10/22/13 Goiter

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Goiter

Author: James R Mulinda, MD, FACP, FACE; Chief Editor: George T Griffing, MD more...

Updated: Apr 9, 2013

Background

In 1656, Thomas Wharton described the distinct nature of what he termed the thyroid gland, distinguishing it fromthe larynx, as this structure had been considered a laryngeal gland from the time of Andreas Vesalius in the 16thcentury. It was nearly 200 more years before the function of the thyroid was elucidated. The normal adult thyroidgland weighs 10-25 g and has 2 lobes connected by an isthmus. Nearly 50% of thyroid glands exhibit a pyramidallobe arising from the center of the isthmus. Longitudinal dimensions of the lobes of the thyroid range up to 5 cm,as shown in the image below.

Thyroid nuclear scan of a patient w ith a euthyroid goiter show ing different projections.

A goiter is an enlarged thyroid gland, and it may be diffuse or nodular. A goiter may extend into the retrosternalspace, with or without substantial anterior enlargement. Because of the anatomic relationship of the thyroid glandto the trachea, larynx, superior and inferior laryngeal nerves, and esophagus, abnormal growth may cause a varietyof compressive syndromes. Thyroid function may be normal (nontoxic goiter), overactive (toxic goiter), orunderactive (hypothyroid goiter).

Pathophysiology

The thyroid gland is controlled by thyroid-stimulating hormone (TSH; also known as thyrotropin), secreted from thepituitary gland, which in turn is influenced by the thyrotropin-releasing hormone (TRH) from the hypothalamus. TSHpermits growth, cellular differentiation, and thyroid hormone production and secretion by the thyroid gland.Thyrotropin acts on TSH receptors located on the thyroid gland. Serum thyroid hormones levothyroxine andtriiodothyronine feed back to the pituitary, regulating TSH production. Interference with this TRH-TSH thyroidhormone axis causes changes in the function and structure of the thyroid gland. Stimulation of the TSH receptorsof the thyroid by TSH, TSH-receptor antibodies, or TSH receptor agonists, such as chorionic gonadotropin, mayresult in a diffuse goiter. When a small group of thyroid cells, inflammatory cells, or malignant cells metastatic tothe thyroid is involved, a thyroid nodule may develop.

A deficiency in thyroid hormone synthesis or intake leads to increased TSH production. Increased TSH causesincreased cellularity and hyperplasia of the thyroid gland in an attempt to normalize thyroid hormone levels. If this

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process is sustained, a goiter is established. Causes of thyroid hormone deficiency include inborn errors of thyroid

hormone synthesis, iodine deficiency,[1] and goitrogens.

A goiter may result from a number of TSH receptor agonists. TSH receptor stimulators include TSH receptorantibodies, pituitary resistance to thyroid hormone, adenomas of the hypothalamus or pituitary gland, and tumorsproducing human chorionic gonadotropin.

Epidemiology

Frequency

United States

Autopsy studies suggest a frequency of greater than 50% for thyroid nodules; with high-resolutionultrasonography, the value approaches 40% of patients with nonthyroidal illness. In the Wickham study from the

United Kingdom, 16% of the population had a goiter.[2] In the Framingham study, ultrasonography revealed that 3%

of men older than 60 years had thyroid nodules, while 36% of women aged 49-58 years had thyroid nodules.[3] Inthe United States, most goiters are due to autoimmune thyroiditis (ie, Hashimoto disease).

The incidence of thyroid cancer has been rising worldwide. The reasons are unclear, but this trend may be related

to better detection and diagnostic methods.[4]

International

Worldwide, the most common cause of goiter is iodine deficiency.[1] It is estimated that goiters affect as many as200 million of the 800 million people who have a diet deficient in iodine.

In a German study, 635 people underwent ultrasonographic thyroid screening, as well as basal TSH measurement,

during a preventive-health checkup.[5] Thyroid nodules were detected in 432 (68%) of the persons screened; in aprevious German study, ultrasonographic screening of more than 90,000 people detected thyroid nodules in 33%of the normal population. The authors of the latter report attributed this difference to the fact that patients in theirstudy were screened using 13 MHz ultrasonographic scanners, which were more sensitive than the 7.5 MHzscanners used in the previous study. According to the investigators, their results indicated that the question ofroutine iodine supplementation requires renewed attention.

Mortality/Morbidity

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

Race

No racial predilection exists.

Sex

The female-to-male ratio is 4:1.

In the Wickham study, 26% of women had a goiter, compared to 7% of men.[2]

Thyroid nodules are less frequent in men than in women, but when found, they are more likely to bemalignant.

Age

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

Contributor Information and DisclosuresAuthorJames R Mulinda, MD, FACP, FACE Consulting Staff, Department of Endocrinology, Endocrinology

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Associates, Inc

James R Mulinda, MD, FACP, FACE is a member of the following medical societies: American College ofClinical Endocrinologists and American College of Physicians

Disclosure: Nothing to disclose.

Specialty Editor BoardSteven R Gambert, MD Professor of Medicine, Johns Hopkins University School of Medicine; Director ofGeriatric Medicine, University of Maryland Medical Center and R. Adams Cowley Shock Trauma Center

Steven R Gambert, MD is a member of the following medical societies: Alpha Omega Alpha, American Collegeof Physician Executives, American College of Physicians, American Geriatrics Society, Association ofProfessors of Medicine, Gerontological Society of America, and The Endocrine Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical CenterCollege of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Kent Wehmeier, MD Professor, Department of Internal Medicine, Division of Endocrinology, Diabetes, andMetabolism, St Louis University School of Medicine

Kent Wehmeier, MD is a member of the following medical societies: American Society of Hypertension,International Society for Clinical Densitometry, and The Endocrine Society

Disclosure: Nothing to disclose.

Mark Cooper, MBBS, PhD, FRACP Head, Diabetes & Metabolism Division, Baker Heart Research Institute,Professor of Medicine, Monash University

Disclosure: Nothing to disclose.

Chief EditorGeorge T Griffing, MD Professor of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for theAdvancement of Science, American College of Medical Practice Executives, American College of PhysicianExecutives, American College of Physicians, American Diabetes Association, American Federation for MedicalResearch, American Heart Association, Central Society for Clinical Research, International Society for ClinicalDensitometry, Southern Society for Clinical Investigation, and The Endocrine Society

Disclosure: Nothing to disclose.

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