid goiter should have TSH checked every 6–12 months, as progression to overt hypothyroidism is common and often gradual.

Jod-Basedow phenomenon: Patients with autonomous thyroid nodules (subclinical or overt toxic MNG) are at risk of precipitating overt hyperthyroidism if exposed to a large iodine load — a risk named after the German and Danish physicians who first described it. The most common modern scenario is iodinated intravenous contrast used in CT scans. In a patient with known autonomous nodules who needs a contrast CT for an unrelated reason, it is prudent to check TSH before and 4–6 weeks after the contrast exposure, and to consider pretreatment with methimazole in high-risk patients (those with very large multinodular goiters, known low TSH, or cardiovascular disease that would be worsened by hyperthyroidism).

Pregnancy planning: Women with any thyroid condition who are planning pregnancy should optimize thyroid function before conception. Autoimmune thyroid disease — both Graves' and Hashimoto's — can flare in the first trimester and in the postpartum period, so TSH monitoring every trimester during pregnancy is standard. Women planning pregnancy who have had I-131 therapy should wait at least 6 months before conceiving. Iodine supplementation (at least 150 micrograms per day above baseline dietary intake, per the American Thyroid Association's pregnancy guidelines) should begin before conception in women known to have iodine deficiency.

After thyroidectomy: Patients who have undergone total thyroidectomy need lifelong levothyroxine replacement, with TSH monitoring every 6–12 months once the dose is stable. Those who have had hemithyroidectomy need TSH checked at 6 weeks postoperatively and then annually — approximately 20–30% will develop hypothyroidism in the years following lobectomy and require levothyroxine. Calcium and parathyroid hormone (PTH) levels should be monitored in the immediate postoperative period after total thyroidectomy to detect hypoparathyroidism.

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Key Research Papers

  1. Vanderpump MPJ (2011). The epidemiology of thyroid disease. Br Med Bull, 99:39–51. PMID 21893493. DOI: 10.1093/bmb/ldr030
  2. Zimmermann MB, Boelaert K (2015). Iodine deficiency and thyroid disorders. Lancet Diabetes Endocrinol, 3(4):286–295. PMID 25591468. DOI: 10.1016/S2213-8587(14)70225-6
  3. Haugen BR et al (2016). 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer. Thyroid, 26(1):1–133. PMID 26462967. DOI: 10.1089/thy.2015.0020
  4. Ross DS et al (2016). 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid, 26(10):1343–1421. PMID 27521067. DOI: 10.1089/thy.2016.0229
  5. Knudsen N et al (2002). Risk factors for goiter and thyroid nodules. Thyroid, 12(10):879–888. PMID 12487771. DOI: 10.1089/105072502761016562
  6. Mazzaferri EL (1993). Management of a solitary thyroid nodule. N Engl J Med, 328(8):553–559. PMID 8426623. DOI: 10.1056/NEJM199302253280807
  7. Hegedüs L et al (2003). Management of simple nodular goiter: current status and future perspectives. Endocr Rev, 24(1):102–132. PMID 12588812. DOI: 10.1210/er.2002-0016
  8. Bahn RS et al (2011). Hyperthyroidism and Other Causes of Thyrotoxicosis: Management Guidelines of the American Thyroid Association. Thyroid, 21(6):593–646. PMID 21510801. DOI: 10.1089/thy.2010.0417
  9. Durante C et al (2015). The natural history of benign thyroid nodules. JAMA, 313(9):926–935. PMID 25734734. DOI: 10.1001/jama.2015.0956
  10. Tessler FN et al (2017). ACR Thyroid Imaging, Reporting and Data System (TI-RADS): White Paper of the ACR TI-RADS Committee. J Am Coll Radiol, 14(5):587–595. PMID 28372962. DOI: 10.1016/j.jacr.2017.01.046
  11. Gharib H et al (2010). AACE/AME/ETA Task Force on Thyroid Nodules. Endocr Pract, 16 Suppl 1:1–43. PMID 20360146. DOI: 10.4158/10024.GL
  12. Braverman LE, Cooper DS, eds. Werner & Ingbar's The Thyroid: A Fundamental and Clinical Text. 10th ed. Philadelphia: Lippincott Williams & Wilkins; 2012. (Standard reference textbook in thyroidology.)

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Connections

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