Nontoxic Goiter 

  • Author: Stephanie L Lee, MD, PhD; Chief Editor: George T Griffing, MD   more...
 
Updated: Sep 14, 2011
 

Background

A nontoxic goiter is a diffuse or nodular enlargement of the thyroid gland that does not result from an inflammatory or neoplastic process and is not associated with abnormal thyroid function. Endemic goiter is defined as thyroid enlargement that occurs in more than 10% of a population, and sporadic goiter is a result of environmental or genetic factors that do not affect the general population.

Intrathoracic goiter causing obstruction. This patIntrathoracic goiter causing obstruction. This patient has a visible goiter on physical examination. In addition, he has distension of his left external jugular vein, facial erythema (when compared with his shoulder), and cutaneous varicosities of venous blood draining from his head into his chest because of jugular obstruction from his goiter.
Next

Pathophysiology

The histopathology varies with etiology and age of the goiter. Initially, uniform follicular epithelial hyperplasia (diffuse goiter) is present, with an increase in thyroid mass. As the disorder persists, the thyroid architecture loses uniformity, with the development of areas of involution and fibrosis interspersed with areas of focal hyperplasia. This process results in multiple nodules (multinodular goiter). On nuclear scintigraphy, some nodules are hot, with high isotope uptake (autonomous) or cold, with low isotope uptake, compared with the normal thyroid tissue (as demonstrated in the images below). The development of nodules correlates with the development of functional autonomy and reduction in thyroid-stimulating hormone (TSH) levels. Clinically, the natural history of a nontoxic goiter is growth, nodule production, and functional autonomy (resulting in thyrotoxicosis in a minority of patients).

The overall risk of malignancy is the same in a patient with a nodular goiter as with a solitary nodule.

See the images below.

Technetium-99m (99mTc) thyroid scan of a large, noTechnetium-99m (99mTc) thyroid scan of a large, nontoxic multinodular goiter. Multiple cold and hot nodules are observed in the enlarged thyroid gland. The white arrow indicates sternal notch marker. Areas of autonomy with excess thyroid hormone secrAreas of autonomy with excess thyroid hormone secretion in a large nodular goiter. This technetium-99m (99mTc) thyroid scan shows hot and cold nodules in a multinodular goiter. Although the patient's thyroid-stimulating hormone level had become progressively suppressed, it was within the reference range, at 0.4 mU/mL (reference range 0.35-5.5 mU/mL).
Previous
Next

Epidemiology

Frequency

United States

Iodine comes from ingestion of food. Iodine content of the soil determines the iodine content of plants and animals. Iodine is washed from the soil by water and is eventually washed out to the oceans. In general, areas with mountain ranges or heavy rainfall and flooding are iodine deficient. Iodine deficiency occurs in populations that depend on locally grown food and rely on vegetable protein rather than on animal or fish protein.

Studies have shown that iodine supplementation can eliminate cretinism and is highly effective in the prevention of endemic goiter. When urinary iodide falls below 25 micrograms per gram of creatinine, a palpable goiter occurs in 40-90% of the population, hypothyroidism occurs in 30-50% of the population, and cretinism occurs in 1-10% of the population. The seminal studies by David Marine, MD, in 1917 demonstrated the reduction in goiter among adolescent girls in Ohio from 20% to 5% by iodine supplementation.

Table salt has been supplemented in the United States since the 1920s for the prevention of cretinism and endemic goiter. The iodine intake in the United States, according to the National Health and Nutrition Examination Survey III (NHANES III), is adequate at 145 mcg/mg of creatinine. This adequate iodine intake in the United States eliminates the most common cause of endemic goiter in most populations.

Sporadic goiter is the most common cause of nontoxic goiter in the United States. The incidence of sporadic nontoxic goiter has been estimated in North America at approximately 5%. Sporadic goiter does not usually occur in people before puberty, and it does not have a peak incidence. Generally, the development of palpable thyroid nodules and goiter progressively increases with age. The prevalence of palpable nodules is approximately 5-6% in people aged 60 years, but on autopsy and ultrasonographic imaging findings, the incidence of small, nonpalpable nodules approaches 50% in people aged 60 years.

International

More than 2.2 billion people worldwide have some form of iodine deficiency disorder. Twenty-nine percent of the world's population lives in a region that has iodine deficiency (primarily in Asia, Latin American, central Africa, and regions of Europe). Of those at risk, 655 million were known to have goiter. In the iodine-deficient regions of the world, goiter is more common than in the United States. The prevalence of goiter can be estimated based on the iodine intake of the population.

As reported by the World Health Organization (WHO), the United Nations Children's Fund (UNICEF), and the International Council for the Control of Iodine Deficiency Disorders (ICCIDD), the absence of iodine deficiency (ie, median urine iodine >100 mg/dL) is associated with a goiter prevalence of less than 5%; mild iodine deficiency (ie, median urine iodine 50-99 mg/dL), with a goiter prevalence of 5-20%; moderate iodine deficiency (ie, median urine iodine 20-49 mg/dL), with a goiter prevalence of 20-30%; and severe iodine deficiency (ie, median urine iodine 20-49 mg/dL), with a goiter prevalence of greater than 30%.

Mortality/Morbidity

Endemic goiters arising from iodine deficiency are associated with sometimes immense thyroid hypertrophy, hypothyroidism, and cretinism. Sporadic goiters are generally asymptomatic and found either by a clinician's physical examination or by the patient's observation of neck enlargement. Occasionally, the goiter may produce symptoms caused by pressure on anterior neck structures, including the trachea (wheezing, cough, globus hystericus [anterior neck pressure]), the esophagus (dysphagia), and the recurrent laryngeal nerve (hoarseness).

Rarely, the obstruction can be dangerous because of narrowing of the trachea and the development of tracheitis with edema and tracheomalacia, leading to severe narrowing of the airway with serious obstruction resulting in a respiratory emergency. (Tracheal compression and the results of its surgical treatment are seen in the images below.)

Nontoxic goiter of the thyroid gland with trachealNontoxic goiter of the thyroid gland with tracheal compression. An axial, noncontrast computed tomography scan through the thyroid shows significant tracheal compression. Relief of tracheal compression after subtotal thyrRelief of tracheal compression after subtotal thyroidectomy of large, obstructive, nontoxic multinodular goiter. (A) Laryngoscopy demonstrating critical tracheal narrowing before thyroidectomy; (B) laryngoscopy showing widened patent trachea after thyroidectomy.

Race

No convincing epidemiologic studies suggest that race plays an important role in the development of nontoxic goiter. Generally, the lower socioeconomic conditions in nonindustrialized countries resulting in iodine deficiency have a more important role than race does in the development of a goiter.

Sex

Diffuse and nodular goiter is more common in women than in men. According to the best estimate, the incidence of goiter in women is 1.2-4.3 times as great as that in men.

Age

Sporadic goiter from dyshormonogenesis, a genetic error in proteins that are necessary for thyroid hormone synthesis, occurs during childhood. Endemic goiter due to iodine deficiency occurs during childhood, with the goiter's size increasing with age. Other causes of sporadic goiter rarely occur before puberty and do not have a peak age of occurrence. Thyroid nodules increase in incidence with age.

Previous
 
 
Contributor Information and Disclosures
Author

Stephanie L Lee, MD, PhD  Associate Professor, Department of Medicine, Boston University School of Medicine; Director of Thyroid Health Center, Associate Chief, Section of Endocrinology, Diabetes and Nutrition, Boston Medical Center; Fellow, Association of Clinical Endocrinology

Stephanie L Lee, MD, PhD is a member of the following medical societies: American College of Endocrinology, American Thyroid Association, and Endocrine Society

Disclosure: Nothing to disclose.

Coauthor(s)

Sonia Ananthakrishnan, MD  Assistant Professor of Medicine, Section of Endocrinology, Diabetes and Nutrition, Boston University School of Medicine, Boston Medical Center

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, Endocrine Society, and Gerontological Society of America

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, Endocrine Society, and International Society for Clinical Densitometry

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

Disclosure: Nothing to disclose.

References
  1. Bahn RS, Castro MR. Approach to the patient with nontoxic multinodular goiter. J Clin Endocrinol Metab. May 2011;96(5):1202-12. [Medline].

  2. Cooper DS, Doherty GM, Haugen BR, et al. Revised American Thyroid Association management guidelines for patients with thyroid nodules and differentiated thyroid cancer. Thyroid. Nov 2009;19(11):1167-214. [Medline].

  3. Baloch ZW, LiVolsi VA. Fine-needle aspiration of the thyroid: today and tomorrow. Best Pract Res Clin Endocrinol Metab. Dec 2008;22(6):929-39. [Medline].

  4. Agarwal G, Aggarwal V. Is total thyroidectomy the surgical procedure of choice for benign multinodular goiter? An evidence-based review. World J Surg. Jul 2008;32(7):1313-24. [Medline].

  5. Weetman AP. Radioiodine treatment for benign thyroid diseases. Clin Endocrinol (Oxf). Jun 2007;66(6):757-64. [Medline].

  6. Baczyk M, Pisarek M, Czepczynski R, Ziemnicka K, Gryczynska M, Pietz L, et al. Therapy of large multinodular goitre using repeated doses of radioiodine. Nucl Med Commun. Mar 2009;30(3):226-31. [Medline].

  7. Bonnema SJ, Hegedus L. A 30-year perspective on radioiodine therapy of benign nontoxic multinodular goiter. Curr Opin Endocrinol Diabetes Obes. Oct 2009;16(5):379-84. [Medline].

  8. Duntas LH, Cooper DS. Review on the occasion of a decade of recombinant human TSH: prospects and novel uses. Thyroid. May 2008;18(5):509-16. [Medline].

  9. Medeiros-Neto G, Marui S, Knobel M. An outline concerning the potential use of recombinant human thyrotropin for improving radioiodine therapy of multinodular goiter. Endocrine. Apr 2008;33(2):109-17. [Medline].

  10. Braverman L, Kloos RT, Law B Jr, Kipnes M, Dionne M, Magner J. Evaluation of various doses of recombinant human thyrotropin in patients with multinodular goiters. Endocr Pract. Oct 2008;14(7):832-9. [Medline].

  11. Fast S, Nielsen VE, Grupe P, et al. Optimizing 131I uptake after rhTSH stimulation in patients with nontoxic multinodular goiter: evidence from a prospective, randomized, double-blind study. J Nucl Med. May 2009;50(5):732-7. [Medline].

  12. Bahn Chair RS, Burch HB, Cooper DS, et al. Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists. Thyroid. Jun 2011;21(6):593-646. [Medline].

  13. Yetkin G, Uludag M, Onceken O, et al. Does unilateral lobectomy suffice to manage unilateral nontoxic goiter?. Endocr Pract. Jan-Feb 2010;16(1):36-41. [Medline].

  14. Phitayakorn R, McHenry CR. Follow-up after surgery for benign nodular thyroid disease: evidence-based approach. World J Surg. Jul 2008;32(7):1374-84. [Medline].

  15. Barczynski M, Konturek A, Hubalewska-Dydejczyk A, et al. Five-year Follow-up of a Randomized Clinical Trial of Total Thyroidectomy versus Dunhill Operation versus Bilateral Subtotal Thyroidectomy for Multinodular Nontoxic Goiter. World J Surg. Feb 20 2010;[Medline].

  16. [Best Evidence] Worni M, Schudel HH, Seifert E, et al. Randomized controlled trial on single dose steroid before thyroidectomy for benign disease to improve postoperative nausea, pain, and vocal function. Ann Surg. Dec 2008;248(6):1060-6. [Medline].

  17. Erbil Y, Barbaros U, Temel B, et al. The impact of age, vitamin D(3) level, and incidental parathyroidectomy on postoperative hypocalcemia after total or near total thyroidectomy. Am J Surg. Apr 2009;197(4):439-46. [Medline].

  18. Berghout A, Wiersinga WM, Drexhage HA, et al. Comparison of placebo with L-thyroxine alone or with carbimazole for treatment of sporadic non-toxic goitre. Lancet. Jul 28 1990;336(8709):193-7.

  19. Bonnema SJ, Bertelsen H, Mortensen J, et al. The feasibility of high dose iodine 131 treatment as an alternative to surgery in patients with a very large goiter: effect on thyroid function and size and pulmonary function. J Clin Endocrinol Metab. Oct 1999;84(10):3636-41. [Medline]. [Full Text].

  20. Braverman LE, Utiger RD, Hermus AR, Huysmans DA:. Clinical manifestations and treatment of nontoxic diffuse and nodular goiter. In: Werner & Ingbar's The Thyroid. Baltimore, Md: Lippincott Williams & Wilkins;. 2000;866-871.

  21. Hegedus L, Gerber H. Multinodular goiter. In: DeGroot LJ, Jameson JL, eds. Endocrinology. 2001;2:1517-1528.

  22. Hermus AR, Huysmans DA. Treatment of benign nodular thyroid disease. N Engl J Med. May 14 1998;338(20):1438-47. [Medline].

  23. Hollowell JG, Staehling NW, Hannon WH, et al. Iodine nutrition in the United States. Trends and public health implications: iodine excretion data from National Health and Nutrition Examination Surveys I and III (1971-1974 and 1988-1994). J Clin Endocrinol Metab. Oct 1998;83(10):3401-8. [Medline]. [Full Text].

  24. Huysmans D, Hermus A, Edelbroek M, et al. Radioiodine for nontoxic multinodular goiter. Thyroid. Apr 1997;7(2):235-9. [Medline].

  25. Huysmans DA, Hermus AR, Corstens FH, et al. Large, compressive goiters treated with radioiodine. Ann Intern Med. Nov 15 1994;121(10):757-62. [Medline].

  26. Huysmans DA, Nieuwlaat WA, Erdtsieck RJ, et al. Administration of a single low dose of recombinant human thyrotropin significantly enhances thyroid radioiodide uptake in nontoxic nodular goiter. J Clin Endocrinol Metab. Oct 2000;85(10):3592-6. [Medline]. [Full Text].

  27. Netterville JL, Coleman SC, Smith JC, et al. Management of substernal goiter. Laryngoscope. Nov 1998;108(11 Pt 1):1611-7. [Medline].

  28. Perrild H, Hansen JM, Hegedus L. Triiodothyronine and thyroxine treatment of diffuse non-toxic goitre evaluated by ultrasonic scanning. Acta Endocrinol (Copenh). Jul 1982;100(3):382-7. [Medline].

  29. Rios A, Rodriguez JM, Canteras M, et al. Surgical management of multinodular goiter with compression symptoms. Arch Surg. Jan 2005;140(1):49-53. [Medline]. [Full Text].

  30. Ross DS. Thyroid hormone suppressive therapy of sporadic nontoxic goiter. Thyroid. Fall 1992;2(3):263-9. [Medline].

Previous
Next
 
Intrathoracic goiter causing obstruction. This patient has a visible goiter on physical examination. In addition, he has distension of his left external jugular vein, facial erythema (when compared with his shoulder), and cutaneous varicosities of venous blood draining from his head into his chest because of jugular obstruction from his goiter.
Technetium-99m (99mTc) thyroid scan of a large, nontoxic multinodular goiter. Multiple cold and hot nodules are observed in the enlarged thyroid gland. The white arrow indicates sternal notch marker.
Areas of autonomy with excess thyroid hormone secretion in a large nodular goiter. This technetium-99m (99mTc) thyroid scan shows hot and cold nodules in a multinodular goiter. Although the patient's thyroid-stimulating hormone level had become progressively suppressed, it was within the reference range, at 0.4 mU/mL (reference range 0.35-5.5 mU/mL).
Nontoxic goiter of the thyroid gland with tracheal compression. An axial, noncontrast computed tomography scan through the thyroid shows significant tracheal compression.
Relief of tracheal compression after subtotal thyroidectomy of large, obstructive, nontoxic multinodular goiter. (A) Laryngoscopy demonstrating critical tracheal narrowing before thyroidectomy; (B) laryngoscopy showing widened patent trachea after thyroidectomy.
Multinodular goiter. On visual inspection of the neck (image on left), this patient appears to have a goiter. The computed tomography scan (image on right) shows the asymmetrical goiter, measuring 9.3 x 7.4 cm, with tracheal deviation, although no tracheal obstruction is present.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.