Goiter is an enlargement of the thyroid gland. The thyroid gland is the largest endocrine organ in our body. It is located in our neck, in the anterior lower region of the trachea, close to the sternum. It secretes thyroid hormones. The thyroid gland measures 4-4.8 cm from top to bottom, 1-1.8 cm in width, and 0.8-1.6 cm from front to back.

What is goiter?

Goiter is an enlargement of the thyroid gland. The thyroid gland is the largest endocrine organ in our body. It is located in our neck, in the anterior lower region of the trachea, close to the sternum. It secretes thyroid hormones. The thyroid gland measures 4-4.8 cm from top to bottom, 1-1.8 cm in width, and 0.8-1.6 cm from front to back.

The thyroid gland can become enlarged for various reasons. Normally males are slightly larger than females. If the thyroid gland overgrows and travels down the neck to the back of the breastbone, it’s called a retrosternal goiter. The probability of developing goiter is at least 4 times more than men.



Goiter can also be associated with thyroid hormone levels. Patients with goiter may have hypothyroidism, euthyroidism with normal thyroid levels, or hyperthyroidism. Goiter patients may or may not have nodules in the thyroid gland. If nodules are present, they may be single or multinodular.

The enlargement of the thyroid is a result of the inflammatory process that develops for any reason. Therefore, with the improvement of inflammation, thyroid enlargement decreases. Therefore, the term goiter is not used to describe the disorder in the thyroid gland. Goiter is a symptom. It is among the signs and symptoms of inflammatory thyroid disorder.

When any pathological condition develops that prevents the production of thyroid hormones in the thyroid gland, the thyroid follicles begin to grow in order to provide the thyroid hormone level that the body needs. Goiter is actually the adaptive response of the thyroid gland to this situation, its reaction.

The most common possible causes of thyroid gland enlargement (goiter):

  • Congenital causes
    • Congenital thyroid hormone synthesis defects
    • Congenital hypothyroidism
    • Development of postpartum thyroiditis
  • Subsequent causes
    • Physiological reasons
    • Adolescence period
    • Pregnancy
  • Pathological causes
    • Thyroid diseases
    • Diffuse goiter
    • euthyroid goiter
    • Endemic or sporadic diffuse goiter
  • Drug-induced goiter
  • Goiter due to hormone synthesis abnormalities
  • Goiter due to thyroiditis
    • Acute thyroiditis
    • Subacute thyroiditis
    • Chronic thyroiditis
    • Radiation thyroiditis
    • Hashimoto’s thyroiditis
    • Postpartum portpartum thyroiditis
  • Hypothyroid goiter
  • Cretinism
  • Juvenile hypothyroidism
  • Thyroiditis and Hashimoto’s disease
  • Radiation thyroiditis
  • Hormone synthesis abnormalities
  • Hyperthyroid goiter
  • Graves’ disease
  • Subacute thyroiditis (De Quervain’s thyroiditis)
  • Multinodular goiter (may be endemic or sporadic)
  • Toxic multinodular goiter
  • Non-toxic multinodular goiter
  • Solitary nodular goiter
  • Toxic nodular goiter
  • Non-toxic nodular goiter
  • Benign non-toxic nodular goiter
  • Radiation
  • Genetic factors
  • Insulin resistance
  • Metabolic syndrome
  • Malignant non-toxic nodular goiter
  • Geographical reasons (endemic goiter)
  • Iodine deficiency
  • Sporadic (random) causes
  • Genetic factors
  • TSH-secreting pituitary adenoma
  • Thyroid hormone resistance syndromes
  • Gonadotropin-secreting tumors

The most common cause of goiter is iodine deficiency. There are endemic areas of goiter in different parts of the world, depending on dietary iodine intake. In these regions, goiter and other thyroid diseases such as hypothyroidism, hyperthyroidism, thyrotoxicosis, thyroiditis or thyroid cancers are more common.



During puberty or pregnancy, it may be necessary to increase the thyroid hormone level according to the increasing needs of the body, and in this case, the thyroid gland may develop itself.

Lithium, dietary goitrogens, and some endocrine disruptors can block any of the thyroid hormone production steps. In this case, more TSH is secreted from the pituitary gland in order to maintain the thyroid hormone balance in the blood. The increased TSH level makes the thyroid glands work harder. The follicles of the thyroid glands, which work harder, begin to grow.

Drugs such as amiodarone, interleukin-2, sunitinib, sorafenib, ipilimumab, pembrolizumab and nivolumab may also cause thyroiditis and therefore goiter. In addition, chemicals such as thiocyanate, perchlorate and NO3- cause disruptions in thyroid hormone metabolism, causing the thyroid gland to work and enlarge more.

Certain foods containing phthalates, isoflavones and organochlorides, cyanogenic glycosides such as cassava, sorghum, maize, millet, or thioglucosides such as cabbage, cabbage, Brussels sprouts, cauliflower, kohlrabi, rutabaga, mustard can also cause goiter with similar effects.

Goiter may be the first symptom in autoimmune thyroid diseases. In response to hypothyroidism seen in autoimmune thyroid disorders, the thyroid gland has to develop itself. In order to produce more thyroid hormone, the thyroid follicles have to grow.

Depending on hereditary factors, the probability of developing thyroid disease increases in the clichés with a family history of thyroid disease. This can also be expressed as a kind of predisposition.

Symptoms of goiter:

Since goiter is a slowly growing picture, patients usually apply to the physician for aesthetic reasons. Because the thyroid hormone balance that the body needs is mostly provided. The patient usually presents to the physician with the complaint of a mass in the neck. However, if there is hypothyroidism or hyperthyroidism in patients who develop goiter, symptoms and clinical picture specific to these conditions may develop. Hypothyroidism or hyperthyroidism’s own symptoms dominate the picture.

It may be due to rapidly growing goiter conditions, bleeding inside the thyroid gland, acute inflammatory conditions or malignancy. In rapidly growing goiters, compression around the chest and chest may develop. The patient may develop neck pain, shortness of breath, limitation of movement, difficulty in swallowing or pathologies in the veins. Rarely, neurological symptoms such as Horner’s syndrome may also occur.

In some types of goiter, symptoms may not occur. These are usually endemic goiter, sporadic goiter, drug-induced goiter, initial period of thyrotoxicosis, Hashimoto’s thyroiditis.

Hypothyroidism is more likely if patients have fatigue, weight gain, intolerance to cold, dry skin or joint pain. This condition may develop in some thyroiditis, goiters that progress with abnormal thyroid synthesis, drug-induced goiters or multinodular goiter.

Patients who develop thyrotoxicosis may experience weakness, heat intolerance, palpitations, weight loss and enlargement of the eyeballs called exophthalmos.



If patients who have difficulty in swallowing or have pain during swallowing have goiter, subacute thyroiditis such as De Quervain’s thyroiditis, cancer, bleeding, ademon or cyst may be present. Inflammatory changes in adenomas or cysts can also trigger this picture. Difficulty in swallowing should also raise the possibility of pressure on the esophagus due to chronic thyroiditis or cancer. If the thyroid is overgrown, it can press on the esophagus without cancer, etc.

If the goiter has advanced and the thyroid gland is pressing up to the trachea or bronchi, patients may develop shortness of breath.

Diseases associated with goiter should also be evaluated. For example, patients who develop rheumatoid arthritis with goiter may also have Addison’s disease.

The possibility of thyroid cancers or multinodular goiter should not be forgotten in newborns or children who received excessive radiation to the neck or face during childhood.

Diagnosis of goiter:

In patients who are found to have goiter on examination, the underlying main cause and all other factors affecting the patient’s clinic should be evaluated. The thyroid hormone profile of the patient is examined. Hypothyroidism or hyperthyroidism is evaluated.

If the patient’s thyroid is hard and woody on examination, it should be evaluated for malignancy or Riedel’s thyroiditis (Riedel struma). If the thyroid gland is diffusely and symmetrically enlarged, endemic or sporadic goiters, thyroiditis, Graves’ disease or neonatal goiter come to mind.

Since the blood vessels in the thyroid gland are very strong, if a thyroid murmur is detected by listening, hyperthyroidism may be considered.

In the ultrasonographic evaluation of the thyroid gland, if there is a multinodular growth, there is a possibility of carcinoma or chronic thyroiditis. The appearance of solitary nodules suggests toxic or non-toxic conditions, adenomas or carcinomas or cysts.

If the patient has lymphadenopathy in the neck together with goiter, it brings to mind Hashimoto’s thyroiditis or cancers.



If the thyroid gland is fixed and not moving, it often suggests thyroid cancers or some thyroiditis. However, in patients with hoarseness, detailed evaluation is required primarily in terms of thyroid malignancies and Hashimoto’s disease.

In patients with goiter, other hematological tests are evaluated together with the evaluation of thyroid hormones. Especially low platelet counts and low leukocyte count are common in thyrotoxicosis.

Thyroglobulin antibodies are also commonly used tests along with the thyroid profile. The elevation of thyroglobulin antibodies is typical, especially in patients with suspected Hashimoto’s disease.

Thyroid ultrasonography is valuable for investigations such as determining the size of the thyroid gland, presence of nodules, follicular structures, capsule, compression findings, and presence of cysts.

If there are other organ disorders (hepatitis, nephrosis, etc.) with goiter or if the patient has a history of suspected drug use, thyroxine-binding globulin test can be performed.

Radioactive iodine uptake test can add an interpretation of whether the follicles are active or passive according to the iodine uptake level of the thyroid gland.

Thyroid scintigraphy with iodine 131 can be useful in differentiating toxic or non-toxic goiters. It can be evaluated especially in patients who have undergone radiotherapy to the head and neck region at a young age.

In some patients, a definitive diagnosis with fine needle aspiration biopsy may be required. Classical surgical biopsy may be required in some patients with fibrosis.

Some patients may require further investigations. Pulmonary function tests, chest X-ray, Barium swallow tests, computed tomography, magnetic resonance imaging, thyroid scintigraphy with technetium, serum calcium and phosphorus levels, TRH stimulation test, perchlorate test, thyroid stimulating immunoglobulins, laryngoscopy, genetic tests, hearing and genetic tests in some children. Tests such as taste tests may be required.

Treatment of goiter:

The priority in the treatment of goiter is to reduce the pressure around and to ensure the patient’s thyroid hormone balance. Surgical treatment may be considered to reduce the pressure. Oral thyroid hormone support can be given in patients who develop hypothyroidism. In any case, it should be clarified that there is no malignancy in the thyroid gland.

The treatment of goiter mainly depends on the main cause of the goiter and the patient’s clinic. Surgical treatment is a priority in patients with a possibility of malignancy. Surgical treatment may be considered in patients with ongoing thyroid enlargement.

 

   



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