Iodine Deficiency Medication

  • Author: Stephanie L Lee, MD, PhD; Chief Editor: George T Griffing, MD   more...
 
Updated: Jan 27, 2012
 

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Medications used in iodine deficiency include antithyroid agents (potassium iodide) and thyroid products (levothyroxine).

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Antithyroid Agents

Class Summary

Iodine deficiency has been treated at a population level by several methods, including voluntary use of iodized salt, iodine supplementation in bread and water, and oral/intramuscular administration of iodized oil. The simplest and least expensive treatment is to have the patient purchase and use iodized salt.

Potassium iodide (SSKI)

 

Potassium iodide is an option in industrialized counties. Absorption from the gastrointestinal tract is rapid and complete. The skin and lungs also can absorb iodine. Iodine equilibrates in extracellular fluids and is specifically concentrated by the thyroid gland.

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Thyroid Products

Class Summary

Thyroid hormone, L-thyroxine, may be used to treat iodine deficiency, because the chemical content of iodine is approximately 60% by weight.

Levothyroxine (Synthroid, Levothroid, Levoxyl)

 

Levothyroxine (L-T4) is generally effective in treating iodine deficiency. It is a considerably more expensive preparation than other forms of iodine (eg, iodized salt), especially when its cost is combined with the added expense of measuring TSH levels to assure that the supplemental L-T4 has not resulted in iatrogenic hyperthyroidism.

Alternatively, thyroid hormone therapy has been used with caution to shrink the goiter of iodine deficiency. An L-T4 dose is chosen that maintains the TSH in the lower part of the reference range. TSH levels should be monitored carefully to avoid thyrotoxicosis due to autonomous nodules in the iodine deficiency goiter.

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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, 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 Medical Center, Boston University School of Medicine

Disclosure: Nothing to disclose.

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, and Massachusetts Medical Society

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.

Additional Contributors

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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  4. WHO Secretariat, Andersson M, de Benoist B, Delange F, Zupan J. Prevention and control of iodine deficiency in pregnant and lactating women and in children less than 2-years-old: conclusions and recommendations of the Technical Consultation. Public Health Nutr. Dec 2007;10(12A):1606-11. [Medline].

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  14. Zimmermann MB, Wegmuller R, Zeder C, et al. Rapid relapse of thyroid dysfunction and goiter in school-age children after discontinuation of salt iodization. Am J Clin Nutr. Apr 2004;79(4):642-5. [Medline]. [Full Text].

  15. Santiago-Fernandez P, Torres-Barahona R, Muela-Martínez JA, et al. Intelligence quotient and iodine intake: a cross-sectional study in children. J Clin Endocrinol Metab. Aug 2004;89(8):3851-7. [Medline]. [Full Text].

  16. Zimmermann MB, Moretti D, Chaouki N, et al. Development of a dried whole-blood spot thyroglobulin assay and its evaluation as an indicator of thyroid status in goitrous children receiving iodized salt. Am J Clin Nutr. Jun 2003;77(6):1453-8. [Medline]. [Full Text].

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  18. Cerqueira C, Knudsen N, Ovesen L, et al. Association of iodine fortification with incident use of anti-thyroid medication - A Danish nationwide study. J Clin Endocrinol Metab. Apr 14 2009;[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 1
Iodine DeficiencyNoneMildModerateSevere
Median urine iodine, mcg/L>10050-9920-49< 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%
Cretinism00++
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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