Many at times, goiter is often depicted as a result of iodine deficiency. Though this well-known fact is acknowledged worldwide, there is more to the cause of goiter than iodine deficiency.

But before you are educated on goiter in this article, it is best we know what the thyroid gland is and its functions.

The thyroid gland is a small gland, measuring about 5 centimeters in length and lies just under the skin below the laryngeal prominence (Adam’s apple) in the neck.

It consists of two lobes connected in the middle (known as the isthmus), giving the gland a shape of a bow tie or ribbon. Normally, the thyroid gland cannot be felt or can barely be seen. Hence, if it becomes enlarged, physicians can feel it and a prominent swelling (goiter) is noted below or to the sides of the Adam’s apple.


Goiter simply refers to an enlarged thyroid gland. This could be diffuse (involving the entire gland) or nodular (involving a single lobe). The enlarged thyroid gland can extend affecting structures such as the trachea, superior and inferior laryngeal nerves, and esophagus due to its anatomic relationship and abnormal growth.

Thyroid function could be affected and may be normal (nontoxic goiter), overactive (toxic goiter) or underactive (hypothyroid goiter).

What then are the causes of goiter?.


Goiter as already known is associated with iodine deficiency, however there are a variety of different mechanisms that can cause goiter. They are as follows:

• Autoimmune thyroiditis – Hashimoto or postpartum thyroiditis.
• Excess iodine (Wolff-Chaikoff effect) or lithium ingestion, which decrease release of thyroid hormone.
• Stimulation of TSH (thyroid stimulating hormone) receptors by TSH from pituitary tumors, pituitary thyroid hormone resistance, gonadotropins, and/or thyroid-stimulating immunoglobulins.
• Inborn errors of metabolism causing defects in biosynthesis of thyroid hormones.
• Exposure to radiation.
• Deposition diseases/infiltrative disease.
• Thyroid hormone resistance (pituitary thyroid hormone resistance with resultant elevated TSH).
• Subacute thyroiditis (de Quervain thyroiditis).
• Silent thyroiditis.
• Riedel thyroiditis.
• Infectious agents (Acute–Bacterial) and (Chronic–Mycobacteria, fungal and parasitic).
• Granulomatous disease.
• Thyroid malignancy.


Worldwide, the most common cause of goiter is iodine deficiency. An estimate of 200 million of the 800 million people who have a diet deficient in iodine have goiter.

A Wickham study from the United Kingdom, reported 16% of the population had goiter. A German study, involving ultrasonographic screening of more than 90,000 people, detected thyroid nodules in 33% of the normal population.

In sub-Saharan Africa, goiter is influenced by population isolation and absence of food self-sufficiency, which are both factors affecting the onset and persistence of iodine-deficiency goiters.

Mainly women are affected about (94.2%) of the normal population, most often with euthyroid goiters accounting for (54.7%), followed by Graves disease (13.1%), hypothyroidism (8.8%), thyroiditis (6.6%), toxic multinodular goiters (6.6%), and unclassified goiters (10%).

The scarcity of laboratories specializing in endocrinology and of nuclear medicine facilities and delay in diagnosis has resulted in compressive or recurrent goiters and endemic goiters being typical in Africa.

Most goiters are benign, causing only cosmetic disfigurement. Morbidity or mortality may result from compression of surrounding structures, thyroid cancer, hyperthyroidism or hypothyroidism.

The frequency of goiters decreases with advancing age. The decrease in frequency differs from the incidence of thyroid nodules, which increases with advancing age.


Now what actually takes place in the thyroid gland leading to its enlargement? First of all, the thyroid gland is controlled by the thyroid stimulating hormone (TSH) also referred to as thyrotropin. This hormone is secreted from the pituitary gland, which is influenced by the thyrotropin releasing hormone (TRH) from the hypothalamus.

TSH permits the growth of cells in the thyroid gland known as thyroid follicles and stimulates thyroid hormone production and secretion by the thyroid gland.

Thyrotropin acts on TSH receptors found on the thyroid gland. Thyroid hormones are then produced from iodination of tyrosine. Iodine transport from the plasma into the thyroid cell is facilitated via a sodium-iodide symporter. The iodine transport activity is controlled by TSH.
Any disruption with the TRH-TSH thyroid hormone axis causes changes in the structure and function of the thyroid gland.

Therefore, any stimulation of TSH receptors by TSH-receptor antibodies and TSH agonists such as chorionic gonadotropin can lead to a diffuse goiter. Inflammatory cells or malignant metastatic cells of the thyroid can lead to the development of a nodular goiter.

Deficiency in thyroid hormone synthesis or intake leads to elevated TSH production. This results in an increased cellularity and hyperplasia of the thyroid in an attempt to maintain normal levels of thyroid hormone. This process when sustained leads to a goiter being formed.


Goiter normally presents in a variety of ways. Below are a few ways it can be noticed:

• Presence of swelling at the base of the neck, normally on routine physical examination or on personal observation in a mirror.
• Local compression resulting in dysphagia, dyspnea, stridor or hoarseness
• Pain resulting from inflammation, necrosis, bleeding or malignant transformation.
• Signs and symptoms of hyperthyroidism or hypothyroidism.


Doctors would usually perform blood tests to determine how the thyroid gland is functioning (thyroid function tests). These tests measure the blood levels of thyroid hormones (T4 or thyroxine), (T3 or triiodothyronine) and the thyroid-stimulating hormone (TSH).

Sometimes, investigations are also done to look for antibodies that attack the thyroid gland (antithyroid antibodies) in the blood. This serves as a sign of an immune reaction to the thyroid gland leading to inflammation.

A radioactive iodine uptake test and a thyroid scan can also be done. This detects how much iodine is taken up by the gland and a picture of the gland is taken using a gamma camera (which detects radiation). This scan displays any physical abnormalities of the thyroid gland suggestive of Graves disease, thyroid nodules or thyroiditis.

Imaging studies such as ultrasonography is also performed to identify any nodules that could be cancerous by acquiring an image of the thyroid gland through the use of sound waves.


Most goiters do not require treatment, especially if they are small, benign and euthyroid. However, large and complicated goiters require medical and surgical treatment. This is also required for malignant goiters. Medical treatment involves the following:

• Thyroid hormone replacement after surgical and radiation treatment of a goiter.
• Ethanol infusion into benign thyroid nodules.
• Treatment of hyperthyroidism or hypothyroidism.

Surgical treatment involves subtotal thyroidectomy or total thyroidectomy. Surgical treatment is indicative for the following:
• Large goiters with compression symptoms.
• Malignancy.
• Ineffective medical treatment.


Complications from goiter include the following:

• Compression of the trachea, with asphyxiation and tracheomalacia caused by large goiters.
• Hyperthyroidism.
• Malignant transformation in multinodular goiters.
• Pain, intra-nodular necrosis, and bleeding in nodular goiters.
• Bacteremia, sepsis, pain, and fever from thyroid abscess.
• Lymphoma development in autoimmune goiters.