Iodine Deficiency Treatment & Management

  • Author: Stephanie L Lee, MD, PhD; Chief Editor: George T Griffing, MD  more...
 
Updated: Dec 16, 2015
 

Approach Considerations

Treatment of iodine deficiency

Correction of an individual's iodine deficiency should be instituted at a level recommended by the US Institute of Medicine (IOM) and the World Health Organization (WHO). In a nonpregnant adult, 150 mcg/day is sufficient for normal thyroid function.

Consultation with an endocrinologist should be considered when the etiology of thyroid abnormalities is unclear. Thyroidectomy may be indicated for patients with compressive symptoms of a large goiter.

Prevention

At a population level, iodine deficiency disorder (IDD) can be prevented by the iodization of food products or the water supply. In practice, this is usually achieved by iodization of salt. An alternative in some developing countries has been the periodic injection of iodized oil supplements.[13, 16]

Iodine treatment-related hyperthyroidism

The primary complication of iodine therapy for IDD is the development of hyperthyroidism. This may occur, especially in patients older than 45 years, because of the hyperfunctioning areas of autonomy that tend to develop in patients with long-standing iodine-deficient goiters.[21]

A Danish study investigating the incidence of hyperthyroidism associated with Denmark's iodine fortification program found that, based on the incident use of antithyroid medication in various parts of the country, the incidence of hyperthyroidism was greater among persons who had suffered from moderate iodine deficiency than it was among those who had had only a mild deficiency.[22] In the moderately deficient population, the incident use of antithyroid medication increased the most in persons younger than 40 years or older than 75 years. Four years after iodine fortification began, the incidence of hyperthyroidism apparently began to decline, returning to prefortification rates in most population groups by the end of 6 years.

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Sources of Iodine Replacement

Iodine replacement should be based on the recommendations of IOM and WHO. In an adult, 150 mcg/day is sufficient for normal thyroid function. Replacement of iodine is most easily achieved by requesting that the patient use iodized salt in his or her cooking and at the table or an iodine-containing daily multiple vitamin. Other dietary sources of iodine include milk, egg yolks, and saltwater fish. Not all daily or prenatal multiple vitamins contain iodine, but those that do, typically contain 150 mcg of iodine per tablet.

While a person who follows a vegan diet still might consume iodized salt, only 70% of salt sold from US supermarket shelves currently is iodized. Other major sources of US dietary iodine are saltwater fish, milk and milk products, and eggs. These food items are not included in a true vegan diet.[23]

The Institute of Medicine (IOM) recommended dietary allowance (RDA) is 220 mcg/d of iodine for pregnant women. Not all daily or prenatal multiple vitamins contain iodine, but those that do typically contain 150 mcg of iodine per tablet. The IOM recommends 290 mcg/d for lactating women and 90-120 mcg/d for children aged 1-11 years. The adequate intake for infants is 110-130 mcg/d.

In developing countries, eradication of iodine deficiency has been accomplished by adding iodine drops to well water or by injecting people with iodized oil.

Using highly concentrated pharmaceutical agents such as a saturated solution of potassium iodide (SSKI), which has a concentration of 35,000-50,000 mcg/drop, is impractical and potentially dangerous.

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Treatment of Nontoxic Goiters Caused by Iodine Deficiency

Long-term dietary iodine replacement at levels recommended by IOM and WHO may decrease the size of iodine-deficient goiters in very young children and pregnant women and is indicated for all patients with iodine deficiency.[5] Generally, long-standing goiters associated with iodine deficiency disorder respond with only small amounts of shrinkage after iodine supplementation, and patients are at risk for developing hyperthyroidism. Patients do not routinely require specific therapy unless the goiter is large enough to cause compressive symptoms (eg, tracheal obstruction, thoracic inlet occlusion, hoarseness).

Levothyroxine

Exogenous levothyroxine (L-T4) can also be used to decrease goiter size but generally is not effective in adults and older children. Supplemental L-T4, when added to the T3 and T4 secretion by the autonomous nodules in the endemic goiter, may cause thyrotoxicosis. Long-term L-T4 therapy that results in the suppression of the TSH level to below-normal levels may have deleterious effects on cardiac and bone health; therefore, L-T4 therapy is no longer routinely administered to patients with goiter.

Radioactive iodine

Radioactive iodine (iodine-131 [131 I]) has been used, primarily in Europe, to decrease thyroid volume in patients with euthyroid goiters (40-60% volume reduction). In the United States,131 I is the most common treatment for toxic multinodular goiters associated with hyperthyroidism. Risks associated with131 I therapy include permanent hypothyroidism.

Surgery

The standard of care for large goiter associated with obstructive symptoms such as dough, stridor, and dysphagia is thyroidectomy. If the goiter extends into the anterior mediastinum, surgery is the recommend treatment even without obstructive symptoms. After the surgery, the patient need levothyroxine replacement therapy.

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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, 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, Endocrine Society

Disclosure: Nothing to disclose.

Coauthor(s)

Elizabeth N Pearce, MD, MSc Associate Professor of Medicine, Boston Medical Center, Boston University School of Medicine

Elizabeth N Pearce, MD, MSc is a member of the following medical societies: American Association of Clinical Endocrinologists, American Thyroid Association, Endocrine Society, Massachusetts Medical Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: consulted for Scientific Consulting Company GmbH; advisory board for Endocrine Advisor Website; Member of the Management Council of the Iodine Global Network.

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

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD Professor Emeritus 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, International Society for Clinical Densitometry, Southern Society for Clinical Investigation, American College of Medical Practice Executives, American Association for Physician Leadership, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society

Disclosure: Nothing to disclose.

Acknowledgements

Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS Professor of Medicine (Endocrinology, Adj), Johns Hopkins School of Medicine; Affiliate Research Professor, Bioinformatics and Computational Biology Program, School of Computational Sciences, George Mason University; Principal, C/A Informatics, LLC

Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Nutrition, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Informatics Association, American Society for Bone and Mineral Research, Endocrine Society, and International Society for Clinical Densitometry

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

References
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  13. Zimmermann MB, Aeberli I, Torresani T, et al. Increasing the iodine concentration in the Swiss iodized salt program markedly improved iodine status in pregnant women and children: a 5-y prospective national study. Am J Clin Nutr. 2005 Aug. 82(2):388-92. [Medline]. [Full Text].

  14. Bath SC, Steer CD, Golding J, Emmett P, Rayman MP. Effect of inadequate iodine status in UK pregnant women on cognitive outcomes in their children: results from the Avon Longitudinal Study of Parents and Children (ALSPAC). Lancet. 2013 Jul 27. 382(9889):331-7. [Medline].

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  20. Krejbjerg A, Pedersen IB, Laurberg P. Can Elastography Predict Growth of Incidental Thyroid Nodules? A Pilot Two-Year Follow-Up Study. Ultrason Imaging. 2015 Sep 7. [Medline].

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  24. Zimmermann MB, Boelaert K. Iodine deficiency and thyroid disorders. Lancet Diabetes Endocrinol. 2015 Apr. 3 (4):286-95. [Medline].

 
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Distribution of iodine deficiency in developing countries.
Typical endemic goiters in 3 women from the Himalayas, an area of severe iodine deficiency. Image courtesy of F. DeLange.
A man and 3 females (age range, 17-20 y) with myxedematous cretinism from the Republic of the Congo in Africa, a region with severe iodine deficiency. Image courtesy of F. DeLange.
Histologic sections from a normal thyroid and from an endemic goiter that was removed because of compressive symptoms. The normal thyroid (A) contains thyroid cells arranged in a monolayered sheet around a storage form of thyroid hormone, colloid, while the endemic goiter (B) shows intense hyperplasia with no colloid. Image courtesy of F. DeLange.
Table.
Iodine Deficiency None Mild Moderate Severe
Median urine iodine, mcg/L >100 50-99 20-49 < 20
Goiter prevalence < 5% 5-20% 20-30% >30%
Neonatal thyroid-stimulating hormone (TSH),



>5 IU/mL whole blood



< 3% 3-20% 20-40% >40%
Cretinism 0 0 + +
Adapted from the World Health Organization (WHO)/United Nations Children's Fund (UNICEF)/International Council for Control of Iodine Deficiency Disorders (ICCIDD).
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