Goiter

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

Goiter is the abnormal enlargement of the thyroid gland. Development of goiter doesn’t imply the malfunction of the thyroid gland and Goiter occurs in a gland which is either in hypothyroid, euthyroid or hyperthyroid state. Lack of iodine in the diet is the most common cause of goiters worldwide. Goiter is usually painless but if large in size may lead to compression symptoms such as dysphagia, dyspnea and hoarseness of voice. Ancient documented texts with reference to goiter have been seen dating back to 2700 BC. In 1949, commercial synthesis of levothyroxine was done successfully. In 1974, an international committee of thyroid pathologists published the first WHO histological classification of thyroid tumors which had served as a basis for various clinical, pathological, and epidemiological studies. Goiter may also be classified according to various classification methods based on etiologic, epidemiological, anatomical, pathological, functional and morphological factors. When the TRH–TSH thyroid hormone axis is interfered, it results in the structural and functional changes of the thyroid gland. Increased TSH production is triggered by a deficiency in thyroid hormone synthesis or intake. In order to normalize thyroid hormone levels, the increase in TSH leads to increased cellularity and hyperplasia of the thyroid gland and when this process is continuous, it leads to goiter. Various factors have been associated with the cause of goiter such as hereditary, hormonal, dietary, pharmacological, physiological, environmental and pathological factors. The most common causes being, iodine deficiency, Grave’s disease and Hashimoto’s disease. Goiter may be caused by a mutation in the genes such as the thyroglobulin (Tg) gene, thyroid-stimulating hormone receptor (TSHR) gene and the sodium-iodide symporter (NIS) gene. As goiter manifests in a variety of clinical forms, differentiation must be established in accordance with the particular sub-type. The incidence of goiter is approximately 1400 – 1700 per 100,000 individuals in females and 900 per 100,000 individuals in males, worldwide. The prevalence of goiter is approximately 3000 per 100,000 individuals worldwide, for single thyroid nodules. The frequency of goiter increases in women over 45 years of age. The rate of occurrence of goiter in females is higher than that in males by a ratio of 4:1. There is no racial predilection to goiter. Screening for goiter initially involves physical examination followed by blood tests for free T4 and TSH and finally thyroid scan, ultrasound and biopsy to rule out malignancy. Slow growth of the nodules is observed in benign goiter. Rapid growth and large size of goiter causing compressive symptoms may be suggestive of thyroid cancer. Common complications of goiter include those related to the enlarged gland and to thyroidectomy. Prognosis is generally good for benign goiter. Although the prognosis is good and the risk is low, caution is advised for the possible development of malignancy. Careful monitoring of size, shape and consistency associated with pain is advised. Radiation exposure has been attributed to the possible development of malignancy. A history of low iodine intake, history of use of therapeutic drugs that hinder normal thyroid hormonal activity, radiation exposure and positive family history of thyroid diseases. Symptoms of goiter include, swelling at the base of the neck, dysphagia, hoarseness of voice and dyspnea. Physical examination of patients with Goiter is usually remarkable for swelling at the base of the neck. Patients with Goiter may be in a euthyroid, hypothyroid or hyperthyroid state. Patients should be evaluated for free T4, T3, TSH levels and TPO antibodies. Plain x-ray findings of the neck suggestive of goiter include tracheal deviation or compression and calcification within the goiter. Ultrasound may be helpful in determining the physical characteristics of the thyroid gland and also aids in ultrasound guided FNAC. Thyroid radioisotope scan may be helpful in the diagnosis of goiter. Barium swallow may be helpful in assessing compression of the esophagus due to goiter. Indirect laryngoscopy helps assess the mobility of the vocal cords. Pharmacologic therapy for goiter involves normalizing hormone levels and treating the inflammation. Treatment regimen involves Lugol’s iodine, antithyroid drugs and β-adrenergic blockers. In some cases, radioactive iodine may be used to treat an overactive thyroid gland. Thyroid surgery may be advised in cases of goiter depending upon the symptoms and extent as well as type of gland pathology such as, compressive symptoms, thyroid hyper-functioning and thyroid cancer. Effective measures for the primary prevention of goiter include iodine supplementation and smoking cessation.

Ancient documented texts with reference to goiter have been seen dating back to 2700 BC. In 1949, commercial synthesis of levothyroxine was done successfully.

In 1974, an international committee of thyroid pathologists published the first WHO histological classification of thyroid tumors which had served as a basis for various clinical, pathological, and epidemiological studies. Goiter may also be classified according to various classification methods based on etiological, epidemiological, anatomical, pathological, functional and morphological factors.

When the TRH–TSH thyroid hormone axis is interfered, it results in the structural and functional changes of the thyroid gland. Increased TSH production is triggered by a deficiency in thyroid hormone synthesis or intake. In order to normalize thyroid hormone levels, the increase in TSH leads to increased cellularity and hyperplasia of the thyroid gland and when this process is continuous, it leads to goiter.

Various factors have been associated with the cause of goiter such as hereditary, hormonal, dietary, pharmacological, physiological, environmental and pathological factors. The most common causes being, iodine deficiency, Grave’s disease and hashimoto’s disease. Goiter may be caused by a mutation in the genes such as the thyroglobulin (Tg) gene, thyroid-stimulating hormone receptor (TSHR) gene and the Na+/I- symporter (NIS) gene.

As goiter manifests in a variety of clinical forms, differentiation must be established in accordance with the particular subtype.

The incidence of goiter is approximately 1400 to 1700 per 100,000 individuals in females and 900 per 100,000 individuals in males, worldwide. The prevalence of goiter is approximately 3000 per 100,000 individuals worldwide, for single thyroid nodules. The frequency of goiter increases in women over 45 years of age. The rate of occurrence of goiter in females is higher than that in males by a ratio of 4:1. There is no racial predilection to goiter.

Common risk factors in the development of goiter include non-iodized salt, age over 45 years, female gender, drugs and radiation therapies.

Screening for goiter initially involves physical examination followed by blood tests for free T4 and TSH and finally thyroid scan, ultrasound and biopsy to rule out malignanacy.

Slow growth of the nodules is observed in benign goiter. Rapid growth and large size of goiter causing compressive symptoms may be suggestive of thyroid cancer. Common complications of goiter include those related to the enlarged gland and those related to thyroidectomy. Prognosis is generally good for benign goiter. Although the prognosis is good and the risk is low, caution is advised to prevent the possible development of malignancy. Careful monitoring of size, shape and consistency associated with pain is recommended. Radiation exposure has been attributed to the possible development of malignancy.

A history of low iodine intake, history of use of therapeutic drugs that hinder normal thyroid hormonal activity, radiation exposure and positive family history of thyroid diseases. Symptoms of goiter include, swelling at the base of the neck, difficulty swallowing, hoarseness of voice and difficulty in breathing.

Physical examination of patients with goiter is usually remarkable for swelling at the base of the neck.

Patients with goiter may be in a euthyroid, hypothyroid or hyperthyroid state. Patients should be evaluated for free T4, T3, TSH levels and thyroid peroxidase (TPO) antibodies.

There are no ECG findings associated with goiter.

Plain x-ray radiography findings of the neck suggestive of goiter may include tracheal deviation or compression and calcification within the goiter.

Although CT scan gives an excellent anatomical detail of thyroid swelling but has no role as the first line of investigation. CT scan also helps to assess recurrence and intrathoracic or retrosternal goiter.

Although MRI gives an excellent anatomical detail of thyroid swelling but has no role as the first line of investigation. MRI also helps to assess recurrence and intrathoracic or retrosternal goiter.

Ultrasound may be helpful in determining the physical characteristics of the goiter. Ultrasound also aids in guided FNA.

Thyroid radioisotope scan may be helpful in the diagnosis of goiter. It is helpful in determining the functional activity by distinguishing a nodule as hot, warm, or cold, based on the relative amount of uptake of radioactive isotope. The radioactive isotopes that are most commonly used include Iodine-123, Technetium-99m and Iodine-131

Barium swallow may be helpful in assessing compression of the esophagus due to goiter. Indirect laryngoscopy helps assess the mobility of the vocal cord.

Pharmacologic medical therapy for goiter involves normalizing hormone levels and treating the inflammation. Treatment regimen involves Lugol’s iodine, antithyroid drugs and β-adrenergic blockers. In some cases, radioactive iodine may be used to treat an overactive thyroid gland.

Thyroid surgery may be advised in cases of goiter depending upon the symptoms and adverse effects associated with the development of goiter such as, compression related symptoms, thyroid hyper-function and thyroid cancer.

Effective measures for the primary prevention of goiter include iodine supplementation and smoking cessation.

Secondary prevention measures for goiter are similar to the primary prevention for goiter.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

Ancient texts with reference to goiter date back to 2700 BC. In the 7th century, steatomatous goiter and hyperplastic or hyperemic goiter were described by Paulus Aegineta. In 1917, Marine introduced prevention of goiter with iodine by suggesting a low dose of 1:100000 parts of iodine. In 1949, commercial synthesis of levothyroxine was done successfully.

• Ancient texts with reference to goiter have been seen dating back to 2700 BC.^[1]
• In 1400 BC, goiter was described as ‘galaganda’ and details regarding this disease were explained in Indian ayurvedic medicine.^[1][2]
• In the 7th century, steatomatous goiter and hyperplastic or hyperemic goiter were described by Paulus Aegineta.^[1]
• In 1656, Thomas Wharton, a famous anatomist, discovered the exact anatomical structure of the thyroid gland.^[1]
• In 1836, Thomas Wilkinson King, also known as father of endocrinology, described thyroid colloid in his article on ‘Observations on the Thyroid Gland’.^[1]
• Between 1884 and 1886, Sir Horsley discovered the association of thyroidectomy with myxedema and cretinism, during his experiments on monkeys.^[1]
• In the 19th century iodine was discovered by the Parisians Courtois.^[1]
• In 1974, an international committee of thyroid pathologists published the first WHO classification of tumors of the thyroid gland based on histology, which served as a basis for various clinical, pathological, and epidemiological studies.^[3]

• In the 6th century, the surgical treatment of goiter was mentioned by Aetius. Aetius also made references to ‘atheromatous’ goiters. ^[4]
• In the 7th century, thyroid surgery on struma was performed by Paulus Aegineta. ^[1]
• In the 10th century, Albucasis removed a large goiter of a man under opium sedation which is supposedly the first reliable account of a thyroid surgery. ^[1]
• In the 14th century, Guy de Chaliac, a French surgeon reported goiter as a hereditary disease and recommended surgical treatment for it.^[1][2]
• Coindet of Geneva was the first person to use iodine as a remedy for goiter and prescribed hydriodate of potash or ‘tincture of iodine’. ^[1]
• In 1833, salt iodization was suggested by Boussingault in order to prevent goiter. In 1835, he also demonstrated that the incidence of goiter was reduced when salt from goiter-free regions was used in regions with endemic goiter.^[1]
• In 1907, David Marine proved that iodine is necessary for thyroid function.^[1]
• In 1909, the nobel prize was awarded to Emil Theodor Kocher, for his work on thyroid gland.^[1]
• In 1917, Marine introduced prevention of goiter with iodine by suggesting a low dose of 1:100000 parts of iodine.^[1]
• In 1943, Hertz, Roberts and Leblond used radioactive iodine was used in the treatment of Grave’s disease.^[1]
• In 1949, commercial synthesis of levothyroxine was done successfully.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

In 1974, the international committee of thyroid pathologists published the first WHO histological classification of thyroid tumors which had served as a basis for various clinical, pathological, and epidemiological studies. Goiter may also be classified according to various classification methods based on etiological, epidemiological, anatomical, pathological, functional and morphological factors.

In 1974, an international committee of thyroid pathologists published the first WHO histological classification of thyroid tumors which had served as a basis for various clinical, pathological, and epidemiological studies.^[1]

• WHO Histological Classification of Thyroid Tumors, Second edition (1988):^[1][2]
  • Epithelial tumors
    • Benign
      • Follicular adenoma
      • Others
    • Malignant
      • Follicular carcinoma
      • Papillary carcinoma
      • Medullary carcinoma
      • Undifferentiated (anaplastic) carcinoma
      • Others
  • Nonepithelial tumors
    • Benign
    • Malignant
  • Malignant lymphomas
  • Miscellaneous tumors
  • Secondary tumors
  • Unclassified tumors
  • Tumor-like lesions

• Goiter may be also be classified according to various classification methods based on the following criteria:^{[3][4][5][6][7][8][9][10][11][12][13][14]}
  • Classification based on etiology
  • Classification based on epidemiology
  • Classification based on anatomy
  • Classification based on pathology
  • Classification based on function
  • Classification based on morphology

• Classification based on etiology:
  • Physiological goiter: Goiter occurring due to increased metabolic demand of thyroid hormones (during pregnancy or puberty).
  • Pathological goiter: Goiter occurring as a result of the diseases affecting the thyroid gland e.g. neoplastic or inflammatory conditions.

• Classification based on epidemiology:
  • Familial goiters: Goiter occurring as an inherited defect of thyroid hormone synthesis.
  • Endemic goiters: Thyroid enlargement observed in a significant number of population in a particular locality.
  • Sporadic goiters: Goiter occuring sporadically.

• Classification based on anatomy:
  • Cervical goiter: Goiter situated on the anterior aspect of the neck.
  • Retrosternal goiter: Goiter situated behind the sternum and extending downwards.
  • Intrathoracic goiter: Goiter extending into thoracic cavity.

• Classification based on pathology:
  • Simple goiter
  • Toxic goiter
  • Neoplastic goiter
  • Inflammatory goiter
  • Miscellaneous (other rare types)

• Classification based on function:
  • Toxic goiter: Goiter associated with thyroid hyperfunction (hyperthyroidism)
  • Non-toxic goiter: Goiter associated with thyroid hypofunction (hypothyroidism) or normal thyroid function (Euthyroid)

• Classification based on morphology:

• According to the texture of the thyroid gland:
  • Diffuse goiter
  • Nodular goiter:
    • Solitary nodular goiter
    • Multinodular goiter

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

When the thyrotrophin releasing hormone–thyroid stimulating hormone axis (TRH–TSH thyroid hormone axis) is interfered, it results in structural and functional changes in the thyroid gland. Increased TSH production is trigerred by a deficiency in thyroid hormone synthesis or intake. In order to normalize thyroid hormone levels, the increase in TSH leads to increased cellularity and hyperplasia of the thyroid gland and when this process occurs continuously, it leads to goiter.

Pathogenesis:^{[1][2][3][4][5][6][7][8][9][10][11]}

• Goiters may occur as a result of either hypothyroidism, hyperthyroidism, or even with normal levels of thyroid hormone.
• Thyroid enlargement (goiter) and hypothyroidism may occur due to compensatory responses as a result of a severe underlying disorder.
• When the thyroid gland cannot secrete enough thyroid hormone to cater to the metabolic requirements, it may lead to simple goiter (smooth enlargement).
• In order to compensate for inadequate hormone synthesis, the thyroid gland enlarges, this type of compensation overcomes mild to moderate hormonal impairment.
• When the TRH–TSH thyroid hormone axis is interfered, it results in the structural and functional changes of the thyroid gland.
• Increased TSH production is triggered by a deficiency in thyroid hormone synthesis or intake.
• In order to normalize thyroid hormone levels, the increase in TSH leads to increased cellularity and hyperplasia of the thyroid gland and when this process is continuous, it leads to goiter.
• Thyroid hormone deficiency may occur secondary to to iodine deficiency, inborn errors of thyroid hormone synthesis and goitrogens.
• Goiters may form as a result of many TSH receptor agonists. The TSH receptor gets stimulated under the following conditions:
  • Adenoma of the pituitary
  • Adenoma of the hypothalamus
  • Pituitary resistance to thyroid hormone
  • TSH receptor antibodies
  • Tumors producing hCG (human chorionic gonadotropin)

• The pathophysiological consequences of goitres results from one of the following:
  • Thyroid hormone dysfunction
  • Enlarged thyroid gland
  • The effect of primary disease causing goiter

• The effect of thyroid hormone dysfunction:
  • Thyroid hyperfunction (hyperthyroidism) → Features of hyperthyroidism
  • Thyroid hypofunction (hypothyroidism) → Features of hypothyroidism

• The effect of enlarged thyroid gland:
  • Effect on the trachea results in dyspnea
  • Effect on the esophagus results in dysphagia
  • Effect on the superior vena cava results in distended neck veins
  • Effect on the recurrent laryngeal nerve results in hoarseness of voice

• The effect of primary disease causing goitre:
  • The effect depends on the underlying disease

• Goiter may be caused by a mutation in the following genes which vary from one family to the other: ^{[12][13][14][15][16][17]}

• Thyroglobulin (Tg) gene
• Thyroid-stimulating hormone receptor (TSHR) gene
• Sodium–iodine (Na+/I-) symporter (NIS) gene ^[18]

The following conditions are associated with goiter:^[19][20]

• Grave’s disease
• Hashimoto’s thyroiditis

• On gross pathology the following features are observed:^[21][22][23]
  • Enlarged thyroid gland
  • Multiple nodules lacking fibrous capsule
  • Secondary changes such as hemorrhage, calcification and cystic degeneration are observed

Goiter histologic findings:

• Simple non-toxic goiters demonstrate:
  • Hyperplasia
  • Colloid accumulation
  • Nodularity

• Nodular hyperplasia is commonly seen in multinodular goiter. Cytologic findings include:
  • Benign appearing follicular cells
  • Abundant colloid, macrophages
  • Hürthle cells (occasionally)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

Various factors have been associated with the cause of goiter such as hereditary, hormonal, dietary, pharmacological, physiological, environmental and pathological factors. The most common causes being, iodine deficiency, Grave’s disease and hashimoto’s disease. Goiter may be caused by a mutation in the genes such as the thyroglobulin (Tg) gene, thyroid-stimulating hormone receptor (TSHR) gene and the sodium-iodide symporter (NIS) gene.

Factors associated with goiter can be classified as follows:

Hereditary factors

• Inherited defect(Familial goiter) of thyroid hormone synthesis such as:
  • Enzymatic defect deficiency
  • Dyshormonogenesis

Hormonal factors

Thyroid hormone dysfunction:

• Hyperthyroidism (overproduction of thyroid hormones)
• Hypothyroidism (underproduction of thyroid hormones)

Dietary factors

• Dietary iodine deficiency
• Goitrogens (play a major role in endemic goitre)

Pharmacological factors

• Use of goitrogenic drugs like para-aminosalicylic acid (PAS), thiocyanate and antithyroid drugs [e.g. thiouracil, carbimazole] results in hypothyroidism

Physiological factors

• Increased metabolic demand of thyroid hormones e.g. during pregnancy or puberty results in physiological goiter.

Environmental factors

• Exposure to radiations leading to:
  • Thyroid cancer
  • Hypothyroidism

Pathological factors

Intrinsic thyroid gland diseases:

• Inflammatory goitres
• Neoplastic goitres
  • Benign adenoma (follicular adenoma)
  • Malignant
    • Primary: Well differentiated, poorly differentiated, arising from parafollicular cells
    • Secondary

Goiter may be caused by:

• Iodine deficiency
• Grave’s disease
• Hashimoto’s disease

Less common causes of Goiter include:

• Pregnancy
• Radiation exposure
• Thyroid cancer
• Multinodular goiter
• Solitary thyroid nodules

• Goiter may be caused by a mutation in the following genes which vary from one family to the other: ^[1]

• Thyroglobulin (Tg) gene
• Thyroid-stimulating hormone receptor (TSHR) gene
• Sodium-iodide symporter (NIS) gene

• Multinodular goiter marker 1 (MNG1) on chromosome 14 ^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

As goiter manifests in a variety of clinical forms, differentiation must be established in accordance with the particular subtype.

• As goiter manifests in a variety of clinical forms, differentiation must be established in accordance with the particular subtype. The following are the various differential diagnoses: ^[1]
  • Anaplastic Thyroid Carcinoma
  • Follicular Thyroid Carcinoma
  • Medullary Thyroid Carcinoma
  • Papillary Thyroid Carcinoma
  • Sarcoma
  • Lipomas
  • Fibroma
  • Thyroid lymphoma
  • Hashimoto thyroiditis
  • Riedel thyroiditis
  • Subacute thyroiditis
  • Infectious thyroiditis
  • Parathyroid adenoma
  • Parathyroid cyst
  • Thyroglossal duct cyst
  • Branchial cleft cyst
  • Pseudo-goiter
  • Thyroid abscess
  • Thyroid nodule
  • Granulomatous disease of the thyroid
  • Lymphadenopathy
  • Carotid artery aneurysm
  • Lymphatic malformation (cystic hygroma)
  • Tumors of other structures in the neck

The table below outlines the differential diagnoses of neck swelling due to thyroid gland enlargement:^[2]

Disease	Findings
Multinodular goiter	Multinodular goiter is the multinodular enlargement of the thyroid gland. They are large nodules of more than 1 cm that produces symptoms of hyperthyroidism.
Grave’s disease	Grave’s disease is an autoimmune disease that affects the thyroid. It frequently results in hyperthyroidism and an enlarged thyroid. Pretibial myxedema and ophthalmopathy are some of the findings of grave’s disease.
Hashimoto’s disease	Hashimoto’s disease is an autoimmune disease in which the thyroid gland is attacked by a variety of cell-mediated and antibody-mediated immune processes, causing primary hypothyroidism.
Medullary thyroid carcinoma	Medullary thyroid carcinoma is a form of thyroid carcinoma which originates from the parafollicular cells (C cells), which produce the hormone calcitonin.
Thyroid lymphoma	Thyroid lymphoma is a rare malignant tumor which manifests as rapidly enlarging neck mass causing respiratory difficulty.
De Quervain’s thyroiditis	De Quervain’s thyroiditis is a subacute granulomatous thyroiditis preceded by an upper respiratory tract infection.
Acute suppurative thyroiditis	Acute suppurative thyroiditis is an uncommon thyroid disorder usually caused by bacterial infection.
Toxic adenoma	Toxic adenoma and toxic multinodular goiter are results of focal/diffuse hyperplasia of thyroid follicular cells independent of TSH regulation. Findings of single or multiple nodules are seen on physical examination or thyroid scan.[3]
Direct chemical toxicity with inflammation	Amiodarone, sunitinib, pazopanib, axitinib, and other tyrosine kinase inhibitors may also be associated with a destructive thyroiditis.[4][5]
Palpation thyroiditis	Manipulation of the thyroid gland during thyroid biopsy or neck surgery and vigorous palpation during the physical examination may cause transient hyperthyroidism.

The following table summarizes the various differential diagnoses of thyroid gland enlargement plus thyrotoxicosis and their major features:

Cause of thyrotoxicosis	TSH receptor antibodies	Thyroid US	Color flow Doppler	Radioactive iodine uptake/Scan	Other features
Graves’ disease	+	Hypoechoic pattern	↑	↑	Ophthalmopathy, dermopathy, acropachy
Toxic nodular goiter	–	Multiple nodules	–	Hot nodules at thyroid scan	–
Toxic adenoma	–	Single nodule	–	Hot nodule	–
Subacute thyroiditis	–	Heterogeneous hypoechoic areas	Reduced/absent flow	↓	Neck pain, fever, and elevated inflammatory index
Painless thyroiditis	–	Hypoechoic pattern	Reduced/absent flow	↓	–
Amiodarone induced thyroiditis-Type 1	–	Diffuse or nodular goiter	↓/Normal/↑	↓ but higher than in Type 2	High urinary iodine
Amiodarone induced thyroiditis-Type 2	–	Normal	Absent	↓/absent	High urinary iodine
Central hyperthyroidism	–	Diffuse or nodular goiter	Normal/↑	↑	Inappropriately normal or high TSH
Factitious thyrotoxicosis	–	Variable	Reduced/absent flow	↓	↓ Serum thyroglobulin

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

The incidence of goiter is approximately 1400 to 1700 per 100,000 individuals in females and 900 per 100,000 individuals in males, worldwide. The prevalence of goiter is approximately 3000 per 100,000 individuals worldwide, for single thyroid nodules. The frequency of goiter increases in women over 45 years of age. The rate of occurrence of goiter in females is higher than in males by a ratio of 4:1. There is no racial predilection to goiter.

• Worldwide, the incidence of goiter is approximately 1400 to 1700 per 100,000 individuals in females and 900 per 100,000 individuals in males.^[1][2][3]

• Worldwide, the prevalence of goiter is approximately 3000 for single thyroid nodules per 100,000 individuals.^[4][5][6]

• Goiter occurs more commonly in women over 45 years of age.^[4][7]

• The rate of occurrence of goiter in females is higher than that in males by a ratio of 4:1.^[8]

• There is no racial predilection of goiter.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

Risk factors in the development of goiter include non-iodized salt, age over 45 years, female gender, drugs and radiation therapies.

Risk factors in the development of goiter include the following:^{[1][2][3][4][5][6][7][8][9][10]}

• Common risk factors in the development of goiter may be occupational, diet related, environmental, genetic, age and sex related
• Common risk factors in the development of goiter include:
  • Table salt deficient in dietary iodine.
  • Individuals above the age of 40 years may have a higher chance of developing goiters.
  • Females are more more likely to develop goiters and prone to get affected by thyroid disorders.
  • For reasons unclear, thyroid disorders tend to occur more during pregnancy and during menopause.
  • Drugs used in the treatment of heart ailments such as amiodarone and also in psychiatric treatments such as lithium. Some other drugs include phenylbutazone, or aminoglutethimide and propylthiouracil.
  • Radiation therapies focused on the neck and the chest regions.
  • Positive family history of goiter.

• Less common risk factors in the development of goiter include:
  • Family history of autoimmune disorders, ^[11]
  • Radiation leak and exposure to hazardous radiations as a result of nuclear reactor accidents, ^[12]
  • Cigarette smoking, ^[13][14]
  • Emotional stress, ^[15]
  • Infections (rare), ^[15]
  • Goitrogenic foods: ^[16]
    • Higher risk (higher amounts of goitrogens):
      • Cabbage, cauliflower, bok choy, broccoli, brussel sprouts, kale, kohlrabi, mustard and mustard greens, radishes, rutabagas, soybeans and turnips.
    • Lower risk (smaller amounts of goitrogens):
      • Fruits (peaches, pears, strawberries), nuts (peanuts, pine nuts), bamboo shoots, sweet potatoes and spinach.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

Screening for goiter initially involves physical examination followed by blood tests for free T4 and TSH and finally thyroid scan, ultrasound and biopsy to rule out malignancy.

Screening for goiter includes the following approaches and progresses to the next approach based on the result of earlier screening procedure: ^{[1][2][3][4][5][6]}

Physical exam:

• Involves the assessment of the size and the extent of enlargement of the thyroid gland. If the gland is enlarged, blood tests for free T4 and TSH are evaluated.

Blood Tests:

• Blood tests are carried out in order to determine whether the goiter is affecting the production of thyroid hormone:
  • Free thyroxine (T4)
  • Thyroid stimulating hormone (TSH)

Further evaluation to rule out malignancy:

• Based on the results of the physical exam and blood tests, further evaluation involving the following is advised in order to rule out malignant transformation of the thyroid gland:
  • Thyroid scan
  • Ultrasound
  • Biopsy of the thyroid gland

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

If left untreated, goiter will continue to grow in size. Slow growth of the nodules is observed in benign goiter. Rapid growth and large size of goiter causing compressive symptoms may be suggestive of thyroid cancer. Common complications of goiter include those related to the enlarged thyroid gland and those related to thyroidectomy. Prognosis is generally good for benign goiter. Although the prognosis is good and the risk is low, caution is advised to prevent the possible development of malignancy. Careful monitoring of size, shape and consistency associated with pain is recommended. Radiation exposure has been attributed to the possible development of malignancy.

• If left untreated, goiter will continue to grow in size.
• Slow growth of the nodules is observed in benign goiter.
• Rapid growth and large size of goiter causing compressive symptoms (such as dysphagia, hoarseness and dyspnoea) may be suggestive of thyroid cancer. ^[1][2]

• Common complications of goiter include:^[1][2][3][4]
  • Complications related to the enlarged gland,
  • Complications related to thyroidectomy.

Complications related to the enlarged gland:

• Tracheal obstruction leading to airway obstruction,
• Secondary thyrotoxicosis,
• Malignant transformation.

Complications related to thyroidectomy:

• Haemorrhage
• Respiratory obstruction
• Recurrent laryngeal nerve palsy
• Thyroid storm
• Thyroid insufficiency
• Parathyroid insufficiency
• Wound infection
• Hypertrophic scar
• Keloids

• Prognosis is generally good for benign goiters. ^[5]
• Although the prognosis is good and the risk is low, caution is advised for the possible development of malignancy.
• Careful monitoring of size, shape and consistency associated with pain is advised.
• Radiation exposure has been attributed to the possible development of malignancy.

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