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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 from the larynx, as this structure had been considered a laryngeal gland from the time of Andreas Vesalius in the 16th century. It was nearly 200 more years before the function of the thyroid was elucidated. The normal adult thyroid gland weighs 10-25 g and has 2 lobes connected by an isthmus. Nearly 50% of thyroid glands exhibit a pyramidal lobe 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 retrosternal space, with or without substantial anterior enlargement. Because of the anatomic relationship of the thyroid gland to the trachea, larynx, superior and inferior laryngeal nerves, and esophagus, abnormal growth may cause a variety of compressive syndromes. Thyroid function may be normal (nontoxic goiter), overactive (toxic goiter), or underactive (hypothyroid goiter).

Pathophysiology
The thyroid gland is controlled by thyroid-stimulating hormone (TSH; also known as thyrotropin), secreted from the pituitary gland, which in turn is influenced by the thyrotropin-releasing hormone (TRH) from the hypothalamus. TSH permits 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 and triiodothyronine feed back to the pituitary, regulating TSH production. Interference with this TRH-TSH thyroid hormone axis causes changes in the function and structure of the thyroid gland. Stimulation of the TSH receptors of the thyroid by TSH, TSH-receptor antibodies, or TSH receptor agonists, such as chorionic gonadotropin, may result in a diffuse goiter. When a small group of thyroid cells, inflammatory cells, or malignant cells metastatic to the thyroid is involved, a thyroid nodule may develop. A deficiency in thyroid hormone synthesis or intake leads to increased TSH production. Increased TSH causes increased 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 receptor antibodies, pituitary resistance to thyroid hormone, adenomas of the hypothalamus or pituitary gland, and tumors producing human chorionic gonadotropin.

Epidemiology
Frequency
United States Autopsy studies suggest a frequency of greater than 50% for thyroid nodules; with high-resolution ultrasonography, 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] In the 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 as 200 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 a previous 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 their study were screened using 13 MHz ultrasonographic scanners, which were more sensitive than the 7.5 MHz scanners used in the previous study. According to the investigators, their results indicated that the question of routine iodine supplementation requires renewed attention.

Mortality/Morbidity
Most goiters are benign, causing only cosmetic disfigurement. Morbidity or mortality may result from compression of 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 be malignant.

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

Contributor Information and Disclosures

Author James 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 of Clinical Endocrinologists and American College of Physicians Disclosure: Nothing to disclose. Specialty Editor Board Steven R Gambert, MD Professor of Medicine, Johns Hopkins University School of Medicine; Director of Geriatric 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 College of Physician Executives, American College of Physicians, American Geriatrics Society, Association of Professors 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 Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment Kent Wehmeier, MD Professor, Department of Internal Medicine, Division of Endocrinology, Diabetes, and Metabolism, 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 Editor George 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 the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, International Society for Clinical Densitometry, Southern Society for Clinical Investigation, and The Endocrine Society Disclosure: Nothing to disclose.

References
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6. Duarte GC, Tomimori EK, de Camargo RY, Catarino RM, Ferreira JE, Knobel M, et al. Excessive iodine intake and ultrasonographic thyroid abnormalities in schoolchildren. J Pediatr Endocrinol Metab . Apr 2009;22(4):327-34. [Medline]. 7. Rasmussen LB, Schomburg L, Kohrle J, et al. Selenium status, thyroid volume, and multiple nodule formation in an area with mild iodine deficiency. Eur J Endocrinol. Apr 2011;164(4):585-90. [Medline]. 8. Pinchot SN, Al-Wagih H, Schaefer S, Sippel R, Chen H. Accuracy of fine-needle aspiration biopsy for predicting neoplasm or carcinoma in thyroid nodules 4 cm or larger. Arch Surg. Jul 2009;144(7):649-55. [Medline]. 9. Arda IS, Yildirim S, Demirhan B, Firat S. Fine needle aspiration biopsy of thyroid nodules. Arch Dis Chil. 2001;85(4):313-7. [Medline]. 10. Bardin CW. Endemic goiter. In: Current Therapy in Endocrinology and Metabolism. 6th ed. Mosby-Year Book; 1997:101-112. 11. Becker KL, Bilezikian JP, Bremner WJ. Nontoxic goiter. In: Principles and Practice of Endocrinology and Metabolism. 2nd ed. Lippincott Williams & Wilkins; 1995:338-345. 12. Bostanci I, Sarioglu A, Ergin H, Aksit A, Cinbis M, Akalin N. Neonatal goiter caused by expectorant usage. J Pediatr Endocrinol Metab . Sep-Oct 2001;14(8):1161-2. [Medline]. 13. Braverman LE, Utiger RD. Thyroid diseases: nontoxic diffuse and multinodular goiter. In: Werner and Ingbar, eds. The Thyroid: A Fundamental and Clinical Text. 7th ed. Lippincott-Raven; 1996:889-900. 14. Gross JL. Ultrasonography in management of nodular thyroid disease. Annals of internal medicine. 2001;135(5):383-4. [Medline]. 15. Romanchishen AF, Iakovlev PN. [Special surgical treatment of patients with nodular tumors of the thyroid gland against the background of diffuse toxic goiter]. Vestn Khir Im I I Grek . 2005;164(1):21-4. [Medline]. 16. Sawin CT, Geller A, Wolf PA, et al. Low serum thyrotropin concentrations as a risk factor for atrial fibrillation in older persons. N Engl J Med. Nov 10 1994;331(19):1249-52. [Medline]. 17. Schumm-Draeger PM. [Every third German has a sick thyroid gland. Nodules and goiter are a challenge that needs to be met]. MMW Fortschr Med. Feb 5 2004;146(6):20. [Medline]. 18. Thompson L. Dyshormonogenetic goiter of the thyroid gland. Ear Nose Throat J . Apr 2005;84(4):200. [Medline]. 19. Vetshev PS, Chilingaridi KE, Bannyi DA, Dmitriev EE. [Repeated surgeries on the thyroid gland in nodular euthyroid goiter]. Khirurgiia (Mosk ). 2004;37-40. [Medline]. 20. Wilson JD, Foster DW. The thyroid gland. In: Williams Textbook of Endocrinology. 8th ed. Harcourt Brace & Co; 1992:463-465. Medscape Reference 2011 WebMD, LLC

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