Hubbry Logo
GoitreGoitreMain
Open search
Goitre
Community hub
Goitre
logo
8 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Contribute something
Goitre
Goitre
Goitre
View on Wikipedia
from Wikipedia

Goitre
Other namesGoiter
Diffuse hyperplasia of the thyroid
SpecialtyEndocrinology
CausesIodine deficiency, autoimmune disease, tumors, cyanide poisoning

A goitre (British English), or goiter (American English), is a swelling in the neck resulting from an enlarged thyroid gland.[1][2] A goitre can be associated with a thyroid that is not functioning properly.

Worldwide, over 90% of goitre cases are caused by iodine deficiency.[3] The term is from the Latin gutturia, meaning throat. Most goitres are not cancerous (benign), though they may be potentially harmful.

Signs and symptoms

[edit]

A goitre can present as a palpable or visible enlargement of the thyroid gland at the base of the neck. A goitre, if associated with hypothyroidism or hyperthyroidism, may be present with symptoms of the underlying disorder. For hyperthyroidism, the most common symptoms are associated with adrenergic stimulation: tachycardia (increased heart rate), palpitations, nervousness, tremor, increased blood pressure and heat intolerance. Clinical manifestations are often related to hypermetabolism (increased metabolism), excessive thyroid hormone, an increase in oxygen consumption, metabolic changes in protein metabolism, immunologic stimulation of diffuse goitre, and ocular changes (exophthalmos).[4] Hypothyroid people commonly have poor appetite, cold intolerance, constipation, lethargy and may undergo weight gain. However, these symptoms are often non-specific and make diagnosis difficult.[citation needed]

According to the WHO classification of goitre by palpation, the severity of goitre is currently graded as grade 0, grade 1, grade 2.[5]

  • Goitre Class II, WHO grade 2
    Goitre Class II, WHO grade 2
  • Goitre Class III, WHO grade 2
    Goitre Class III, WHO grade 2

Causes

[edit]

Worldwide, the most common cause for goitre is iodine deficiency, commonly seen in countries that scarcely use iodized salt. Selenium deficiency is also considered a contributing factor. In countries that use iodized salt, Hashimoto's thyroiditis is the most common cause.[6] Goitre can also result from cyanide poisoning, which is particularly common in tropical countries where people eat the cyanide-rich cassava root as the staple food.[7]

Cause Pathophysiology Resultant thyroid activity Growth pattern Treatment Incidence and prevalence Prognosis
Iodine deficiency Hyperplasia of thyroid to compensate for decreased efficacy Can cause hypothyroidism Diffuse Iodine Constitutes over 90% cases of goitre worldwide[3] Increased size of thyroid may be permanent if untreated for around five years
Congenital hypothyroidism Inborn errors of thyroid hormone synthesis Hypothyroidism
Goitrogen ingestion
Adverse drug reactions
Hashimoto's thyroiditis Autoimmune disease in which the thyroid gland is gradually destroyed. Infiltration of lymphocytes. Hypothyroidism Diffuse and lobulated[8] Thyroid hormone replacement Prevalence: 1 to 1.5 in a 1000 Remission with treatment
Pituitary disease Hypersecretion of thyroid stimulating hormone, almost always by a pituitary adenoma[9] Diffuse Pituitary surgery Very rare[9]
Graves' disease—also called Basedow syndrome Autoantibodies (TSHR-Ab) that activate the TSH-receptor (TSHR) Hyperthyroidism Diffuse Antithyroid agents, radioiodine, surgery Will develop in about 0.5% of males and 3% of females Remission with treatment, but still lower quality of life for 14 to 21 years after treatment, with lower mood and lower vitality, regardless of the choice of treatment[10]
Thyroiditis Acute or chronic inflammation Can be hyperthyroidism initially, but progress to hypothyroidism
Thyroid cancer Usually uninodular Overall relative 5-year survival rate of 85% for females and 74% for males[11]
Benign thyroid neoplasms Usually hyperthyroidism Usually uninodular Mostly harmless[12]
Thyroid hormone insensitivity Secretional hyperthyroidism,
Symptomatic hypothyroidism		 Diffuse

Diagnosis

[edit]
Goitre with toxic adenoma

Goitre may be diagnosed via a thyroid function test in an individual suspected of having it.[13]

Types

[edit]

A goitre may be classified either as nodular or diffuse. Nodular goitres are either of one nodule (uninodular) or of multiple nodules (multinodular).[14] Multinodular goiter (MNG) is the most common disorder of the thyroid gland.[15]

Growth pattern
  • Uninodular goitre: one thyroid nodule; can be either inactive, or active (toxic) – autonomously producing thyroid hormone.
  • Multinodular goitre: multiple nodules;[16] can likewise be inactive or toxic, the latter is called toxic multinodular goitre and associated with hyperthyroidism. These nodules grow up at varying rates and secrete thyroid hormone autonomously, thereby suppressing TSH-dependent growth and function in the rest of gland. Inactive nodules in the same goitre can be malignant.[17] Thyroid cancer is identified in 13.7% of the patients operated for multinodular goitre.[18]
  • Diffuse goitre: the whole thyroid appearing to be enlarged due to hyperplasia.
Size
  • Class I: the goitre in normal posture of the head cannot be seen; it is only found by palpation.
  • Class II: the goitre is palpable and can be easily seen.
  • Class III: the goitre is very large and is retrosternal (partially or totally lying below the sternum), pressure results in compression marks.

Treatment

[edit]

Goitre is treated according to the cause. If the thyroid gland is producing an excess of thyroid hormones (T3 and T4), radioactive iodine is given to the patient to shrink the gland. If goitre is caused by iodine deficiency, small doses of iodide in the form of Lugol's iodine or KI solution are given. If the goitre is associated with an underactive thyroid, thyroid supplements are used as treatment. Sometimes a partial or complete thyroidectomy is required.[19]

Medical and scientific developments

[edit]

The discovery of iodine's importance in thyroid function and its role in preventing goiter marked a significant medical breakthrough. The introduction of iodized salt in the early 20th century became a key public health initiative, effectively reducing the prevalence of goiter in previously affected regions. This measure was one of the earliest and most successful examples of mass preventive health campaigns.[20]

Epidemiology

[edit]
Disability-adjusted life year for iodine deficiency per 100,000 inhabitants in 2002:[21]
  No data
  <50
  50–100
  100–150
  150–200
  200–250
  250–300
  300–350
  350–400
  400–450
  450–500
  500–800
  >800

Goitre is more common among women, but this includes the many types of goitre caused by autoimmune problems, and not only those caused by simple lack of iodine.[22]

Iodine mainly accumulates in the sea and in the topsoil. Before iodine enrichment programs, goiters were common in areas with repeated flooding or glacial activities, which erodes the topsoil. It is endemic in populations where the intake of iodine is less than 10 μg per day.[23]

Examples of such regions include the alpine regions of Southern Europe (such as Switzerland), the Himalayans, the Great Lakes basin, etc. As reported in 1923, all the domestic animals have goiter in some of the glacial valleys of Southern Alaska. It was so severe in Pemberton Meadows that it was difficult to raise young animals there.[24]

History

[edit]
Goitre and congenital iodine deficiency syndrome in Styria, copper engraving, 1815
Woman in Miesbacher Tracht wearing a goitre choker

Chinese physicians of the Tang dynasty (618–907) were the first to successfully treat patients with goitre by using the iodine-rich thyroid gland of animals such as sheep and pigs—in raw, pill, or powdered form.[25] This was outlined in Zhen Quan's (d. 643 AD) book, as well as several others.[25] One Chinese book, The Pharmacopoeia of the Heavenly Husbandman, asserted that iodine-rich sargassum was used to treat goitre patients by the 1st century BC, but this book was written much later.[25]

In the 12th century, Zayn al-Din al-Jurjani, a Persian physician, provided the first description of Graves' disease after noting the association of goitre and a displacement of the eye known as exophthalmos in his Thesaurus of the Shah of Khwarazm, the major medical dictionary of its time.[26][27] The disease was later named after Irish doctor Robert James Graves, who described a case of goitre with exophthalmos in 1835. The German Karl Adolph von Basedow also independently reported the same constellation of symptoms in 1840, while earlier reports of the disease were also published by the Italians Giuseppe Flajani and Antonio Giuseppe Testa, in 1802 and 1810 respectively,[28] and by the English physician Caleb Hillier Parry (a friend of Edward Jenner) in the late 18th century.[29]

Paracelsus (1493–1541) was the first person to propose a relationship between goitre and minerals (particularly lead) in drinking water.[30] Iodine was later discovered by Bernard Courtois in 1811 from seaweed ash.[31]

Goitre was previously common in many areas that were deficient in iodine in the soil. For example, in the English Midlands, the condition was known as Derbyshire Neck. In the United States, goitre was found in the Appalachian,[32][33] Great Lakes, Midwest, and Intermountain regions. The condition is now practically absent in affluent nations, where table salt is supplemented with iodine. However, it is still prevalent in India, China,[34] Central Asia, and Central Africa.

Goitre had been prevalent in the alpine countries for a long time. Switzerland reduced the condition by introducing iodized salt in 1922. The Bavarian tracht in the Miesbach and Salzburg regions, which appeared in the 19th century, includes a choker, dubbed Kropfband (struma band) which was used to hide either the goitre or the remnants of goitre surgery.[35]

In various regions around the world, particularly in mountainous areas, the prevalence of goiter was linked to iodine deficiency in the diet. For example, the Alps, the Himalayas, and the Andes had high rates of goiter due to the iodine-poor soil. In these regions, iodine deficiency led to widespread hormonal imbalances, particularly affecting thyroid function.[36]

Society and culture

[edit]

In the 1920s wearing bottles of iodine around the neck was believed to prevent goitre.[37]

Notable cases

[edit]

Heraldry

[edit]

The coat of arms and crest of Die Kröpfner, of Tyrol, showed a man "afflicted with a large goitre", an apparent pun on the German for the word ("Kropf").[41]

Social Impacts

[edit]

In some historical contexts, goiters were so prevalent that they became normalized within the culture. For instance, in certain Alpine regions, large goiters were sometimes considered a sign of beauty. Conversely, in other areas, individuals with goiters faced social stigma, which could lead to marginalization and discrimination.[42]

See also

[edit]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Goitre

View on Grokipedia
from Grokipedia
A goitre (or goiter) is an abnormal enlargement of the gland, a butterfly-shaped endocrine organ located at the base of the neck that produces hormones regulating , growth, and development. This swelling can be diffuse, affecting the entire gland, or nodular, involving one or more lumps, and it may occur with normal (euthyroid), overactive (hyperthyroid), or underactive (hypothyroid) function. , the primary cause of goitre worldwide, affects an estimated 2.2 billion people, though in iodine-sufficient regions like the , it impacts about 5% of the population, with higher prevalence in females and those over age 40. The most common cause worldwide is iodine deficiency, which impairs thyroid hormone synthesis and triggers compensatory gland growth through elevated thyroid-stimulating hormone (TSH) levels. In developed countries, autoimmune disorders predominate, including Hashimoto's thyroiditis (leading to hypothyroidism) and Graves' disease (causing hyperthyroidism), while other etiologies encompass thyroid nodules, inflammation (thyroiditis), pregnancy-related hormonal changes, certain medications like lithium, radiation exposure, and rarely, thyroid cancer. Multinodular goitres, characterized by multiple benign lumps, often develop over time without a fully understood trigger but can become toxic if overproducing hormones. Risk factors include female sex (four times more common than in males), family history, age over 40, and iodine-poor diets. Symptoms vary by size and function but often include a visible or palpable swelling at the neck's base, which may cause cosmetic concerns or a sensation of tightness. Large goitres can lead to compressive effects such as difficulty swallowing (dysphagia), breathing (dyspnea), hoarseness, or cough due to pressure on the trachea or esophagus. Associated thyroid dysfunction may manifest as hypothyroidism symptoms (fatigue, weight gain, cold intolerance, dry skin) or hyperthyroidism (weight loss, rapid heartbeat, heat intolerance, tremors). Many goitres are asymptomatic and discovered incidentally, with prevalence increasing with advanced imaging detection. Diagnosis typically begins with a physical to assess gland size, followed by blood tests measuring TSH, free thyroxine (T4), and (T3) to evaluate function. ultrasound is the primary imaging tool to characterize nodules (e.g., size, solidity, vascularity), with biopsy recommended for suspicious features like microcalcifications or rapid growth in nodules over 1 cm. Additional tests, such as CT or MRI, assess compression, while radioactive iodine scans differentiate hot (overactive) from (potentially cancerous) nodules. Treatment depends on the underlying cause, size, symptoms, and function: small, nontoxic goitres may require only monitoring with annual exams. Iodine supplementation addresses deficiency-related cases, while suppresses TSH in hypothyroid or nodular goitres to reduce growth. For toxic or symptomatic goitres, options include antithyroid drugs (e.g., methimazole), radioactive iodine ablation (preferred for ), or () for large compressive or cancerous lesions. Prevention focuses on adequate iodine intake through iodized salt, , and , which has dramatically reduced in many regions since its introduction in the early . Prognosis is generally excellent for benign goitres, though lifelong replacement may be needed post-surgery.

Clinical Presentation

Signs and Symptoms

A goitre primarily manifests as an enlargement of the thyroid gland, appearing as a swelling at the base of the neck that can range from subtle and barely noticeable to a pronounced mass causing cosmetic concerns. In many cases, individuals experience no symptoms beyond this visible or palpable swelling, with the goitre often discovered incidentally during routine physical examinations or imaging for unrelated issues. When the goitre grows larger, it may exert on surrounding structures, leading to compressive symptoms such as difficulty swallowing (), a sensation of fullness or tightness in the , hoarseness, persistent cough, or noisy breathing. In severe cases, significant enlargement can cause dyspnea, particularly during exertion, or even sensations due to airway compression. discomfort or is also common, though most goitres remain painless unless associated with . Goitres linked to thyroid hormone imbalances, such as , may present with systemic symptoms of including rapid heartbeat, unintended weight loss, heat intolerance, tremors, and increased sweating, which arise directly from the gland's overactivity amid its enlargement. Conversely, goitres associated with might involve fatigue, weight gain, and cold sensitivity, though these are secondary to the underlying dysfunction rather than the swelling itself. The presentation can progress from an simple enlargement to more complicated forms, with rapid growth potentially indicating hemorrhage or leading to acute , as seen in rare cases of . Substernal extension of the goitre may further complicate symptoms by causing facial flushing or worsened dyspnea upon arm elevation.

Physical Examination

The of a goiter begins with of the , typically performed with seated and the head slightly extended to optimize on the anterior . The examiner observes for any visible swelling or at the base of the , noting whether the enlargement moves upward with , which confirms its origin. Prominent vascular pulsations may also be visible in cases of hypervascularity. Palpation is the cornerstone of thyroid assessment, conducted with the examiner positioned behind or to the side of the patient to facilitate bimanual technique. The , , and sternal notch serve as key landmarks; the examiner gently places fingers along the trachea to palpate the and lobes, avoiding compression of the sternocleidomastoid muscles. To evaluate size, the normal thyroid lobes are approximately 7-10 grams each, and enlargement is gauged by the extent of palpable tissue extending beyond these bounds. Consistency is assessed as soft (common in diffuse goiters like those from ), firm (as in autoimmune ), or nodular (indicating multinodular goiter); tenderness suggests , hemorrhage, or . Mobility is tested by having the patient swallow a sip of water, observing if the gland glides smoothly with the trachea—restricted movement may indicate adhesions from or . The lower border is palpated to detect substernal extension; if not reachable, is elicited by raising the patient's arms overhead for one minute to provoke symptoms of thoracic inlet compression, such as facial flushing or dyspnea. Auscultation follows , using a placed over the lobes to detect a —a continuous whooshing sound signifying increased vascularity, often heard in hyperthyroid states like due to arteriovenous shunting. A palpable thrill may accompany louder bruits. enlargement is graded using the (WHO) system to standardize assessment: Grade 0 indicates no palpable or visible goiter; Grade 1 denotes a palpable not visible with the in normal position; and Grade 2 describes a goiter visible when the is in the normal position. This palpation-based grading helps quantify prevalence in endemic areas but may underestimate small or substernal goiters. Associated features are evaluated concurrently: is palpated in the anterior and posterior triangles, as enlarged nodes may signal thyroid malignancy or metastasis. In suspected , eye signs such as , , or periorbital are inspected for proptosis. is assessed by midline of the trachea; lateral displacement suggests significant compression from a large goiter. Differentiation between diffuse and nodular enlargement relies on palpation findings: a diffuse goiter presents as uniform, symmetrical swelling without discrete lumps, often seen in or , whereas nodular goiter features one or more firm, distinct masses that may be solitary or multiple, warranting further evaluation for autonomy or neoplasia.

Causes

Goitre, or thyroid enlargement, arises from various etiological factors that disrupt normal thyroid function or structure, leading to compensatory growth of the . The most common global cause is , which impairs thyroid hormone synthesis and triggers increased (TSH) secretion from the , resulting in follicular cell and gland enlargement. This mechanism is particularly prevalent in regions with low soil iodine content, where dietary intake is insufficient, affecting an estimated 2.2 billion people worldwide. Endemic goitre refers to enlargement occurring in populations where prevalence exceeds 10%, primarily due to chronic in iodine-poor geographic areas, often exacerbated by goitrogenic factors in local diets or water. In contrast, sporadic goitre develops in iodine-sufficient regions and is typically linked to non-environmental triggers, such as genetic predispositions or isolated physiological demands, though it shares similar hyperplastic pathways. Autoimmune disorders are significant causes of goitre in iodine-replete settings. , an autoimmune condition characterized by lymphocytic infiltration and antibody-mediated destruction of thyroid tissue, leads to and subsequent goitrous enlargement as the gland attempts to compensate for reduced hormone production. Conversely, , another autoimmune thyroiditis, causes through TSH receptor-stimulating antibodies, promoting diffuse thyroid hyperplasia and goitre formation. Certain pharmacological agents interfere with thyroid hormone synthesis or release, inducing goitre. Lithium, commonly used in bipolar disorder treatment, inhibits thyroid hormone release and iodide uptake, leading to elevated TSH levels and glandular hypertrophy in up to 40% of long-term users. Amiodarone, an antiarrhythmic drug rich in iodine, can paradoxically disrupt thyroid function by causing either hypothyroidism through Wolff-Chaikoff effect inhibition or destructive thyroiditis, both resulting in goitre. Physiological states with heightened thyroid hormone demands can cause transient goitre due to temporary . During , , and , increased levels enhance TSH sensitivity and thyroid-binding , elevating hormone requirements and prompting enlargement, particularly in women. In , this goitrogenesis is driven by higher metabolic needs and hCG-mediated TSH suppression, often resolving postpartum. Rare causes include infectious, radiation-induced, and infiltrative processes. , often viral in origin, leads to painful goitre through granulomatous inflammation and follicular disruption, causing transient followed by . External , such as from medical treatments or environmental accidents, damages thyroid follicles and induces or nodular growth, increasing goitre risk dose-dependently. Infiltrative diseases like deposit proteins in the thyroid , causing compressive enlargement and functional impairment.

Types

Goitres are classified based on their structural characteristics, functional status, , and specific morphological features. Structurally, they can be diffuse or nodular. A diffuse goitre involves uniform enlargement of the entire , resulting in a smooth, symmetric swelling without discrete lumps. In contrast, a nodular goitre features one or more focal nodules; these may be solitary (uninodular) or multiple (multinodular), often developing from compensatory in response to chronic stimulation. Multinodular goitres are common in long-standing cases and can lead to irregular contours. Functionally, goitres are categorized as simple (euthyroid), toxic (hyperfunctioning), or hypofunctioning. Simple goitres maintain normal thyroid hormone levels (euthyroidism) despite enlargement, typically arising from physiological adaptations or mild deficiencies without disrupting synthesis. Toxic goitres, however, are hyperfunctioning, producing excess and causing thyrotoxicosis; examples include , where autonomous nodules overproduce hormones, or toxic diffuse goitre as seen in . Hypofunctioning goitres are associated with reduced hormone output, leading to , often due to autoimmune destruction or biosynthetic defects in the gland. Etiologically, goitres are distinguished as endemic or sporadic. Endemic goitre occurs in populations where affects more than 10% of individuals, leading to widespread enlargement as a compensatory response to insufficient iodine for production. Sporadic goitre, conversely, arises in iodine-sufficient areas and affects individuals idiosyncratically, often linked to autoimmune conditions, medications, or isolated genetic factors rather than environmental deficiencies. Congenital goitre manifests at birth and results from fetal exposure to during or intrinsic genetic defects impairing synthesis, such as mutations in genes encoding the sodium-iodide symporter or . These can present as diffuse enlargement and may be associated with if untreated. Certain goitres exhibit specific morphological variants, including cystic or hemorrhagic types. Cystic goitres contain fluid-filled sacs within nodules, which may arise from degeneration of follicular tissue. Hemorrhagic goitres involve bleeding into nodules or the gland parenchyma, potentially causing sudden pain and rapid enlargement due to formation. The (WHO) provides a framework emphasizing physiological, non-toxic, and toxic categories, particularly for multinodular forms. Physiological goitres represent adaptive enlargements, such as during or , without pathological implications. Non-toxic multinodular goitres are euthyroid or hypothyroid enlargements with multiple nodules but no hyperfunction. Toxic multinodular goitres, in contrast, feature hyperfunctioning nodules leading to thyrotoxicosis. This system aids in distinguishing benign adaptive changes from those requiring intervention.

Diagnosis

Diagnostic Tests

Diagnosis of goiter typically begins with laboratory assessments to evaluate thyroid function and potential underlying autoimmune processes. Serum thyroid-stimulating hormone (TSH) levels are measured as the initial test, with subnormal TSH prompting further evaluation for hyperthyroidism and elevated TSH indicating hypothyroidism. Free thyroxine (T4) and triiodothyronine (T3) levels are then assessed to confirm the functional status of the thyroid gland. Additionally, thyroid autoantibodies such as anti-thyroid peroxidase (anti-TPO) antibodies are tested to identify autoimmune etiologies like Hashimoto's thyroiditis, which is a common cause of goitrous hypothyroidism. Ultrasound serves as the first-line imaging modality for characterizing goiter, providing detailed assessment of size, echotexture, nodularity, vascularity, and the presence of calcifications. High-resolution can detect nodules as small as 1-2 mm and is essential for risk stratification using sonographic patterns, such as hypoechoic composition or microcalcifications, which indicate higher risk. For nodules greater than 1 cm with suspicious features, -guided (FNA) is performed to obtain cytology samples, enabling evaluation for . FNA involves inserting a thin needle into the nodule under real-time guidance to minimize complications and improve accuracy. Cytological results from FNA are reported using the , a standardized six-category framework that correlates with the risk of . The categories include: nondiagnostic (risk 1-4%), benign (0-3%), of undetermined significance/follicular lesion of undetermined significance (5-15%), follicular /suspicious for follicular (15-30%), suspicious for (60-75%), and malignant (97-99%). This system facilitates consistent communication between pathologists and clinicians, guiding decisions on whether to pursue diagnostic or molecular testing for indeterminate results. Thyroid scintigraphy, often using technetium-99m pertechnetate or iodine-123, is employed when TSH is subnormal to differentiate hyperfunctioning ("hot") nodules, which are typically benign, from nonfunctioning ("cold") nodules that may harbor malignancy or represent hypofunction. In multinodular goiter, scintigraphy helps identify autonomously functioning areas contributing to hyperthyroidism. The procedure involves intravenous injection of the radiotracer followed by imaging to assess uptake and nodule functionality, providing functional rather than anatomical detail. Computed tomography (CT) or magnetic resonance imaging (MRI) is reserved for cases with suspected compressive symptoms or retrosternal extension, offering superior visualization of the goiter's relationship to surrounding structures like the trachea and . Contrast-enhanced CT is particularly useful for detecting substernal components and vascular involvement, while MRI provides better soft-tissue contrast without radiation exposure. These modalities are not routine but are indicated when is inconclusive or symptoms such as or dyspnea suggest extrinsic compression.

Classification and Staging

Goitre classification and staging involve multiple systems to assess severity, functional status, size, malignancy potential, and complications, guiding clinical management and surgical decisions. These systems interpret diagnostic findings, such as ultrasound and thyroid function tests, to stratify risk and prognosis without overlapping etiological typing. Nodular goitres are classified using the Thyroid Imaging Reporting and Data System (TI-RADS), particularly the American College of Radiology (ACR) TI-RADS, which evaluates ultrasound features to predict malignancy risk. The system assigns points based on five categories: composition (0-2 points), echogenicity (0-3 points), shape (0-3 points), margin (0-3 points), and echogenic foci (0-3 points), with total points determining the TI-RADS level. Nodules are categorized as TR1 (0 points, benign pattern, 0.3% malignancy risk), TR2 (2 points, not suspicious, 1.5% risk), TR3 (3 points, mildly suspicious, 4.8% risk), TR4 (4-6 points, moderately suspicious, 9.1% risk), and TR5 (≥7 points, highly suspicious, 35% risk). This scoring helps prioritize fine-needle aspiration (FNA) biopsy for higher-risk nodules.
Feature CategoryScoring (Points)
CompositionCystic/spongiform: 0; Mixed: 1; Solid: 2
EchogenicityAnechoic: 0; Hyper- or isoechoic: 1; Hypoechoic: 2; Very hypoechoic: 3
ShapeWider-than-tall: 0; Taller-than-wide: 3
MarginSmooth or ill-defined: 0; Lobulated/irregular: 2; Extrathyroidal extension: 3
Echogenic FociNone/comet-tail: 0; Macrocalcifications: 1; Peripheral: 2; Punctate: 3
Functional staging of goitre categorizes it based on thyroid hormone levels from blood tests, determining euthyroid (normal TSH, free T4, and T3), hyperthyroid (low TSH, elevated T4/T3), or hypothyroid (high TSH, low T4) status. Most simple or nodular goitres are euthyroid, while toxic multinodular goitre or Graves' disease may present as hyperthyroid, and Hashimoto's thyroiditis as hypothyroid. This staging influences treatment, with hyperthyroid goitres requiring control of excess hormone production before interventions. Size-based staging quantifies goitre volume using measurements and the formula for each lobe: volume (mL) = length (cm) × width (cm) × depth (cm) × 0.52, with total volume including the if significant. Normal adult volume is 7-20 mL; goitre is typically defined as >20 mL, with larger volumes (>40 mL) indicating substantial enlargement for surgical planning. This approach assesses growth progression and compressive risk, aiding decisions on observation versus intervention. Malignancy risk stratification follows American Thyroid Association (ATA) guidelines, which recommend FNA based on sonographic patterns and nodule size to balance diagnostic yield and procedure risks. Patterns include high suspicion (solid hypoechoic with suspicious features, 70-90% risk, FNA at ≥1 cm), intermediate (hypoechoic solid, 10-20% risk, FNA at ≥1 cm), low (isoechoic solid or partially cystic, 5-10% risk, FNA at ≥1.5 cm), very low (spongiform, <3% risk, FNA at ≥2 cm optional), and benign (purely cystic, <1% risk, no FNA). These thresholds reduce unnecessary biopsies while identifying cancers early. Complication staging evaluates airway obstruction and cosmetic impact through clinical scales, focusing on symptom severity and structural effects. For cosmetic and size assessment, the World Health Organization (WHO) grading system is used: Grade 0 (no palpable or visible goitre), Grade 1 (palpable but not visible with head extended), and Grade 2 (visible with head in normal position), highlighting visible enlargement as a key indicator for intervention. Airway obstruction is staged clinically by symptoms (e.g., dyspnea, stridor) and imaging evidence of tracheal compression, with severe cases involving >50% narrowing prompting urgent management to prevent respiratory compromise.

Management

Nonsurgical Treatments

For iodine deficiency-related goitre, supplementation is the primary nonsurgical treatment, typically administered as oral or iodized oil in endemic areas, with a recommended daily intake of 150 micrograms for adults to restore synthesis and reduce goitre size. In regions with widespread deficiency, universal salt iodization programs, endorsed by the , fortify table salt with 20–40 milligrams of iodine per kilogram to achieve population-level correction, leading to a significant decline in goitre prevalence over months to years. These programs have been shown to reduce rates globally by over 75% from 1993 to 2019, particularly in school-aged children, when coverage is high. In cases of toxic goitre associated with , such as , antithyroid drugs like methimazole are used to inhibit thyroid hormone production by blocking iodine organification and coupling in the . Methimazole is typically initiated at 10–30 milligrams daily, titrated to normalize thyroid function within 4–8 weeks, providing effective control of symptoms like and in over 80% of patients. Long-term may be required for sustained euthyroidism, particularly in older patients unfit for other interventions. Levothyroxine suppression is employed for non-toxic, euthyroid goitre to reduce (TSH) levels, thereby decreasing goitre growth and promoting shrinkage by minimizing pituitary stimulation of the thyroid. Administered at doses of 1.6–1.8 micrograms per kilogram daily to achieve subclinical (TSH <0.1 mU/L), it is most effective for small, diffuse goitres, with volume reductions of 20–50% observed in responsive cases after 6–12 months. However, efficacy diminishes in longstanding multinodular goitre, and requires monitoring for risks like . Radioiodine therapy using (I-131) targets hyperfunctioning nodules within goitre by leveraging the 's selective uptake of iodine, where beta particles from I-131 decay ablate overactive tissue through , leading to nodule inactivation and goitre size reduction of 40–60% within 6–12 months. is calculated based on uptake and mass, with fixed empiric doses of 15–30 millicuries (555–1110 megabecquerels) commonly used for toxic nodules to deliver 100–300 gray , achieving euthyroidism in 70–90% of cases after one treatment. Pretreatment with antithyroid drugs may optimize uptake, and a low-iodine diet for 7–14 days enhances . For small, asymptomatic goitres without compressive symptoms or suspicious features, the American Thyroid Association recommends active observation with annual clinical examination and , supplemented by ultrasonography every 6–12 months to monitor for growth or nodularity changes. This approach avoids unnecessary intervention in stable cases. To manage complications such as symptomatic in goitre, beta-blockers like provide rapid relief by antagonizing adrenergic effects, reducing , , and anxiety without altering hormone levels. Doses of 20–40 milligrams every 6–8 hours are typically used initially, titrated to control symptoms until definitive therapy takes effect, with nonselective agents preferred for their additional peripheral conversion blockade of T4 to T3.

Surgical and Other Interventions

Surgical intervention is indicated for goitre when there are compressive symptoms such as , dyspnoea, or airway obstruction, suspicion of based on diagnostic evaluation, or significant cosmetic concerns due to gland enlargement. For benign multinodular goitre, thyroidectomy types include partial procedures like for unilateral nodules, which effectively addresses localized disease while preserving remaining thyroid function. In contrast, total is preferred for diffuse goitre, bilateral involvement, or when is suspected, as it removes the entire gland to prevent recurrence and facilitate comprehensive treatment. During surgery, intraoperative considerations focus on preventing complications through techniques such as recurrent laryngeal nerve (RLN) monitoring, which aids in nerve identification and reduces injury rates by providing real-time feedback on nerve function. Parathyroid gland preservation is equally critical, involving in situ maintenance of blood supply or autotransplantation if devascularization occurs, to minimize the risk of postoperative hypoparathyroidism. For benign nodules, minimally invasive alternatives to open include (RFA), which uses heat to shrink nodules under guidance, offering reduced recovery time and complication rates compared to traditional excision, with recent long-term data confirming sustained efficacy as of 2024. injection, particularly effective for cystic or predominantly cystic nodules, involves aspiration followed by sclerosant injection to induce and volume reduction, with high success rates in symptom relief. Postoperative care emphasizes monitoring for through serial serum calcium levels, with supplementation initiated if develops to prevent or cardiac issues. Following total , lifelong replacement is required to maintain euthyroidism, with dosing adjusted based on TSH levels to avoid over- or under-replacement. Recent advancements include robotic-assisted thyroidectomy, adopted widely since the early 2000s, which enhances precision through three-dimensional visualization and articulated instruments, particularly in remote-access approaches like transaxillary or bilateral axillo-breast to reduce visible scarring. These techniques have demonstrated comparable outcomes to conventional in terms of oncologic safety and complication rates for goitre management.

Epidemiology and Public Health

Prevalence and Distribution

Goitre affects an estimated 5% to 20% of the global population, particularly in regions with , while approximately 1.9 billion people—nearly 30% of the world's inhabitants—remain at risk of iodine deficiency disorders that contribute to its development. These figures underscore the condition's persistence as a major issue, despite widespread interventions. The classifies areas as endemic for goitre when prevalence exceeds 5% in school-aged children, with total goitre rates globally estimated at 10% to 20%, affecting around 700 million individuals. As of 2025, the Iodine Global Network reports 23 countries with , up from 19 in 2017, indicating ongoing challenges. Endemic goitre is most prevalent in , , and remote mountainous regions including the in Asia and the in , where glacial soils and erosion result in severe iodine depletion, limiting dietary intake from local food sources. In these areas, prevalence can reach 30% or higher in affected communities, far exceeding global averages. Since the widespread adoption of universal salt iodization programs in the mid-20th century, goitre rates have declined dramatically in many countries, reducing endemicity from severe to mild levels in regions like parts of and . However, resurgences have been noted in economically challenged areas where access to affordable iodized salt is limited by and supply disruptions, leading to renewed iodine insufficiency. The condition shows distinct demographic patterns, occurring more frequently in women than in men, attributed to physiological demands during reproductive years. Prevalence typically peaks in , when rapid growth increases iodine needs, and during , when hormonal changes and fetal requirements exacerbate thyroid enlargement. In severe endemic zones, goitre contributes to significant morbidity, including endemic cretinism—a form of causing profound , motor deficits, and in up to 10% of children in the most affected communities.

Risk Factors and Prevention

Risk factors for goitre encompass both non-modifiable demographic elements and modifiable environmental influences that contribute to thyroid enlargement, primarily through iodine insufficiency or interference with thyroid function. Women face a significantly higher than men, with ratios often exceeding 5:1, particularly in iodine-deficient regions where hormonal fluctuations during , , and exacerbate vulnerability. Family history of thyroid disorders also elevates susceptibility, as genetic predispositions affect iodine uptake and thyroid hormone synthesis. Age-related factors further play a role, with heightened incidence during due to rapid growth demands and in older adults from cumulative iodine depletion. Environmental risks predominantly stem from low dietary iodine intake, which remains the leading global cause of goitre, affecting over 2 billion people in endemic areas where and are naturally deficient. Certain foods containing goitrogens—compounds that inhibit iodine absorption or activity—can compound this risk when consumed excessively, such as (e.g., , ) or in staple diets of iodine-poor regions. Emerging environmental threats include , which may alter iodine levels through shifts in ocean chemistry and atmospheric deposition, potentially worsening deficiency in vulnerable coastal and agricultural zones. Additionally, certain medications like or can induce goitre in susceptible individuals by disrupting iodine organification, particularly in those with pre-existing mild deficiency. Prevention strategies focus on ensuring adequate iodine supply, with the (WHO) endorsing universal salt iodization since 1994 as a cost-effective to eliminate deficiency disorders, targeting iodization of all household and food-grade salt at 20-40 mg/kg. For pregnant women, daily iodine supplementation of 150-250 mcg is recommended to meet elevated requirements (220-250 mcg RDA), reducing neonatal goitre risk and supporting fetal development. Public health programs bolster these efforts through neonatal -stimulating hormone (TSH) screening, which detects early iodine deficiency indicators in newborns and enables timely intervention in endemic areas. policies, including mandatory iodization in salt and staples like in high-risk regions, have successfully lowered goitre prevalence by over 50% in implemented programs.

Historical and Societal Context

Medical History

Goitre, an enlargement of the thyroid gland, has been recognized since ancient times, with early descriptions appearing in Chinese medical texts around 2700 BCE, where it was noted as a neck swelling treatable with and burnt , substances later understood to contain iodine. In ancient , the Ayurvedic texts from approximately 1400 BCE to 400 CE referred to goitre as "gala-ganda," associating it with imbalances in bodily humors and recommending herbal remedies, though without a clear etiological understanding. These early observations highlighted regional prevalence in iodine-deficient areas but lacked insight into the underlying nutritional cause. By the 16th century, the Swiss physician (1493–1541) advanced the understanding by linking goitre to environmental factors, attributing it to mineral impurities in drinking water, particularly in mountainous regions. This marked an early recognition of endemic patterns, though treatment remained empirical, often involving local remedies like animal thyroid extracts. In the , significant progress occurred with Carl Adolph von Basedow's 1840 description of exophthalmic goitre, characterizing the triad of thyroid enlargement, , and , which differentiated hyperthyroid forms from simple enlargements. Concurrently, Kocher refined surgical techniques for ; in 1883, he reported on his first 100 cases with improved safety through meticulous and nerve preservation, reducing operative mortality dramatically and earning him the in Physiology or Medicine in 1909 for contributions to thyroid physiology and pathology. The discovery of iodine's role revolutionized treatment. In 1820, Jean-François Coindet in demonstrated that effectively reduced goitre size, attributing efficacy to the element isolated by Bernard Courtois in 1811, though initial enthusiasm waned due to risks of in hyperthyroid cases. By the early , global surveys confirmed as the primary cause of , prompting interventions. In the United States, iodized salt was introduced in the mid-1920s following trials by David Marine in schoolgirls, which showed a marked reduction in goitre incidence—approaching 50% within decades in affected regions—establishing fortification as a cost-effective strategy. In the mid-20th century, diagnostic advancements included the adoption of thyroid ultrasound in the 1970s, enabling non-invasive visualization of gland structure and nodules, which improved preoperative assessment and reduced reliance on invasive biopsies. From the onward, genetic research elucidated congenital forms of goitre, identifying mutations in genes such as and DUOX2 as causes of dyshormonogenesis, leading to familial screening and targeted therapies that addressed inherited defects beyond environmental iodine supplementation.

Cultural and Social Impacts

Goitre has been depicted in art and folklore across various cultures, often reflecting regional endemic prevalence due to . In Renaissance-era paintings, particularly from and the , enlarged glands appear frequently in portraits and religious scenes, such as those by artists like and , symbolizing either realistic portrayals of common deformities in mountainous areas or deliberate markers of , , or moral traits like . In from regions like the and , goitre was associated with negative connotations, including low intelligence or phlegmatic humors, and sometimes linked to supernatural cures involving dead hands or animal parts, underscoring its role as a visible stigma in rural communities. The visible neck swelling of goitre has historically contributed to , particularly affecting women who comprised the majority of cases in endemic areas, leading to , marginalization, and exclusion from social or marital opportunities. In artistic representations, such as portraits of the biblical figure Judith, the goitre symbolized both strength and , potentially evoking pity or ridicule to emphasize themes of otherness. Modern studies highlight ongoing psychosocial burdens, with over two-thirds of goitre patients reporting daily and reduced , exacerbating issues like anxiety and depression, especially among women facing cosmetic concerns. Public health efforts have significantly mitigated goitre's societal impacts through global campaigns promoting iodized salt. The International Council for Control of Iodine Deficiency Disorders (ICCIDD), founded in 1985 and renamed the in 2014 as a partnership with the and , has coordinated technical support for iodization programs, averting millions of cases worldwide and reducing the global burden of iodine deficiency disorders by over 50% since the 1990s. As of 2023, the IGN reports that while household coverage of iodized salt has reached 88% globally, iodine deficiency remains a problem affecting an estimated 1.5 billion people. Economically, untreated goitre and related contribute to substantial productivity losses in endemic regions, including cognitive impairments that diminish workforce output and . A 2020 analysis estimated that ongoing affects 4.8 million newborns annually, resulting in lifetime productivity losses valued at $12.5 billion in , primarily in low- and middle-income countries. In high-income settings like , annual healthcare costs for diagnosing and treating exceed one billion euros, highlighting the broader fiscal strain on public resources.

References

  1. https://www.ncbi.nlm.nih.gov/books/NBK562161/
  2. https://www.thyroid.org/goiter/
  3. https://my.clevelandclinic.org/health/diseases/12625-goiter
  4. https://www.mayoclinic.org/diseases-conditions/goiter/symptoms-causes/syc-20351829
  5. https://www.hopkinsmedicine.org/health/conditions-and-diseases/goiter
  6. https://www.ncbi.nlm.nih.gov/books/NBK244/
  7. https://www.who.int/publications/i/item/WHO-NMH-NHD-EPG-14.5
  8. https://pmc.ncbi.nlm.nih.gov/articles/PMC3100137/
  9. https://pmc.ncbi.nlm.nih.gov/articles/PMC9459956/
  10. https://pubmed.ncbi.nlm.nih.gov/1718324/
  11. https://www.ncbi.nlm.nih.gov/books/NBK285556/
  12. https://www.ncbi.nlm.nih.gov/books/NBK459262/
  13. https://www.ncbi.nlm.nih.gov/books/NBK557859/
  14. https://pmc.ncbi.nlm.nih.gov/articles/PMC2723027/
  15. https://pmc.ncbi.nlm.nih.gov/articles/PMC3113168/
  16. https://www.ncbi.nlm.nih.gov/books/NBK279059/
  17. https://www.ncbi.nlm.nih.gov/books/NBK285553/
  18. https://emedicine.medscape.com/article/120034-overview
  19. https://www.dynamed.com/condition/nontoxic-multinodular-goiter
  20. https://www.ncbi.nlm.nih.gov/books/NBK279158/
  21. https://emedicine.medscape.com/article/919758-overview
  22. https://www.thyroid.org/thyroid-function-tests/
  23. https://doi.org/10.1089/thy.2015.0020
  24. https://pmc.ncbi.nlm.nih.gov/articles/PMC4739132/
  25. https://radiopaedia.org/articles/acr-thyroid-imaging-reporting-and-data-system-acr-ti-rads?lang=us
  26. https://ajronline.org/doi/10.2214/AJR.04.0816
  27. https://www.medicalalgorithms.com/who-classification-of-goiter-size
  28. https://pmc.ncbi.nlm.nih.gov/articles/PMC7757618/
  29. https://www.ncbi.nlm.nih.gov/books/NBK545223/
  30. https://www.thyroid.org/patient-thyroid-information/ct-for-patients/september-2019/vol-12-issue-9-p-11-12/
  31. https://www.e-enm.org/journal/view.php?number=2346
  32. https://emedicine.medscape.com/article/120392-treatment
  33. https://academic.oup.com/jcem/article/87/9/4154/2846546
  34. https://www.uptodate.com/contents/thyroid-hormone-suppressive-therapy-for-thyroid-nodules-and-benign-goiter
  35. https://pmc.ncbi.nlm.nih.gov/articles/PMC10542302/
  36. https://jnm.snmjournals.org/content/53/10/1633
  37. https://www.radiologyinfo.org/en/info/radioiodine
  38. https://www.aafp.org/pubs/afp/issues/2005/0815/p623.html
  39. https://emedicine.medscape.com/article/121865-medication
  40. https://pmc.ncbi.nlm.nih.gov/articles/PMC5778395/
  41. https://pubmed.ncbi.nlm.nih.gov/21365410/
  42. https://pmc.ncbi.nlm.nih.gov/articles/PMC5756755/
  43. https://www.ncbi.nlm.nih.gov/books/NBK563279/
  44. https://www.mayoclinic.org/tests-procedures/thyroidectomy/about/pac-20385195
  45. https://pubmed.ncbi.nlm.nih.gov/3689014/
  46. https://pmc.ncbi.nlm.nih.gov/articles/PMC4583592/
  47. https://pmc.ncbi.nlm.nih.gov/articles/PMC8035947/
  48. https://pmc.ncbi.nlm.nih.gov/articles/PMC10266226/
  49. https://pubmed.ncbi.nlm.nih.gov/25605285/
  50. https://pmc.ncbi.nlm.nih.gov/articles/PMC5676165/
  51. https://pmc.ncbi.nlm.nih.gov/articles/PMC3485526/
  52. https://pmc.ncbi.nlm.nih.gov/articles/PMC5381163/
  53. https://www.sciencedirect.com/science/article/pii/S266639612500041X
  54. https://pmc.ncbi.nlm.nih.gov/articles/PMC10839701/
  55. https://www.mayoclinic.org/medical-professionals/endocrinology/news/ethanol-ablation-for-the-treatment-of-cystic-and-predominantly-cystic-thyroid-nodules/mac-20439196
  56. https://pmc.ncbi.nlm.nih.gov/articles/PMC9884003/
  57. https://pmc.ncbi.nlm.nih.gov/articles/PMC8353683/
  58. https://pmc.ncbi.nlm.nih.gov/articles/PMC3003466/
  59. https://pubmed.ncbi.nlm.nih.gov/21173898/
  60. https://pmc.ncbi.nlm.nih.gov/articles/PMC3821511/
  61. https://pmc.ncbi.nlm.nih.gov/articles/PMC5503928/
  62. https://pmc.ncbi.nlm.nih.gov/articles/PMC4561655/
  63. https://pmc.ncbi.nlm.nih.gov/articles/PMC7402570/
  64. https://pmc.ncbi.nlm.nih.gov/articles/PMC11109269/
  65. https://lpi.oregonstate.edu/mic/minerals/iodine
  66. https://www.who.int/teams/nutrition-and-food-safety/databases/vitamin-and-mineral-nutrition-information-system
  67. https://journals.lww.com/jehp/fulltext/2023/06300/goiter_prevalence_and_iodine_deficiency_disorder.10.aspx
  68. https://ign.org/scorecard/
  69. https://www.sciencedirect.com/topics/medicine-and-dentistry/endemic-goitre
  70. https://pmc.ncbi.nlm.nih.gov/articles/PMC5359876/
  71. https://www.hindustantimes.com/lifestyle/health/gastroenterologist-warns-iodine-deficiency-is-reemerging-due-to-popularity-of-himalayan-salt-over-iodised-salt-101751523621561.html
  72. https://pubmed.ncbi.nlm.nih.gov/23238875/
  73. https://www.nejm.org/doi/full/10.1056/NEJM196902062800604
  74. https://pubmed.ncbi.nlm.nih.gov/12487770/
  75. https://emedicine.medscape.com/article/122714-overview
  76. https://pmc.ncbi.nlm.nih.gov/articles/PMC7282437/
  77. https://pmc.ncbi.nlm.nih.gov/articles/PMC11046319/
  78. https://www.ncbi.nlm.nih.gov/books/NBK285560/
  79. https://www.who.int/publications/i/item/WHO-NUT-94.4
  80. https://www.thyroid.org/patient-thyroid-information/ct-for-patients/february-2017/vol-10-issue-2-p-7-8/
  81. https://pmc.ncbi.nlm.nih.gov/articles/PMC5471633/
  82. https://www.sciencedirect.com/science/article/pii/S0022316622108102
  83. https://karger.com/hrp/article/95/6/546/828530/History-of-the-Thyroid
  84. http://www.hormones.gr/115/article/article.html
  85. https://pmc.ncbi.nlm.nih.gov/articles/PMC6367459/
  86. https://www.nobelprize.org/prizes/medicine/1909/kocher/article/
  87. https://www.thyroid.org/wp-content/uploads/timeline/sawin-discoverers-thyroid-landmarks-coindet.pdf
  88. https://pmc.ncbi.nlm.nih.gov/articles/PMC3509517/
  89. https://www.endocrinepractice.org/article/S1530-891X%2820%2939933-X/fulltext
  90. https://pmc.ncbi.nlm.nih.gov/articles/PMC1736062/
  91. https://www.sciencedirect.com/science/article/pii/S1521690X23000192
  92. https://www.liebertpub.com/doi/10.1089/thy.2014.0494
  93. https://scholarworks.smith.edu/cgi/viewcontent.cgi?article=1000&context=museum_books
  94. https://publishing.cdlib.org/ucpressebooks/view?docId=ft2d5nb1b2&chunk.id=d0e2690&toc.depth=1&toc.id=d0e2690
  95. https://pmc.ncbi.nlm.nih.gov/articles/PMC6198785/
  96. https://pmc.ncbi.nlm.nih.gov/articles/PMC4743372/
  97. https://www.scirp.org/journal/paperinformation?paperid=88753
  98. https://www.ign.org/cm_data/IDD-NL-2011-1.pdf
  99. https://iris.who.int/bitstream/handle/10665/71343/80%285%29410-417.pdf
  100. https://www.ign.org/scorecard/
  101. https://www.liebertpub.com/doi/full/10.1089/thy.2019.0719
  102. https://pmc.ncbi.nlm.nih.gov/articles/PMC7849460/
Add your contribution
Related Hubs
Contribute something
User Avatar
No comments yet.