Endemic goiter

Last updated date: 30-Aug-2023

Originally Written in English

Endemic goiter

Overview

Endemic goiter occurs when the prevalence of thyroid enlargement in a community surpasses 10%. With a few exceptions, its etiology is iodine shortage along with other goitrogenic variables that are generally present and responsible for sporadic goitre. Iodine insufficiency causes serious health concerns, hence the term iodine deficiency diseases (IDD) was developed.

The most common symptom of IDD is goitre, however these illnesses also include cretinism, neonatal hypothyroidism, and congenital abnormalities, as well as delays in mental and physical development, among other things. IDD are a worldwide problem: the WHO estimates that more than 800 million people are at risk, and more than 190 million suffer from IDD; over 3 million individuals have cretinism, and many millions suffer from mental and physical developmental impairments in the most severely afflicted areas.

Prophylaxis with iodine in salt, oil, or another vehicle can completely remove endemic goiter. Problems in preventing iodine deficiency stem from challenges in the handling and distribution of iodized vehicles in some regions of the world, as well as a lack of political will to implement preventative measures.

Despite adequate iodine availability, the presence of goitrogenic chemicals in the environment causes endemic goitre in just a few regions. Excess iodine from seaweed used as a staple meal causes endemic goitre in a few regions.

 

Goiter

Goiter

The swelling of the thyroid gland is known as goiter. Nontoxic goiter is defined as thyroid gland enlargement with no disruption in thyroid function. It isn't the result of inflammation or neoplasia. The goiter might be widespread or confined. The goiter may spread into the retrosternal region if it is big. The goiter might compress the upper trachea, laryngeal nerves, and esophagus because to the restricted space in the mediastinum.

Nontoxic goiter is always caused by iodine supply or metabolic problems. Normally, the thyroid gland weighs around 25 grams. It is a butterfly-shaped gland found in the front triangle of the neck, right below the larynx and trachea. It is made up of two lobes, right and left, joined by an isthmus.

The isthmus is located between the second and third tracheal rings, with lobes reaching from the thyroid cartilage superiorly to the fourth tracheal ring inferiorly on either side. In response to pituitary gland thyrotropic hormone (TSH) stimulation, the thyroid gland secretes thyroid hormones (thyroxin/T4 and triiodothyronine/T3). They are necessary for the metabolism of bodily cells.

It also secretes the calcitonin hormone, which is essential for calcium metabolism. TSH release will rise if thyroid hormone production is reduced owing to iodine shortage, for example, and this, in the long run, will lead to thyroid follicular hyperplasia and, as a consequence, an increase in thyroid gland size.

 

Endemic goiter definition

Endemic goiter definition

The isthmus is located between the second and third tracheal rings, with lobes reaching from the thyroid cartilage superiorly to the fourth tracheal ring inferiorly on either side. In response to pituitary gland thyrotropic hormone (TSH) stimulation, the thyroid gland secretes thyroid hormones (thyroxin/T4 and triiodothyronine/T3). They are necessary for the metabolism of bodily cells.

It also secretes the calcitonin hormone, which is essential for calcium metabolism. TSH release will rise if thyroid hormone production is reduced owing to iodine shortage, for example, and this, in the long run, will lead to thyroid follicular hyperplasia and, as a consequence, an increase in thyroid gland size.

 

Epidemiology

Internationally, 2.2 billion individuals suffer from some sort of iodine deficiency, with the majority of them living in iodine-deficient regions. The degree of iodine shortage correlates with the prevalence of goiter. According to research, the lack of iodine deficiency is connected with a 5% frequency of goiter. The incidence of goiters ranges from 5% to 20% when there is a slight iodine deficit. The prevalence of mild deficit is between 20% and 30%.

The frequency climbs to more than 30% in places with severe insufficiency. Females are 1.2 to 4.3 times more likely than males to have goiter. A low socioeconomic status increases the risk of goiter. This might be due to a decrease in iodine consumption. Sporadic goiter owing to dysmorphogenesis and endemic goiter are most common in childhood, and the thyroid gland grows larger with age. There is no racial difference in the frequency of goiter.

 

Endemic goiter causes

  • Causes
    • Iodine deficiency (most common)
    • Certain foods (eg, sorghum, millet, maize, cassava)
    • Mineral deficiencies (selenium, iron, zinc)
    • Water pollutants
    • Congenital partial defects in thyroid enzyme activity

 

The most frequent kind of goitre is endemic goitre, which is caused by a lack of iodine. Iodine is an important vitamin that is necessary for thyroid hormone synthesis. When iodine consumption is low, thyroid hormone production is low, and the pituitary gland secretes more thyrotropin (thyroid-stimulating hormone, TSH) to try to return thyroid hormone production to normal.

Excess thyrotropin enhances thyroid hormone production as well as thyroid development. Endometrial goitre affects more girls than boys and more women than males. It is especially common in inland or hilly areas where the natural iodine content of the water and soil is quite low. It is readily avoided by consuming salt or foods containing iodine.

Increased iodine consumption causes goitre regression in young people; however, the chance of regression decreases with age. If the goitre interferes with breathing or swallowing, the thyroid gland may need to be surgically removed. 

 

Pathophysiology

The major function of iodine shortage in goitrogenesis is well recognized, as is the prevention and treatment of endemic goiter with iodine supplementation. Unfortunately, the execution of iodine prophylactic programs has been fraught with technical and economical challenges.

Furthermore, a lack of understanding about some of the other endemic goiter causative variables has impeded the development of effective procedures for its total eradication in locations where goiter persists despite extended and adequate iodine administration. At the moment, no less than 5% of the world's population has goiters and related problems, resulting in a huge public health and economical burden.

Seventy-five percent of persons with goiter reside in developing nations, where iodine shortage is common. In endemic areas with extreme iodine shortage, goiter prevalence rates of more than 50% and the highest incidence of severe instances of iodine deficiency diseases, such as cretinism, congenital hypothyroidism, and various degrees of growth and mental development impairment, are seen. Goiters are often multinodular and quite enormous in size, causing indications of compression that necessitate surgery. Recurrence rates range from 25 to 30 percent, with a second operation accounting for 16 percent of all thyroidectomies.

Unfortunately, the majority of these goiters occur in places with limited medical and surgical resources. 25% of persons with goiters live in more industrialized nations, where goiter persists in some locations despite iodine prophylaxis. Autoimmune thyroiditis, hypothyroidism, hyperthyroidism, and thyroid cancer are all associated with iodine-sufficient goiters.

Goiter is surgically significant in iodine-sufficient endemic locations and, to a lesser extent, in nonendemic places where it is referred to as "sporadic" goiter. Following thyroidectomy, the recurrence rate of iodine-sufficient goiter is 10-19%. Because most of these goiters grow by mechanisms other than enhanced thyrotropin (TSH) activation, suppressive dosages of L-thyroxine are ineffective and, due to potential consequences, are not suggested.

Although Graves' hyperthyroidism is not directly associated to endemic goiter, it does have a negative relationship with iodine consumption or administration. Currently, 131I or antithyroid medications are used to treat Graves' illness in more than 90% of patients. The prevalence of papillary, follicular, and anaplastic thyroid carcinomas appears to be linked to endemic goiter and iodine supplementation, with surgery necessary in nearly all of these cases.

 

Endemic goiter symptoms

Endemic goiter symptoms

Symptoms and Signs

  • Thyroid may become multinodular and very large
  • Growth often occurs during pregnancy and may cause compressive symptoms
  • Substernal goiters usually asymptomatic but can cause
    • Tracheal compression
    • Respiratory distress
    • Dysphagia
    • Superior vena cava syndrome
    • Phrenic or recurrent laryngeal nerve palsy, or Horner syndrome
    • Gastrointestinal bleeding from esophageal varices
    • Pleural or pericardial effusions (rare)
  • Cerebral ischemia and stroke can result from arterial compression or thyrocervical steal syndrome
  • Malignancy in < 1%
  • Some patients with goiter become hypothyroid
  • Other patients become thyrotoxic as goiter grows and becomes more autonomous, especially if iodine added to diet
  • Congenital hypothyroidism
    • Isolated deafness
    • Short stature
    • Impaired mentation

 

Fetal Development

In iodine-deficient areas, severe endemic goiter and cretinism are found. After an experiment in Papua New Guinea, the association between ID and cretinism was verified in 1966. When iodized oil was supplied to a population before to the commencement of pregnancy, the incidence of cretinism and goiter was reduced in the treated group.

Maternal dietary I and T4 are essential during pregnancy. Even when the fetus' thyroid begins to produce THs, the mother's T4 supply remains critical. Maternal T4 accounts for 20% to 50% of the T4 detected in cord blood at delivery. Maternal I, which is transported into milk by NIS after birth, is essential for the newborn's growth. The iodine intake guideline during breastfeeding is based on the woman's daily need plus the amount of iodine lost in human milk.

Thyroid hormone receptors are present in the embryonic brain by nine weeks, rendering the development of the central nervous system (CNS) vulnerable to TH deficit as early as the first trimester. THs have an important function in the fetal and neonatal CNS, influencing neuronal migration, differentiation, myelination, and synaptogenesis. Thyroid hormones are required for the development of the cerebral cortex, cochlea, and basal ganglia during the first trimester of pregnancy. They are also required for brain development and differentiation throughout the third trimester.

 

Diagnosis

Laboratory Tests

Laboratory Test

  • Serum thyroxine and thyroid-stimulating hormone (TSH) usually normal
    • TSH low if multinodular goiter becomes autonomous in presence of sufficient iodine for thyroid hormone synthesis, causing hyperthyroidism
    • TSH high in hypothyroidism
  • Serum levels of antithyroid antibodies usually undetectable or low
  • Serum thyroglobulin often elevated above 13 mcg/L

Imaging Studies

  • Thyroid radioactive iodine uptake usually elevated, but may be normal if iodine intake has improved

 

Management

Management of endemic goiter

Medications

Dietary iodine supplementation (eg, addition of potassium iodide to table salt)

  • Reduces the frequency of endemic goiter and cretinism significantly, but is less efficient in decreasing existing goiter.
  • Has not been shown to be useful in treating people with big multinodular goiter and may instead increase their chance of acquiring thyrotoxicosis.

Surgery

  • Thyroidectomy indicated for cosmesis, compressive symptoms, or thyrotoxicosis in adults with very large multinodular goiters

Procedures

  • Patients may be treated with 131I for large compressive goiters

 

Complications

  • Supplementing with dietary iodine raises the risk of autoimmune thyroid dysfunction, which can result in hypothyroidism or hyperthyroidism.
  • Excessive iodine supplementation increases the risk of goiter
  • Levothyroxine supplementation
    • May induce hyperthyroidism in individuals with autonomous multinodular goiters
    • Therefore, levothyroxine suppression should not be started in patients with suppressed TSH levels
  • Rarely, Graves disease can develop 3–10 months after 131I treatment in patients with large multinodular goiters

 

Prevention

  • Iodized salt contains iodine at about 20 mg per kg salt
  • Other sources of iodine include commercial bread, milk, and seafood.
  • Minimum dietary requirement for iodine is about 50 mcg daily
    • Optimal iodine intake is 150–300 mcg daily
    • Iodine sufficiency is demonstrated by urinary iodide excretion > 10 mcg/dL

 

When to Refer

  • Refer to an endocrinologist if you have hyperthyroidism, a growing goiter, or suspicious nodules.
  • In individuals with very large multinodular goiters, see a thyroid surgeon about having a thyroidectomy for cosmesis, compressive symptoms, or thyrotoxicosis.

 

Conclusion 

The goiter is the most common clinical symptom of an iodine deficit. Goiter is considered endemic if it affects more than 5% of the general population or 10% of school-aged children in a certain geographic area. Endemic goiter is an adaptive illness caused by chronic stimulation of the thyroid gland as a result of increased thyrotropin release owing to iodine shortage.

If iodine shortage is severe or chronic, various indications of iodine deficiency diseases (IDD), such as cretinism, might be seen in the clinical picture. In general, goiter is not accompanied with additional symptoms during the early stages of the disease, although nodular and toxic development are common complications of long-term sickness.