Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Goiter

  • Author: James R Mulinda, MD, FACP; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
 
Updated: Jul 13, 2016
 

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 with a euthyroid Thyroid nuclear scan of a patient with a euthyroid goiter showing 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).

Next

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. Thyroid hormones are synthesized from iodination of tyrosine. The iodine is transported from plasma into the thyroid cell via a sodium-iodide symporter. This is an active process resulting in an intracellular iodine level exceeding 20 times the plasma iodine level. This iodine transport activity is controlled by TSH.[1] 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 process is sustained, a goiter is established. Causes of thyroid hormone deficiency include inborn errors of thyroid hormone synthesis, iodine deficiency,[2] 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.

Previous
Next

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.[3] 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.[4] 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.[5]

International

Worldwide, the most common cause of goiter is iodine deficiency.[2] 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.[6] 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. [3]
  • 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.

Previous
Next

Prognosis

Benign goiters have a good prognosis. However, all goiters should be monitored by examination and biopsy for possible malignant transformation, which may be signaled by a sudden change in size, pain, or consistency. Fortunately, the risk of this is low. In patients exposed to low levels of radiation the risk rises.

Based on the Wickham study, a few of the goiters increased in size.[3]

A small percentage of multinodular goiters do cause hyperthyroidism. Lifelong surveillance is necessary.

Patients with chronic lymphocytic thyroiditis generally have glands that become atrophic.

Previous
Next

Patient Education

Educate a patient about potential etiologies, eg, adequate dietary iodine intake, avoidance of goitrogens, regular personal neck examination, and physician examination.

For patients on medical therapy, reinforce the need to take medications on a regular basis. Review symptoms of hyperthyroidism.

For excellent patient education resources, visit eMedicineHealth's Thyroid and Metabolism Center. Also, see eMedicineHealth's patient education article Thyroid Problems.

Previous
 
 
Contributor Information and Disclosures
Author

James R Mulinda, MD, FACP Consulting Staff, Department of Endocrinology, Endocrinology Associates, Inc

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

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, Endocrine Society, International Society for Clinical Densitometry

Disclosure: Nothing to disclose.

Chief Editor

Romesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School

Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society

Disclosure: Nothing to disclose.

Additional Contributors

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 Association for Physician Leadership, American College of Physicians, American Geriatrics Society, Endocrine Society, Gerontological Society of America, Association of Professors of Medicine

Disclosure: Nothing to disclose.

References
  1. Dohan O, De la Vieja A, Paroder V, et al. The sodium/iodide Symporter (NIS): characterization, regulation, and medical significance. Endocr Rev. 2003 Feb. 24(1):48-77. [Medline].

  2. Triggiani V, Tafaro E, Giagulli VA, et al. Role of iodine, selenium and other micronutrients in thyroid function and disorders. Endocr Metab Immune Disord Drug Targets. 2009 Sep 1. [Medline].

  3. Tunbridge WM, Evered DC, Hall R, Appleton D, Brewis M, Clark F, et al. The spectrum of thyroid disease in a community: the Wickham survey. Clin Endocrinol (Oxf). 1977 Dec. 7(6):481-93. [Medline].

  4. Sawin CT, Geller A, Hershman JM, Castelli W, Bacharach P. The aging thyroid. The use of thyroid hormone in older persons. JAMA. 1989 May 12. 261(18):2653-5. [Medline].

  5. Cossu A, Budroni M, Paliogiannis P, et al. Epidemiology of thyroid cancer in an area of epidemic thyroid goiter. J Cancer Epidemiol. 2013. 2013:584768. [Medline]. [Full Text].

  6. Guth S, Theune U, Aberle J, Galach A, Bamberger CM. Very high prevalence of thyroid nodules detected by high frequency (13 MHz) ultrasound examination. Eur J Clin Invest. 2009 Aug. 39(8):699-706. [Medline].

  7. 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. 2009 Apr. 22(4):327-34. [Medline].

  8. 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. 2011 Apr. 164(4):585-90. [Medline].

  9. 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. 2009 Jul. 144(7):649-55. [Medline].

  10. Li Y, Li Y, Zhou X. Total Thyroidectomy versus Bilateral Subtotal Thyroidectomy for Bilateral Multinodular Nontoxic Goiter: A Meta-Analysis. ORL J Otorhinolaryngol Relat Spec. 2016. 78(3):167-75. [Medline]. [Full Text].

  11. Khan MN, Goljo E, Owen R, et al. Retrosternal Goiter: 30-Day Morbidity and Mortality in the Transcervical and Transthoracic Approaches. Otolaryngol Head Neck Surg. 2016 May 24. [Medline].

  12. Arda IS, Yildirim S, Demirhan B, Firat S. Fine needle aspiration biopsy of thyroid nodules. Arch Dis Chil. 2001. 85(4):313-7. [Medline].

  13. Bardin CW. Endemic goiter. Current Therapy in Endocrinology and Metabolism. 6th ed. Mosby-Year Book; 1997. 101-112.

  14. Becker KL, Bilezikian JP, Bremner WJ. Nontoxic goiter. Principles and Practice of Endocrinology and Metabolism. 2nd ed. Lippincott Williams & Wilkins; 1995. 338-345.

  15. Bostanci I, Sarioglu A, Ergin H, Aksit A, Cinbis M, Akalin N. Neonatal goiter caused by expectorant usage. J Pediatr Endocrinol Metab. 2001 Sep-Oct. 14(8):1161-2. [Medline].

  16. Braverman LE, Utiger RD. Thyroid diseases: nontoxic diffuse and multinodular goiter. Werner and Ingbar, eds. The Thyroid: A Fundamental and Clinical Text. 7th ed. Lippincott-Raven; 1996. 889-900.

  17. Gross JL. Ultrasonography in management of nodular thyroid disease. Annals of internal medicine. 2001. 135(5):383-4. [Medline].

  18. 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].

  19. 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. 1994 Nov 10. 331(19):1249-52. [Medline].

  20. 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. 2004 Feb 5. 146(6):20. [Medline].

  21. Thompson L. Dyshormonogenetic goiter of the thyroid gland. Ear Nose Throat J. 2005 Apr. 84(4):200. [Medline].

  22. Vetshev PS, Chilingaridi KE, Bannyi DA, Dmitriev EE. [Repeated surgeries on the thyroid gland in nodular euthyroid goiter]. Khirurgiia (Mosk). 2004. 37-40. [Medline].

  23. Wilson JD, Foster DW. The thyroid gland. Williams Textbook of Endocrinology. 8th ed. Harcourt Brace & Co; 1992. 463-465.

  24. Wang P, Sun H, Shang L, Zhang Q, He Y, et al. Low Goiter Rate Associated with Small Average Thyroid Volume in Schoolchildren after the Elimination of Iodine Deficiency Disorders. PLoS One. 2015. 10 (10):e0141552. [Medline].

  25. Lee SJ, Lim GY, Kim JY, Chung MH. Diagnostic performance of thyroid ultrasonography screening in pediatric patients with a hypothyroid, hyperthyroid or euthyroid goiter. Pediatr Radiol. 2015 Aug 23. [Medline].

 
Previous
Next
 
Patient with a goiter. Prominent side-view outline.
Thyroid nuclear scan of a patient with a euthyroid goiter showing different projections.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.