eMedicine Specialties > Pediatrics: General Medicine > Endocrinology

Congenital Hypothyroidism

Author: Daniel C Postellon, MD, Clinical Associate Professor, College of Human Medicine, Pediatrics and Human Development, Michigan State University; Consulting Staff, Pediatric Endocrine Clinic, DeVos Children's Hospital
Coauthor(s): Michael J Bourgeois, MD, Director of Pediatric Undergraduate Medical Education, Associate Professor, Department of Pediatrics, Division of Pediatric Endocrinology and Metabolism, Texas Tech University School of Medicine; Surendra Varma, MD, Vice-Chairman and Program Director, University Distinguished Professor, Department of Pediatrics, Texas Tech University School of Medicine
Contributor Information and Disclosures

Updated: May 28, 2008

Introduction

Background

Congenital hypothyroidism is inadequate thyroid hormone production in newborn infants. This can occur because of an anatomic defect in the gland, an inborn error of thyroid metabolism, or iodine deficiency.

The term endemic cretinism is used to describe clusters of infants with goiter and cretinism in defined geographic areas. These areas were discovered to be low in iodine, and the cause of endemic cretinism was determined to be iodine deficiency. In the 1930s, adequate dietary intake of iodine was found to prevent this goiter and cretinism. Thus, the wholesale iodization of salt was established. Despite its efforts, the World Health Organization (WHO) has not been able to completely eliminate iodine deficiency throughout the world. As a result, endemic goiter and cretinism are still observed in some areas, such as regions of Bangladesh, Chad, China, Indonesia, Nepal, Peru, and Zaire.

The term sporadic cretinism was initially used to describe the random occurrence of cretinism in nonendemic areas. The cause of these abnormalities was identified as nonfunctioning or absent thyroid glands. This led to replacement of the descriptive term sporadic cretinism with the etiologic term congenital hypothyroidism. Treatment with animal thyroid extract was found to elicit some improvement in these infants, although many remained impaired.

The morbidity from congenital hypothyroidism can be reduced to a minimum by early diagnosis and treatment, which was made feasible by the development of radioimmunoassay for thyroid-stimulating hormone (TSH) and thyroxine (T4) from blood spots on filter paper, obtained for neonatal screening tests.

Pathophysiology

The thyroid gland develops from the buccopharyngeal cavity between 4 and 10 weeks' gestation. The thyroid arises from the fourth brachial pouches and ultimately ends up as a bilobed organ in the neck. Errors in the formation or migration of thyroid tissue can result in thyroid aplasia, dysplasia, or ectopy. By 10-11 weeks' gestation, the fetal thyroid is capable of producing thyroid hormone. By 18-20 weeks' gestation, blood levels of T4 have reached term levels. The fetal pituitary-thyroid axis is believed to function independently of the maternal pituitary-thyroid axis.

The thyroid gland uses tyrosine and iodine to manufacture T4 and triiodothyronine (T3). Iodide is taken into the thyroid follicular cells by an active transport system and then oxidized to iodine by thyroid peroxidase. Organification occurs when iodine is attached to tyrosine molecules attached to thyroglobulin, forming monoiodotyrosine (MIT) and diiodotyrosine (DIT). The coupling of 2 molecules of DIT forms tetraiodothyronine (ie, T4). The coupling of one molecule of MIT and one molecule of DIT forms T3. Thyroglobulin, with T4 and T3 attached, is stored in the follicular lumen. TSH activates the enzymes needed to cleave T4 and T3 from thyroglobulin. In most situations, T4 is the primary hormone produced by and released from the thyroid gland.

Inborn errors of thyroid metabolism can result in congenital hypothyroidism in children with anatomically normal thyroid glands. 

T4 is the primary thyronine produced by the thyroid gland. Only 10-40% of circulating T3 is released from the thyroid gland. The remainder is produced by monodeiodination of T4 in peripheral tissues. T3 is the primary mediator of the biologic effects of thyroid hormone and does so by interacting with a specific nuclear receptor. Receptor abnormalities can result in thyroid hormone resistance.

The major carrier proteins for circulating thyroid hormones are thyroid-binding globulin (TBG), thyroid-binding prealbumin (TBPA), and albumin. Unbound, or free, T4 accounts for only about 0.03% of circulating T4 and is the portion that is metabolically active. Infants born with low levels of TBG, as in congenital TBG deficiency, have low total T4 levels but are physiologically normal. Familial congenital TBG deficiency can occur as an X-linked recessive or autosomal recessive condition.

The contributions of maternal thyroid hormone levels to the fetus are thought to be minimal, but maternal thyroid disease can have a substantial influence on fetal and neonatal thyroid function. Immunoglobulin G (IgG) autoantibodies, as observed in autoimmune thyroiditis, can cross the placenta and inhibit thyroid function. Thioamides used to treat maternal hyperthyroidism can also block fetal thyroid hormone synthesis. Most of these effects are transient. Radioactive iodine administered to a pregnant woman can ablate the fetus's thyroid gland permanently.

The importance of thyroid hormone to brain growth and development is demonstrated by comparing treated and untreated children with congenital hypothyroidism. Thyroid hormone is necessary for normal brain growth and myelination and for normal neuronal connections. The most critical period for the effect of thyroid hormone on brain development is the first few months of life.

Frequency

United States

The incidence of congenital hypothyroidism, as detected through newborn screening, is approximately 1 per 4000 births.1

International

In areas of iodine deficiency, the prevalence of goiter is reported to range from 5-15% of the population, with a lower incidence of hypothyroidism.

Data from most countries with well-established newborn screening programs indicate an incidence of congenital hypothyroidism of about 1 per 3000-4000.2,3  Some of the highest incidences (1 in 1400 to 1 in 2000) have been reported from various locations in the Middle East.4

Although percentages of specific etiologies vary from country to country, ranges are as follows:

  • Ectopic thyroid - 25-50%
  • Thyroid agenesis - 20-50%
  • Dyshormonogenesis - 4-15%
  • Hypothalamic-pituitary dysfunction - 10-15%

Mortality/Morbidity

Profound mental retardation is the most serious effect of untreated congenital hypothyroidism. Severe impairment of linear growth and bone maturation also occurs. Affected infants whose treatment is delayed can have neurologic problems such as spasticity and gait abnormalities, dysarthria or mutism, and autistic behavior.

Two clinical forms of endemic cretinism are described, with considerable overlap between them. The neurologic form is characterized by mental retardation, spasticity, ataxia, and defects in speech and hearing to the point of deaf-mutism. Thyroid function and stature are usually normal. Iodine deficiency in early fetal life is thought to be the cause. In the myxedematous form, marked growth delay, myxedema (a doughy edema of the skin and subcutaneous tissue from proteinaceous fluid), and mental retardation without other neurologic features are present. Considerable geographic variation among the predominant forms and findings is noted.

Race

Congenital hypothyroidism is observed in all populations. The racial differences observed in endemic cretinism are probably related more to geographic location and socioeconomic status than to any particular racial predilection. Some researchers have observed variability in symptoms and signs when comparing groups from one part of the world to another. The explanation for these differences is unclear.

  • The prevalence at birth is increased in Hispanics, particularly in Hispanic females, who have a birth prevalence of 1 in 1886 births.5
  • Black infants have about one third the prevalence rate of white infants.
  • Twin births are approximately 12 times as likely to have congenital hypothyroidism as singletons.

Sex

Most studies of congenital hypothyroidism suggest a female-to-male ratio of a 2:1. In 1999, Devos et al showed that much of the discrepancy is accounted for by infants with thyroid ectopy.6 The sex ratio for Hispanics is more striking, with a 3:1 female-to-male ratio. The ratio is lower among black infants.

Age

By definition, congenital hypothyroidism is present at, or before, birth. Children who develop primary hypothyroidism when aged 2 years or older have poor growth and slow mentation but generally do not exhibit the profound and incompletely reversible neurologic abnormalities observed in untreated congenital hypothyroidism.

Clinical

History

  • In regions of iodide deficiency and a known prevalence of endemic cretinism, the diagnosis may be straightforward.
  • Infants with congenital hypothyroidism are usually born at term or after term.
  • Symptoms and signs include the following:
    • Decreased activity
    • Large anterior fontanelle
    • Poor feeding and weight gain
    • Small stature or poor growth
    • Jaundice
    • Decreased stooling or constipation
    • Hypotonia
    • Hoarse cry
  • Often, they are described as "good babies" because they rarely cry and sleep most of the time.
  • Family history should be carefully reviewed for information about similarly affected infants or family members with unexplained mental retardation.
  • Maternal history of a thyroid disorder and mode of treatment, whether before or during pregnancy, can occasionally provide the etiology of the infant's problem.
  • Congenital hypothyroidism is more common in infants with birthweights less than 2,000 g or more than 4,500 g.

Physical

  • The physical findings of hypothyroidism may or may not be present at birth.
  • Signs include the following:
    • Coarse facial features
    • Macroglossia
    • Large fontanelles
    • Umbilical hernia
    • Mottled, cool, and dry skin
    • Developmental delay
    • Pallor
    • Myxedema
    • Goiter
  • A small but significant number (3-7%) of infants with congenital hypothyroidism have other birth defects, mainly atrial and ventricular septal defects.
  • Newborn screening involves the following:
    • Infants with congenital hypothyroidism are usually identified within the first 2-3 weeks of life.
    • These infants should be carefully examined for signs of hypothyroidism, and the diagnosis should be confirmed by repeat testing.
    • Infants with obvious findings of hypothyroidism (eg, macroglossia, enlarged fontanelle, hypotonia) at the time of diagnosis have intelligence quotients (IQs) 10-20 points lower than infants without such findings.
  • Anemia may occur, due to decreased oxygen carrying requirement.

Causes

Endemic cretinism is caused by iodine deficiency and is occasionally exacerbated by naturally occurring goitrogens.7 Congenital hypothyroidism can be caused by any of the following:

  • Dysgenesis of the thyroid gland
    • Agenesis (ie, complete absence of thyroid gland)
    • Ectopy (lingual or sublingual thyroid gland)
  • Inborn errors of thyroid hormone metabolism - Dyshormonogenesis (most cases are familial and inherited as autosomal recessive conditions)
    • TSH unresponsiveness (ie, TSH receptor abnormalities)
    • Impaired ability to uptake iodide
    • Peroxidase, or organification, defect (ie, inability to convert iodide to iodine) 
    • Pendred syndrome, a familial organification defect associated with congenital deafness
    • Thyroglobulin defect (ie, inability to form or degrade thyroglobulin)
    • Deiodinase defect
  • Thyroid hormone resistance (ie, thyroid hormone receptor abnormalities)
  • Maternal autoimmune disease (transient or permanent)
  • Iatrogenic causes - Maternal use of thioamides, iodine excess, radioactive iodine therapy
  • TSH or thyrotropin-releasing hormone (TRH) deficiencies
    • Hypothyroidism can also occur in TSH or TRH deficiencies, either as an isolated problem or in conjunction with other pituitary deficiencies (eg, hypopituitarism).
    • If present with these deficiencies, hypothyroidism is usually milder and is not associated with the significant neurologic morbidity observed in primary hypothyroidism. 

More on Congenital Hypothyroidism

Overview: Congenital Hypothyroidism
Differential Diagnoses & Workup: Congenital Hypothyroidism
Treatment & Medication: Congenital Hypothyroidism
Follow-up: Congenital Hypothyroidism
Multimedia: Congenital Hypothyroidism
References
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Further Reading

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Keywords

congenital hypothyroidism, thyroid dysfunction, congenital myxedema, endemic cretinism, hypothyroidism, sporadic cretinism, thyroid, inadequate thyroid hormone production, inborn error of thyroid metabolism, iodine deficiency, goiter, thyroid aplasia, thyroid dysplasia, thyroid ectopy, ectopic thyroid, hyperthyroidism, dyshormonogenesis, hypothalamic-pituitary dysfunction, jaundice, hypotonia, macroglossia, umbilical hernia, developmental delay, myxedema, Pendred syndrome, thyroglobulin defect, deiodinase defect, hypopituitarism

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Contributor Information and Disclosures

Author

Daniel C Postellon, MD, Clinical Associate Professor, College of Human Medicine, Pediatrics and Human Development, Michigan State University; Consulting Staff, Pediatric Endocrine Clinic, DeVos Children's Hospital
Daniel C Postellon, MD is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, and Lawson-Wilkins Pediatric Endocrine Society
Disclosure: Nothing to disclose.

Coauthor(s)

Michael J Bourgeois, MD, Director of Pediatric Undergraduate Medical Education, Associate Professor, Department of Pediatrics, Division of Pediatric Endocrinology and Metabolism, Texas Tech University School of Medicine
Michael J Bourgeois, MD is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Surendra Varma, MD, Vice-Chairman and Program Director, University Distinguished Professor, Department of Pediatrics, Texas Tech University School of Medicine
Surendra Varma, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Diabetes Association, American Medical Association, American Thyroid Association, Endocrine Society, Medical Group Management Association, New York Academy of Sciences, Sigma Xi, Society for Pediatric Radiology, Southern Society for Pediatric Research, and Texas Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Arlan L Rosenbloom, MD, Adjunct Distinguished Service Professor Emeritus of Pediatrics, University of Florida; Fellow of the American Academy of Pediatrics; Fellow of the American College of Epidemiology
Arlan L Rosenbloom, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Epidemiology, American Pediatric Society, Endocrine Society, Florida Pediatric Society, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Barry B Bercu, MD, Professor, Departments of Pediatrics, Molecular Pharmacology and Physiology, University of South Florida College of Medicine, All Children's Hospital
Barry B Bercu, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Federation for Clinical Research, American Medical Association, American Pediatric Society, Association of Clinical Scientists, Endocrine Society, Florida Medical Association, Lawson-Wilkins Pediatric Endocrine Society, Pituitary Society, Society for Pediatric Research, Society for the Study of Reproduction, and Southern Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Merrily P M Poth, MD, Professor, Department of Pediatrics and Neuroscience, Uniformed Services University of the Health Sciences
Merrily P M Poth, MD is a member of the following medical societies: American Academy of Pediatrics, Endocrine Society, and Lawson-Wilkins Pediatric Endocrine Society
Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD, Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas and Arkansas Children's Hospital
Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research
Disclosure: Genentech, Inc. Honoraria Speaking and teaching; Pfiser, Inc. Honoraria Consulting

 
 
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