Iodine Deficiency Clinical Presentation

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

History and Physical Examination

Patients with iodine deficiency tend to come from geographic regions where iodine deficiency disorders (IDDs) are endemic. The first sign of iodine deficiency is diffuse thyroid enlargement, which becomes multinodular over time. In patients with hypothyroidism due to severe iodine deficiency, one might see signs such as dry skin, periorbital edema, and delayed relaxation phase of the deep tendon reflexes.

Goiter

Patients with IDD most commonly present with goiter. Typical endemic goiters are shown in the image below. Children present with diffuse goiters, while adults present with nodular goiters. If a goiter is large enough, patients may complain of compressive symptoms, such as hoarseness, shortness of breath, cough, or dysphagia.

Typical endemic goiters in 3 women from the HimalaTypical endemic goiters in 3 women from the Himalayas, an area of severe iodine deficiency. Image courtesy of F. DeLange.

Hypothyroidism

Individuals with severe iodine deficiency may also have hypothyroidism and may complain of fatigue, weight gain, cold intolerance, dry skin, constipation, or depression.

Cretinism

Cretinism is the most extreme manifestation of IDD. Cretinism can be divided into neurologic and myxedematous subtypes. These subtypes have considerable clinical overlap. Both conditions can be prevented by adequate maternal and childhood iodine intake.

Neurologic cretinism is thought to be caused by severe IDD with hypothyroidism in the mother during pregnancy and is characterized by mental retardation, abnormal gait, and deaf-mutism, but not by goiter or hypothyroidism in the child.

Myxedematous cretinism is considered to result from iodine deficiency and hypothyroidism in the fetus during late pregnancy or in the neonatal period, resulting in mental retardation, short stature, goiter, and hypothyroidism. (See the image below.)

A man and 3 females (age range, 17-20 y) with myxeA 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.

Mental retardation

Worldwide, iodine deficiency is the leading cause of preventable mental retardation. This became a renewed concern as the prevalence of moderate iodine deficiency in the United States among women of childbearing age increased from 4% in the 1970s to 15% by the 1990s. Although children of mothers from iodine-deficient regions may have normal thyroid function test results, they are noted to have lower language and memory performance.

Reduction in IQ has been noted in affected youth from regions of severe and mild iodine deficiency. Mental retardation as a result of iodine deficiency can be exaggerated in the setting of concomitant deficiencies of selenium or vitamin A.[15]

Postnatally, as infants and children are particularly sensitive to fluctuations in iodine intake, this population is at risk for poor mental and psychomotor development (predominantly in language and memory skills). Unlike mental retardation that occurs because of prenatal iodine deficiency, mental retardation from continued postnatal iodine deprivation may be reversible with thyroid hormone replacement.

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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].

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

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  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].

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  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].

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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].

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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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