Iodine Deficiency Workup

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

Approach Considerations

There has been particular interest in monitoring iodine sufficiency in pregnant women and school-aged children. These populations are important, because they are easily accessible and are particularly vulnerable to the adverse effects caused by iodine deficiency.

Surveillance techniques to monitor iodine sufficiency in a population include assessment of thyroid volume, urinary iodine concentration, dried whole-blood spot thyroglobulin (Tg) levels, and dietary questionnaires; the last method is the least reliable. No test that can reliably diagnose iodine deficiency in individual patients is available.

Results from thyroid function studies are usually within the reference range in the presence of mild iodine insufficiency. However, in patients with euthyroidism and iodine deficiency, serum TSH levels may be normal to increased, T3 levels may be normal or slightly elevated, and T4 levels may be normal or decreased. Only in very extreme iodine deficiency does hypothyroidism develop, accompanied by an elevated serum TSH value and decreased T3 and T4 levels.

Population studies have shown that newborns with iodine deficiency disorder (IDD) have elevated TSH levels at birth that normalize when evaluated again several weeks later. The extent of their transient hypothyroidism correlates with the severity of the iodine deficiency.

Measurement of a dried whole-blood spot level of Tg can be a useful indicator of the thyroid function in children and may be a more sensitive early measure of iodine repletion than serum TSH or thyroxine (T4).[16] Current limitations to the use of dried blood spot Tg measurements include assay complexity and the unknown utility of measuring antithyroglobulin antibody levels in children.

Imaging studies

The 24-hour radioactive iodine uptake value is increased substantially in the presence of iodine deficiency disorder because of increased TSH stimulation and reduction in the nonisotopic iodine pool. Therefore, thyroid uptake values in iodine-sufficient areas, such as the United States, are significantly lower than in areas with iodine deficiency, as in many regions of Europe.

Thyroid size estimated on ultrasonograms has been shown to reflect the iodine sufficiency of a population. When goiter appears in more than 5% of a regional population, iodine deficiency should be considered.

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Urinary Iodine Evaluation

The kidneys excrete approximately 90% of ingested iodine. Therefore, the best diagnostic test to identify IDD in a population is a median 24-hour urine iodine collection. If a 24-hour urine collection is not practical, a random urinary iodine-to-creatinine ratio can be used instead. In this case, a median of 50-100 mcg of iodine per liter is consistent with mild iodine deficiency, 20-49 mcg of iodine per liter is consistent with moderate deficiency, and less than 20 mcg of iodine per liter is consistent with severe deficiency.

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Histologic Findings

In young patients with iodine deficiency, the usual finding is diffuse hyperplasia of the thyroid gland. Histologically, extreme hyperplasia can be seen with little or no colloid, as shown in the image below.

Histologic sections from a normal thyroid and fromHistologic 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.

With aging, the diffuse goiter of iodine deficiency becomes more nodular. Histologically, the nodular goiter develops from areas of hyperplasia separated by areas of degeneration and fibrosis. In older patients, the thyroid gland tends to be extremely heterogeneous, with colloid-containing vesicles, hyperplastic areas, degenerating areas, and fibrosis.

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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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  2. de Benoist B, McLean E, Andersson M, Rogers L. Iodine deficiency in 2007: global progress since 2003. Food Nutr Bull. Sep 2008;29(3):195-202. [Medline].

  3. Zimmermann MB. Iodine deficiency in pregnancy and the effects of maternal iodine supplementation on the offspring: a review. Am J Clin Nutr. Feb 2009;89(2):668S-72S. [Medline].

  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].

  5. Delange F. Optimal iodine nutrition during pregnancy, lactation and neonatal period. Int J Endocrinol Metab. 2004;89:3851.

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  7. Pearce EN, Pino S, He X, Bazrafshan HR, Lee SL, Braverman LE. Sources of dietary iodine: bread, cows' milk, and infant formula in the Boston area. J Clin Endocrinol Metab. Jul 2004;89(7):3421-4. [Medline].

  8. 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].

  9. Caldwell KL, Jones R, Hollowell JG. Urinary iodine concentration: United States National Health And Nutrition Examination Survey 2001-2002. Thyroid. Jul 2005;15(7):692-9. [Medline].

  10. Caldwell KL, Miller GA, Wang RY, Jain RB, Jones RL. Iodine status of the U.S. population, National Health and Nutrition Examination Survey 2003-2004. Thyroid. Nov 2008;18(11):1207-14. [Medline].

  11. Caldwell KL, Makhmudov A, Ely E, Jones RL, Wang RY. Iodine Status of the U.S. Population, National Health and Nutrition Examination Survey, 2005-2006 and 2007-2008. Thyroid. Feb 16 2011;[Medline].

  12. 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. Aug 2005;82(2):388-92. [Medline]. [Full Text].

  13. Williams GR. Neurodevelopmental and neurophysiological actions of thyroid hormone. J Neuroendocrinol. Jun 2008;20(6):784-94. [Medline].

  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].

  17. Zimmermann MB. Iodine requirements and the risks and benefits of correcting iodine deficiency in populations. J Trace Elem Med Biol. 2008;22(2):81-92. [Medline].

  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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