eMedicine Specialties > Endocrinology > Thyroid

Goiter

Author: James R Mulinda, MD, FACP, FACE, Consulting Staff, Department of Endocrinology, Endocrinology Associates, Inc
Contributor Information and Disclosures

Updated: Aug 18, 2009

Introduction

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 euthyroi...

Thyroid nuclear scan of a patient with a euthyroid goiter showing different projections.

Thyroid nuclear scan of a patient with a euthyroi...

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).

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 process is sustained, a goiter is established. Causes of thyroid hormone deficiency include inborn errors of thyroid hormone synthesis, iodine deficiency,1 and goitrogens.

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.

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).

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.4 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 later 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.

Clinical

History

A goiter may present in various ways, including the following:

  • Incidentally, as a swelling in the neck discovered by the patient or on routine physical examination
  • A finding on imaging studies performed for a related or unrelated medical evaluation
  • Local compression causing dysphagia, dyspnea, stridor, plethora or hoarseness
  • Pain due to hemorrhage, inflammation, necrosis, or malignant transformation
  • Signs and symptoms of hyperthyroidism or hypothyroidism
  • Thyroid cancer with or without metastases

Physical

The general examination for hyperthyroidism, hypothyroidism, and autoimmune stigmata is followed by systematic examination of the goiter.

  • A retrosternal goiter may not be evident on physical examination.
  • Examination of the goiter is best performed with the patient upright, sitting or standing. Inspection from the side may better outline the thyroid profile, as shown below. Asking the patient to take a sip of water facilitates inspection. The thyroid should move upon swallowing.

    • Patient with a goiter. Prominent side-view outlin...

      Patient with a goiter. Prominent side-view outline.

      Patient with a goiter. Prominent side-view outlin...

      Patient with a goiter. Prominent side-view outline.

  • Palpation of the goiter is performed either facing the patient or from behind the patient, with the neck relaxed and not hyperextended. Palpation of the goiter rules out a pseudogoiter, which is a prominent thyroid seen in individuals who are thin. Each lobe is palpated for size, consistency, nodules, and tenderness. Cervical lymph nodes are then palpated. The oropharynx is visualized for the presence of lingular thyroid tissue.
  • The size of each lobe is measured in 2 dimensions using a tape measure. Some examiners make tracings on a sheet of paper, which is placed in the patient's chart. Suitable landmarks are used and documented to ensure consistent measurement of the thyroid gland.
  • The pyramidal lobe often is enlarged in Graves disease.
  • A firm rubbery thyroid gland suggests Hashimoto thyroiditis, and a hard thyroid gland suggests malignancy or Riedel struma.
  • Multiple nodules may suggest a multinodular goiter or Hashimoto thyroiditis. A solitary hard nodule suggests malignancy, whereas a solitary firm nodule may be a thyroid cyst.
  • Diffuse thyroid tenderness suggests subacute thyroiditis, and local thyroid tenderness suggests intranodal hemorrhage or necrosis.
  • Cervical lymph glands are palpated for signs of metastatic thyroid cancer.
  • Auscultation of a soft bruit over the inferior thyroidal artery may be appreciated in a toxic goiter. Palpation of a toxic goiter may reveal a thrill in the profoundly hyperthyroid patient.
  • Goiters are described in a variety of ways, including the following:
    • Toxic goiter: A goiter that is associated with hyperthyroidism is described as a toxic goiter. Examples of toxic goiters include diffuse toxic goiter (Graves disease), toxic multinodular goiter, and toxic adenoma (Plummer disease).
    • Nontoxic goiter: A goiter without hyperthyroidism or hypothyroidism is described as a nontoxic goiter. It may be diffuse or multinodular, but a diffuse goiter often evolves into a nodular goiter. Examination of the thyroid may not reveal small or posterior nodules. Examples of nontoxic goiters include chronic lymphocytic thyroiditis (Hashimoto disease), goiter identified in early Graves disease, endemic goiter, sporadic goiter, congenital goiter, and physiologic goiter that occurs during puberty.
  • Autonomously functioning nodules may present with inability to palpate the contralateral lobe. Unilobar agenesis may also present like a single thyroid nodule with hyperplasia of the remaining lobe.
  • The Pemberton maneuver raises a goiter into the thoracic inlet when the patient elevates the arms. This may cause shortness of breath, stridor, or distention of neck veins.

Causes

The different etiologic mechanisms that can cause a goiter include the following:

  • Iodine deficiency1
  • Autoimmune thyroiditis - Hashimoto or postpartum thyroiditis
  • Excess iodine (Wolff-Chaikoff effect)5 or lithium ingestion, which decrease release of thyroid hormone
  • Goitrogens
  • Stimulation of TSH receptors by TSH from pituitary tumors, pituitary thyroid hormone resistance, gonadotropins, and/or thyroid-stimulating immunoglobulins
  • Inborn errors of metabolism causing defects in biosynthesis of thyroid hormones
  • Exposure to radiation
  • Deposition diseases
  • Thyroid hormone resistance
  • Subacute thyroiditis (de Quervain thyroiditis)
  • Silent thyroiditis
  • Riedel thyroiditis
  • Infectious agents
    • Acute suppurative - Bacterial
    • Chronic - Mycobacteria, fungal, and parasitic
  • Granulomatous disease
  • Thyroid malignancy

More on Goiter

Overview: Goiter
Differential Diagnoses & Workup: Goiter
Treatment & Medication: Goiter
Follow-up: Goiter
Multimedia: Goiter
References
Further Reading

References

  1. 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. Sep 1 2009;[Medline].

  2. 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). Dec 1977;7(6):481-93. [Medline].

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

  4. 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. Aug 2009;39(8):699-706. [Medline].

  5. 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].

  6. 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].

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

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

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

  10. 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].

  11. 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.

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

  13. 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].

  14. 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].

  15. 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].

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

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

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

Further Reading

Clinical guidelines:
American Association of Clinical Endocrinologists and Associazione Medici Endocrinologi medical guidelines for clinical practice for the diagnosis and management of thyroid nodules.
American Association of Clinical Endocrinologists - Medical Specialty Society
Associazione Medici Endocrinologi - Medical Specialty Society. 1996 Jan (revised 2006 Feb). 40 pages. NGC:004869

Management guidelines for patients with thyroid nodules and differentiated thyroid cancer.
American Thyroid Association - Professional Association. 2006 Feb. 34 pages. NGC:005212

Screening for congenital hypothyroidism: U.S. Preventive Services Task Force reaffirmation recommendation statement.
United States Preventive Services Task Force - Independent Expert Panel. 1996 (revised 2008 Mar). 6 pages. NGC:006354

Clinical trials:
rhTSH, Radioiodine Uptake and Goiter Reduction Following 131I Therapy in Patients With Benign Nontoxic Nodular Goiter

Block-Replacement Therapy During Radioiodine Therapy

Levothyroxine Treatment in Thyroid Benign Nodular Goiter

Keywords

goiter, goiter disease, thyroid disease, thyroid cancer, iodine deficiency, hypothyroidism, hyperthyroidism, thyroid nodules, thyroid gland goiter, nontoxic goiter, toxic goiter, multinodular goiter, endemic goiter, Hashimoto disease, iodine, enlarged thyroid gland, inborn errors of thyroid hormone synthesis, goitrogens, TSH receptor antibodies, pituitary resistance to thyroid hormone, adenomas of hypothalamus, adenomas of pituitary gland, tumors producing human chorionic gonadotropin, autoimmune thyroiditis, Hashimoto disease, swelling in the neck, Graves disease, Hashimoto thyroiditis

Riedel struma, toxic multinodular goiter, subacute thyroiditis, diffuse toxic goiter, toxic adenoma, Plummer disease, chronic lymphocytic thyroiditis, sporadic goiter, congenital goiter, physiologic goiter, Pemberton maneuver, postpartum thyroiditis, Wolff-Chaikoff effect, lithium ingestion, pituitary thyroid hormone resistance, thyroid-stimulating immunoglobulins, thyroid hormone resistance, de Quervain thyroiditis, silent thyroiditis, Riedel thyroiditis, granulomatous disease, thyroid malignancy

Contributor Information and Disclosures

Author

James R Mulinda, MD, FACP, FACE, Consulting Staff, Department of Endocrinology, Endocrinology 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.

Medical Editor

Steven R Gambert, MD, MACP, Chairman, Department of Medicine, Physician-in-Chief, Sinai Hospital of Baltimore; Professor of Medicine, Program Director, Internal Medicine Program, Johns Hopkins University School of Medicine
Steven R Gambert, MD, MACP 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, Endocrine Society, and Gerontological Society of America
Disclosure: Nothing to disclose.

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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, and International Society for Clinical Densitometry
Disclosure: Nothing to disclose.

CME Editor

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, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation
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