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Goiter is defined as enlargement of the thyroid gland. It generally results from focal follicular cell hyperplasia at one or multiple sites within the thyroid gland, and it usually develops over years. Endemic goiter refers to enlargement of the thyroid gland secondary to iodine deficiency affecting more than 10% of the population in a defined geographic area. Sporadic goiter develops in subjects living in iodine-sufficient areas. Goiter encompasses a spectrum of entities, including diffuse, uninodular, or multinodular enlargement of the thyroid gland. The overall hormonal status of the thyroid nodules within the goiter determines the function of the gland and the definition. When enlargement of the thyroid gland is present without clinical or laboratory evidence of thyroid dysfunction, it is euthyroid multinodular goiter (MNG); when accompanied by hyperthyroidism, it is toxic nodular goiter (TNG). Less frequently, thyroid enlargement is caused by two other disorders such as fibrous chronic Hashimoto's thyroiditis, Graves' disease, or neoplasia. Retrosternal or substernal goiter refers to goiter that is associated with extension into the mediastinum.


This chapter discusses the pathogenesis, clinical manifestations, and management of nontoxic goiter.


Goiter prevalence in the general population is estimated to be 15.8%, varying between 4.7% in the Americas to 28.3% in Africa. When comparing current total goiter prevalence (TGP) estimates with the data from 1993, TGP has increased by 31.7% worldwide, but when analysis is restricted to surveys carried out in the past 5 years, TGP shows a decrease of 28.9% compared with 1993.1 Sporadic goiter is the most common form of goiter in the United States, affecting 5% of the population. Goiter is 2- to 10-fold more prevalent in women than in men.2 The association between age and goiter prevalence is dependent on iodine status: in areas of severe iodine deficiency, the prevalence of goiter is maximal in the teenage years,3 but the peak appears around middle age or later in mildly iodine deficient areas.2 African-American ethnicity has been shown to be an independent risk factor for the development of large nodular goiter.4


Iodine deficiency is the most important risk factor for goiter worldwide. The mechanism by which the thyroid gland adapts to an insufficient iodine supply is to increase the trapping of iodide, as well as the subsequent steps of the intrathyroidal metabolism of iodine. This process is triggered and maintained by increased secretion of thyroid-stimulating hormone (TSH), which is ultimately responsible for the development of goiter. The acceleration of the main steps of iodine kinetics and the degree of hyperstimulation by TSH are greater in the pediatric age groups than in adults, and the development of goiter appears as an unfavorable side effect in the process of adaptation to iodine deficiency during growth.3


In patients with sporadic goiter, the cause is usually unknown and involves a combination of environmental and genetic factors. TSH is considered to be the main growth factor in goiter development, but ...

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