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see thyroid glandthyroid gland,
endocrine gland, situated in the neck, that secretes hormones necessary for growth and proper metabolism. It consists of two lobes connected by a narrow segment called the isthmus. The lobes lie on either side of the trachea, the isthmus in front of it.
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in man, enlargement of the thyroid gland caused by the proliferation of its functional lymphoid tissue (parenchyma) or of its connective-tissue stroma. The proliferation of thyroid epithelium may embrace the entire thyroid parenchyma (diffuse goiter), or it may originate in a particular portion of the parenchyma (nodular goiter). Slight enlargement of the gland may occur in puberty or during menstruation, pregnancy, and lactation. Goiter may be associated with a number of conditions—diffuse toxic goiter, thyroiditis, thyroid tumor, and sporadic and endemic goiter.

A goiter may be unilateral or bilateral. Most often it is found in the neck; sometimes it is located behind the sternum (substernal goiter). A goiter usually alters the contours of the neck; although with substernal and deep-lying goiters the contours of the neck may remain normal. A goiter results in malfunction of the thyroid gland, but in the euthyroid form there need not be any functional impairment. Sporadic goiter is found in a number of localities and is caused by an endogenous (depending on internal factors) iodine deficiency in the body. Endemic goiter is found in certain biogeochemical areas where there is an insufficiency of iodine in the air, water, soil, and food products (instead of 200–220 μg, 20–80 μg of iodine or less enters the human body). Insufficiency of iodine in the environment may be aggravated by unfavorable exogenous (social, everyday, and sanitary-hygienic conditions) or endogenous (pregnancy, lactation, hypovitaminoses, helminthiases) factors. Iodine deficiency may result from infectious diseases or intoxications. A relative deficiency may occur when the ratio of iodine to certain chemical compounds (calcium, fluorine, and so forth) in the body is upset. Endemic goiter is found in almost every country, especially in mountainous regions, valleys, foothills, and watersheds and in swampy, sandy, and peaty regions. It is almost never found in chernozem zones.

Goiter prevention includes correcting unhealthy conditions in the throat and mouth, vermifuge treatment, and improvement of the conditions of sanitation and hygiene of daily life (keeping dwellings clean, maintaining the water supply properly, sound nutrition); individual and group iodine prophylaxis (iodized table salt); and early detection and dispensary observation of goiter patients. Treatment, depending on the form and symptoms of goiter, includes iodine preparations, thyroidin, triiodothyronine, and diiodothyrosine. Surgery is indicated for nodular and mixed goiter; it is also recommended for diffuse goiter if more conservative treatment proves ineffective.



An enlargement of all or part of the thyroid gland; may be accompanied by a hormonal dysfunction.


(US), goiter
Pathol a swelling of the thyroid gland, in some cases nearly doubling the size of the neck, usually caused by under- or overproduction of hormone by the gland
References in periodicals archive ?
The Frequency of Micronuclei (MN) observed in [sup.131]I treated hyperthyroid patients-7 & 30 days after therapy Disease Age in years Particulars (Mean [+ or -] SD) GD (n = 25) 46.32 [+ or -] 6.68 TMG (n = 05) 55.00 [+ or -] 8.24 ATN (n = 02) 53.5 [+ or -] 6.36 Disease Frequency of Micronuclei (Mean [+ or -] SD) Particulars 7 days after 30 days after [sup.131]I therapy [sup.131]I therapy GD (n = 25) 2.36 [+ or -] 1.380 1.88 [+ or -] 0.175 * TMG (n = 05) 4.60 [+ or -] 0.96 3.30 [+ or -] 0.97 * ATN (n = 02) 6.00 [+ or -] 0.00 4.25 [+ or -] 0.35 * * Values insignificant at 5% level; GD, graves' disease; TMG, toxic multinodular goiter; ATN, autonomous thyroid nodule.
A significant positive trend was observed for toxic multinodular goiter (3.6% in the 80s versus 46.3% in the 2010s, p < 0.001 for trend), nontoxic multinodular goiter (1.4% in the 1980s versus 4.7% in the 2010s, p = 0.02 for trend), toxic adenoma (0.3% in the 80s versus 4.2% in the 2010s, p < 0.001), diffuse toxic goiter (4.4% in the 80s versus 45.4% in the 2010s, p < 0.001 for trend), unspecified thyroiditis (4.8% in the 80s and 28.5% in the 2010s, p < 0.0001 for trend), and autoimmune thyroiditis (3.8% in the 1980s versus 10.0% in the 2010s, p < 0.0001 for trend).
As shown in Table 4, diagnosis of toxic multinodular goiter between 1982 and 1995 represented 16.9% of thyroid cases, while from 1996 to 2014 it increased to 24.9% of total thyroid cases (p < 0.0001).
(10) Graves' disease and toxic multinodular goiter exhibit increased RAI uptake that is diffuse and nodular, respectively.
Toxic multinodular goiter, also known as Plummer's disease, is the underlying condition in 15% to 20% of hyperthyroidism cases; it is more common in young patients and in iodine-deficient locations (eg, Denmark).
One study [23] reported that urine 8-OHdG levels were significantly higher in the patients diagnosed with toxic multinodular goiter, Graves' disease, and Hashimoto's thyroiditis.
Thyrotoxicosis is defined as a state of thyroid hormone excess and the major etiologies are Grave's disease, toxic multinodular goiter and toxic adenomas.
In the United States, I-131 is the most common treatment for toxic multinodular goiters associated with hyperthyroidism.