INTRODUCTION — Congenital goiter can be caused by a variety of inborn errors of thyroid hormone production or anomalies of thyroid embryology, in utero exposure to maternal antithyroid antibodies, or maternal ingestion of antithyroid drugs and other goitrogens. The infant may have associated hypothyroidism, hyperthyroidism, or have normal thyroid function. For the hereditary causes, the enlarged thyroid gland, and the thyroid dysfunction that often accompanies it, may not be evident at birth.
Once a goiter is detected, the diagnostic evaluation is aimed at assessing thyroid function and identifying the underlying cause. Both of these factors will determine management.
This topic review will consider congenital goiters in newborns and infants. Related content is discussed in separate topic reviews:
THYROID DEVELOPMENT — The thyroid gland arises from an outpouching of the foregut at the base of the tongue (foramen cecum). It then migrates down to its normal location over the thyroid cartilage by 8 to 10 weeks of gestation. This path of migration is marked by the thyroglossal duct, which normally involutes.
Thyroid volume in term neonates is approximately 0.9±0.2 mL (mean±standard deviation [SD]), as measured by ultrasonography in 68 term neonates in Chicago , and increases with age and body surface area. (See "Approach to acquired goiter in children and adolescents", section on 'Thyroid volume in healthy children and adolescents'.)
CLINICAL PRESENTATION — Most cases of congenital goiter are identified after a neonate is detected to have hypothyroidism by newborn screening tests. A goiter may be visible or palpable or, in some cases, only discovered after ultrasonography. Clinically apparent goiters are most commonly associated with one of the inborn errors of thyroid hormone production (dyshormonogenesis). (See 'Inborn errors of thyroid hormone production' below.)
Other cases may be identified on examination of an infant born to a mother with thyroid disease (either Graves disease or autoimmune thyroiditis). Occasionally, a goiter may be detected incidentally by routine fetal ultrasonography.
EVALUATION — Congenital goiter can be caused by a wide range of disorders, including effects from transplacental transfer of maternal antibodies or goitrogens, genetic disorders, congenital anomalies, or iodine excess or deficiency (table 1). The etiology usually can be determined by a combination of history, focused laboratory testing for the infant's thyroid function and maternal antibodies, and thyroid ultrasound. For selected patients, further testing may be needed to establish the etiology of the goiter.
History — Clues to the cause of congenital goiter and to thyroid function often are found on a careful history:
●Maternal Graves disease – A current or past history of maternal Graves disease suggests that the infant's goiter may be caused by one of two mechanisms:
•The goiter may be caused by transplacental passage of maternal thyroid-stimulating hormone (TSH) receptor-stimulating antibodies. Such antibodies may persist for years even though the maternal hyperthyroidism underwent definitive treatment in the past, by either radioactive iodine ablation or thyroidectomy. Affected newborns will have clinical manifestations of hyperthyroidism, known as neonatal Graves disease. (See 'Neonatal Graves disease' below.)
•If the mother's Graves disease was treated with antithyroid drugs during the pregnancy, thyroid function represents a balance of the TSH receptor-stimulating antibody and effects of the maternal antithyroid drug. If the baby is hypothyroid, the antithyroid drug effect is predominant. If the infant is hyperthyroid, the TSH receptor-stimulating effect is predominant. (See 'Prenatal antithyroid drug treatment' below.)
●Maternal autoimmune thyroid disease – If the mother has autoimmune thyroid disease, which is the most common cause of acquired hypothyroidism, the infant's goiter may be caused by transplacental passage of a TSH receptor antibody. In this setting, the infant's goiter is caused by a TSH receptor-stimulating antibody, or a combination of a TSH receptor-stimulating and -blocking antibody, where the stimulating antibody predominates, causing hyperthyroidism in the infant . Production of only a TSH receptor-blocking antibody would be associated with hypothyroidism and a small or normal-sized gland but not a goiter . There also may be a history of congenital goiter with transient hypothyroidism in older (or occasionally, twin) siblings. (See 'Neonatal Graves disease' below.)
●Goiter or thyroid disease in siblings – If there is no history of maternal thyroid disease (and if maternal autoimmune thyroid disease has been excluded by laboratory testing), the presence of goiter or thyroid disease in an older (or twin) sibling suggests a heritable disorder:
•Hypothyroidism in the infant or older siblings suggests the possibility of a heritable inborn error of thyroid hormone production (dyshormonogenesis). (See 'Inborn errors of thyroid hormone production' below.)
•Hyperthyroidism in the infant or older siblings suggests an activating mutation of the TSH receptor. (See 'Other causes' below.)
●Iodine exposure – The history should explore the possibility of excessive iodine exposure or ingestion, either by the mother during her pregnancy or to the neonate in the first few weeks of life. Maternal iodine exposure may occur with drugs such as amiodarone, health food supplements, or by diagnostic studies using radiocontrast agents containing iodine. A unique form of excess iodine ingestion may occur in mothers who consume seaweed soup and are breastfeeding their newborn infants. (See 'Iodine excess' below.)
Physical examination — Most causes of congenital goiter result in a diffusely enlarged, symmetrical gland. If the thyroid enlargement is unilateral, this may represent thyroid hemiagenesis or, rarely, a tumor such as a teratoma. (See 'Thyroid hemiagenesis' below and 'Thyroid neoplasm' below.)
In neonates with hypothyroidism, the majority have no signs or symptoms other than goiter. More severely hypothyroid newborns may exhibit jaundice, myxedematous facies, macroglossia, and umbilical hernia. Infants born in regions of the world that lack newborn screening programs typically present with symptoms and signs of hypothyroidism that develop over the first few months of life. Infants born to mothers with severe iodine deficiency will manifest features of "endemic cretinism," including coarse facial features with macroglossia, wide sutures and large fontanels, distended abdomen with umbilical hernia, cutis marmorata, and sluggish reflexes. (See "Clinical features and detection of congenital hypothyroidism", section on 'Clinical manifestations'.)
In neonates with hyperthyroidism, clinical manifestations may include irritability, hyperphagia, poor weight gain, tachycardia, small anterior fontanel, hepatomegaly and/or splenomegaly, and eye findings such as stare, exophthalmos, and lid lag. These symptoms may be present at birth or may develop during the first days or weeks of life, depending on the presence and timing of maternal antithyroid drug treatment. (See "Evaluation and management of neonatal Graves disease", section on 'Clinical manifestations'.)
Initial testing — Because clinical manifestations of either hyper- or hypothyroidism may be subtle or slow to develop, tests of thyroid function should be performed in all infants with congenital goiter.
●Thyroid function tests – Initial testing should include measurement of serum TSH and free thyroxine (T4). If there is a clinical suspicion of hyperthyroidism, measurement of serum total triiodothyronine (T3) should be included as it may be the first thyroid hormone to be elevated and it often is proportionally more elevated than the free T4. It is important to interpret thyroid test results using age-appropriate reference intervals. (See "Clinical features and detection of congenital hypothyroidism", section on 'Serum tests of thyroid function'.)
●Thyroid receptor antibody tests – Selection of antibody tests depends on the results of the infant's thyroid function tests, sometimes also guided by a history of a maternal thyroid disorder:
•Hypothyroid infant – If the infant is hypothyroid, the goiter usually is the result of maternal antithyroid drugs, one of the inborn errors of thyroid hormone metabolism, or maternal excess iodine ingestion. Measurement of TSH receptor-stimulating antibodies can be deferred, pending periodic monitoring of thyroid function in the neonate. (See 'Hypothyroid infant (TSH elevated, free T4 low or normal)' below.)
If the infant develops hyperthyroidism, measure TSH receptor-stimulating antibodies, as described below.
•Hyperthyroid infant – If the infant is hyperthyroid, measure TSH receptor-stimulating antibodies in the mother and/or infant. This can be accomplished by measurement of either thyrotropin-stimulating immunoglobulins (TSI; a functional bioassay) or thyrotropin-binding inhibitor immunoglobulins (TBII; a competitive inhibition-binding assay). TBII is sometimes labeled TRAb.
Maternal TSH receptor-stimulating antibodies are the most common cause of neonatal hyperthyroidism. Measurement of these antibodies in the infant and/or mother is particularly important if the mother has a history of Graves disease (current or past) but is worthwhile for all hyperthyroid infants since maternal Graves disease may not be recognized. For example, some women with a prior diagnosis of Graves disease who received definitive therapy may have indefinite persistence of TSH-receptor antibodies despite themselves being cured. (See "Evaluation and management of neonatal Graves disease", section on 'Diagnosis'.)
●Ultrasonography – We recommend that ultrasonography be performed in each case of congenital goiter. Ultrasonography will provide more accurate information than the physical examination about the location, shape, and size (transverse, depth, and longitudinal diameter) of each lobe of the thyroid gland, and the procedure is noninvasive and readily available. The size of the gland may provide a clue as to the etiology. As an example, hyperplasia without a history of a maternal thyroid disorder suggests a form of dyshormonogenesis. For some disorders, such as thyroid hemiagenesis, ultrasonographic findings are the only abnormality and can establish the diagnosis.
Subsequent evaluation for selected patients
●Tests of iodine status – Tests of iodine status should be performed if excessive iodine exposure is suspected from the history and may also be performed if the infant has otherwise unexplained hypothyroidism. The most accurate test to confirm excess iodine exposure is measurement of 24-hour urinary iodine in the mother and/or infant. Measurement of a spot urine iodine and creatinine, yielding an iodine-to-creatinine ratio, or sometimes measurement of serum iodine levels, may also be used to confirm goiter due to excess iodine exposure. (See "Clinical features and detection of congenital hypothyroidism", section on 'Urinary iodine concentration'.)
●Radionuclide uptake and scan – Radionuclide studies may be performed if an inborn error of thyroid hormone production (dyshormonogenesis) is suspected. This type of disorder should be suspected in a hypothyroid infant in whom other causes of hypothyroidism (antithyroid drugs, maternal TSH receptor-blocking antibodies, and iodine excess or deficiency) have been excluded. Among infants with congenital hypothyroidism, those with dyshormonogenesis are particularly likely to present with goiter. For most inborn errors of thyroid hormone production, radionuclide uptake is increased (best quantitated using iodine-123), except in the case of a mutation in the sodium-iodide symporter gene (SLC5A5). (See "Clinical features and detection of congenital hypothyroidism", section on 'Thyroid radionuclide uptake and scan'.)
●Molecular testing – If the infant has hypothyroidism and an inborn error of thyroid hormone production (dyshormonogenesis) is suspected, molecular testing may be performed to confirm the specific diagnosis. Such information may facilitate genetic counseling, including recurrence risk in future siblings, but rarely affects the management of the patient. (See "Clinical features and detection of congenital hypothyroidism", section on 'Disorders of thyroid hormone synthesis and secretion'.)
If the infant has hyperthyroidism, the most likely cause is neonatal Graves disease. In the rare case where there is no evidence of Graves disease (ie, negative TSH receptor-stimulating antibodies), the possibility of either an activating mutation of the TSH receptor or McCune-Albright syndrome should be considered. In such cases, specific molecular testing of the TSH receptor gene or the G protein stimulatory alpha subunit gene from an affected tissue, respectively, may confirm one of these diagnoses. (See 'Other causes' below.)
ESTABLISHING THE ETIOLOGY — The thyroid-stimulating hormone (TSH) result narrows the diagnostic possibilities to those that cause hypothyroidism, hyperthyroidism, or euthyroid goiter. The results of the history and antibody tests can establish the diagnosis in most cases (table 1). Management generally depends upon thyroid function and identification of the underlying cause. For the hereditary causes, the enlarged thyroid gland, and the thyroid dysfunction that often accompanies it, may not be evident at birth.
Hypothyroid infant (TSH elevated, free T4 low or normal)
Prenatal antithyroid drug treatment — In infants with prenatal exposure to antithyroid drugs due to maternal Graves disease, congenital goiter and hypothyroidism are most likely the result of transplacental passage of the antithyroid drugs. The antithyroid drugs propylthiouracil, methimazole, and carbimazole all cross the placenta and can cause fetal hypothyroidism and goiter.
For most of these infants, the hypothyroidism resolves by 7 to 10 days of life as the antithyroid drug is metabolized and excreted. Thyroid function should be followed at weekly intervals to confirm that it normalizes. This pattern confirms that the transient goiter and hypothyroidism were caused by the maternal antithyroid drugs. Because thyroid function normalizes in the vast majority of cases by two weeks of age, thyroid hormone treatment is not necessary. Once thyroid function normalizes, we recommend checking TSH and free thyroxine (T4) for another two weeks to assess for possible transition to hyperthyroidism (uncommon).
Occasionally, the infant transitions to hyperthyroidism during the first few days or weeks of life as the antithyroid drug is excreted. When this occurs, it is usually caused by maternal TSH receptor-stimulating antibodies, measurement of which will confirm this etiology (neonatal Graves disease) and distinguish it from other causes of neonatal hyperthyroidism. (See 'Hyperthyroid infant (TSH suppressed, free T4 elevated or normal)' below.)
Other causes — If there is no prenatal exposure to antithyroid drugs, or if TSH receptor-stimulating antibodies (if measured) are negative, the likely causes are an inborn error of thyroid hormone production (dyshormonogenesis), iodine deficiency, or iodine excess. These disorders can be distinguished by further history and testing for these disorders. (See 'Subsequent evaluation for selected patients' above.)
Inborn errors of thyroid hormone production — An inborn error of thyroid hormone production (dyshormonogenesis) accounts for approximately 10 to 15 percent of cases of severe congenital hypothyroidism, usually with goiter. These disorders are usually first detected by newborn screening for congenital hypothyroidism . Occasionally, they come to attention when prenatal ultrasonography identifies fetal goiter with no evidence of maternal thyroid disease or antithyroid antibodies. They also may be identified prenatally because of a family history of congenital hypothyroidism with an autosomal recessive pattern of inheritance.
Ultrasonography typically shows thyroid hyperplasia in a eutopic (normal) location. Further evaluation to establish the cause includes radioactive iodine uptake and molecular testing for the genes involved in thyroid hormone production, which are SLC5A5 (sodium iodide symporter), TPO (thyroid peroxidase), DUOX2 (dual oxidase 2) and its accessory protein DUOXA2, TG (thyroglobulin), IYD (iodotyrosine deiodinase 1), SLC26A4 (pendrin), and GNAS (pseudohypoparathyroidism and Albright hereditary osteodystrophy). The SLC26A4 variants also cause sensorineural hearing loss, known as Pendred syndrome. The pathophysiology, diagnosis, and management of these disorders are discussed separately. (See "Clinical features and detection of congenital hypothyroidism", section on 'Disorders of thyroid hormone synthesis and secretion'.)
Infants with one of these disorders should be treated with thyroid hormone, with periodic monitoring of serum TSH and free thyroxine (T4) and dose adjustment as indicated. (See "Treatment and prognosis of congenital hypothyroidism", section on 'Treatment'.)
If an inborn error of thyroid hormone production is identified prenatally (typically when goiter is identified on prenatal ultrasound and antithyroid antibody tests are normal), prenatal treatment may be considered. Case reports have described prenatal treatment of such cases by injecting T4 into the amniotic fluid. In the largest such series, fetal goiter size decreased during treatment and there were no adverse events . However, the infants were still hypothyroid at birth, suggesting that the treatment did not fully correct the hypothyroidism. There are inadequate data to conclude whether prenatal treatment improves obstetrical or cognitive outcomes in the offspring or to determine the optimal dosing regimen.
Iodine excess — Compounds that can cross the placenta and cause fetal hypothyroidism and goiter are iodine-rich drugs such as expectorants, amiodarone, nutritional supplements, and iodinated radiocontrast agents, in particular, oil-soluble iodinated contrast medium (for example, as used for hysterosalpingography). One report describes several cases of perinatal goiter caused by excess maternal iodine ingestion due to an error in manufacturing a prenatal vitamin [6,7]. Neonates given oral or topical iodine or bathed with iodine soon after birth can develop a goiter. If iodine exposure is suspected, this should be confirmed by testing for iodine status of the infant. (See 'Subsequent evaluation for selected patients' above and "Clinical features and detection of congenital hypothyroidism", section on 'Transient congenital hypothyroidism'.)
In infants with hypothyroidism and goiter caused by excess iodine ingestion, thyroid function generally recovers to normal without treatment within a few weeks after discontinuation of excess iodine. If thyroid function does not normalize within a few weeks, thyroid hormone therapy should be given for several months and then gradually withdrawn. Thyroid function should be followed at weekly intervals to confirm normalization.
Iodine deficiency — Iodine-deficiency goiter can occur in neonates, but it is rare. It may be suspected in infants born in populations living in areas of severe endemic iodine deficiency, particularly if the mother has a goiter due to iodine deficiency. Many neonates and infants with endemic iodine deficiency (cretinism) do not have a goiter , because they are no longer hypothyroid (neurologic cretinism) or their thyroid has been destroyed (hypothyroid cretinism). Data and a map indicating areas of iodine deficiency worldwide are available from the Iodine Global Network website. (See "Clinical features and detection of congenital hypothyroidism", section on 'Transient congenital hypothyroidism' and "Iodine deficiency disorders", section on 'Impact of iodine supplementation'.)
Hyperthyroid infant (TSH suppressed, free T4 elevated or normal)
Neonatal Graves disease — Transplacental passage of TSH receptor-stimulating antibodies causes fetal and neonatal hyperthyroidism, known as neonatal Graves disease. The mother may have had Graves hyperthyroidism during the pregnancy or she may have had it in the past and been treated by thyroidectomy or radioactive iodine. The presence of goiter in affected infants is variable; when goiter is present, it may be detected by physical examination or by ultrasonography. The infant is typically hyperthyroid at birth. However, if the mother's Graves disease was treated with antithyroid drugs during the pregnancy, the infant may be either hyperthyroid or hypothyroid, depending on the balance of the TSH receptor-stimulating antibody and thyroid-suppressing effects of the thionamide drug. (See 'Prenatal antithyroid drug treatment' above.)
The diagnosis of neonatal Graves disease is confirmed by the presence of thyrotropin-stimulating immunoglobulin (TSI). If TSI is negative, the diagnosis can be confirmed by the presence of TBII, a measure of TSH receptor antibodies (TRAb) in the mother and/or infant. Neonatal Graves hyperthyroidism and goiter resolve in three to six months as the antibodies are cleared. (See "Evaluation and management of neonatal Graves disease".)
Transplacental passage of thyroid receptor-blocking antibodies can cause fetal and neonatal hypothyroidism; however, when the size of the thyroid gland is commented on in case reports, typically it is normal or small, and not enlarged unless stimulating antibodies are also present. (See "Clinical features and detection of congenital hypothyroidism", section on 'Transient congenital hypothyroidism'.)
Other causes — Congenital goiter and hyperthyroidism without TSH receptor-stimulating antibodies indicates one of the following causes, which can be distinguished by specific molecular testing:
Activating mutation of the TSH receptor — Germline mutations that result in constitutive activation of the TSH receptor are a rare cause of diffuse goiter and hyperthyroidism, sometimes known as congenital nonimmune hyperthyroidism. The goiter and hyperthyroidism may be present at birth or may become evident years or even decades later . These mutations are inherited as autosomal dominant traits; as a result, there may be a family history of hyperthyroidism and goiter.
Treatment with an antithyroid drug is effective. However, the disorder is permanent, and hyperthyroidism will recur if the drug is discontinued . Consequently, some form of ablative treatment, such as thyroidectomy, is eventually indicated.
McCune-Albright syndrome — McCune-Albright syndrome is caused by somatic activating mutations of the TSH receptor G protein stimulatory alpha subunit . These mutations result in thyroid hyperplasia or formation of nodules and, ultimately, in toxic nodular goiters . The goiter may be present in infancy, but more commonly, patients present later in childhood with toxic multinodular goiter. (See "Definition, etiology, and evaluation of precocious puberty", section on 'McCune-Albright syndrome' and "Approach to acquired goiter in children and adolescents", section on 'Toxic adenoma or multinodular goiter'.)
Although treatment with an antithyroid drug is effective, the disorder is permanent, and hyperthyroidism will recur if the drug is discontinued. Consequently, some form of ablative treatment, such as thyroidectomy, is eventually indicated for the hyperthyroidism. McCune-Albright syndrome is also associated with precocious puberty, fibrous dysplasia of the skeleton, and irregularly bordered cafe-au-lait spots; management of these aspects are discussed separately. (See "Treatment of precocious puberty", section on 'McCune-Albright syndrome'.)
Euthyroid infant (TSH and free T4 normal) — An asymmetric congenital or midline neck mass goiter in an infant with normal thyroid function tests suggests the following possibilities, which usually can be distinguished by ultrasonography:
Thyroid hemiagenesis — Thyroid hemiagenesis may cause unilateral goiter in neonates because of compensatory hypertrophy of the contralateral lobe. In Sicily, screening of 24,032 healthy children identified 12 cases of hemiagenesis (1:2000), all resulting from absence of the left lobe. Although the children did not have hypothyroidism, the average TSH level was higher than in age-matched controls (2.8 versus 1.9 milli-international unit/L) .
Thyroglossal duct cysts — These are cysts of the thyroglossal duct or tract that form behind the thyroid as it moves from the base of the tongue inferiorly before dividing into the left and right thyroid lobes. Normally, the duct involutes, but cysts can form within it. Most are located in the midline between the hyoid bone and the isthmus of the thyroid, but they can occur anywhere along the thyroglossal duct tract. A thyroglossal duct cyst may be present at birth; more often, it appears during childhood or later [14,15].
If a cyst is detected, it should be removed surgically. Most contain no thyroid cells, but a few do (thyroid ectopia). Very rarely, they are the patient's only thyroid tissue, so that the patient becomes hypothyroid after the "cyst" is removed. A thyroid scan is recommended before surgery to determine if other thyroid tissue is present. Rarely, thyroid carcinomas arise in thyroglossal duct cysts . (See "Thyroglossal duct cyst, thyroglossal duct cyst cancer, and ectopic thyroid" and "Thyroid nodules and cancer in children".)
Thyroid neoplasm — Rarely, teratomas of the thyroid present in the neonatal period .
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Hypothyroidism" and "Society guideline links: Hyperthyroidism" and "Society guideline links: Pediatric thyroid disorders".)
SUMMARY AND RECOMMENDATIONS
●Thyroid development – The thyroid gland arises from an outpouching of the foregut at the base of the tongue (foramen cecum). It then migrates down to its normal location over the thyroid cartilage by 8 to 10 weeks of gestation. Normal thyroid volume is approximately 1 mL at birth and increases with age and body surface area. (See 'Thyroid development' above.)
●Causes of congenital goiter – Congenital goiter can be caused by a wide range of disorders, including effects from transplacental transfer of maternal antibodies or goitrogens, genetic disorders, congenital anomalies, or iodine excess or deficiency (table 1). The etiology usually can be determined by a combination of history and focused laboratory testing for the infant's thyroid function and maternal antibodies. In hereditary forms, the goiter, and the thyroid dysfunction that often accompanies it, may not be evident at birth. (See 'Establishing the etiology' above.)
The main causes are:
•Maternal thyroid disease – Maternal hyper- or hypothyroidism may be associated with fetal and neonatal goiter:
-Maternal Graves disease – If the mother has Graves disease (current or past), she may transfer a thyroid-stimulating hormone (TSH) receptor-stimulating antibody to the infant, causing hyperthyroidism (neonatal Graves disease). The TSH receptor-stimulating antibody may be confirmed by measurement of either thyrotropin-stimulating immunoglobulin (TSI; a functional bioassay) or by measurement of thyrotropin-binding inhibitor immunoglobulin (TBII; a competitive binding assay, sometimes designated TRAb). (See "Evaluation and management of neonatal Graves disease".)
However, if the mother's Graves disease was treated with antithyroid drugs during the pregnancy, the infant may be either hyperthyroid or hypothyroid, depending on the balance of the TSH receptor-stimulating antibody and thyroid-suppressing effects of the drug. (See 'Neonatal Graves disease' above and 'Prenatal antithyroid drug treatment' above.)
-Maternal autoimmune thyroid disease – Acquired maternal hypothyroidism is usually caused by autoimmune thyroid disease. Even though the mother is hypothyroid, she may transfer a TSH receptor-stimulating antibody or a combination of stimulating and blocking antibodies, resulting in a goiter and hyperthyroidism in the infant (neonatal Graves disease), which can be confirmed by measurement of TBII. Goiter in the infant suggests that the stimulating antibody predominates. If the blocking antibody predominates, the infant typically has a normal-size or small thyroid. (See 'Neonatal Graves disease' above.)
These disorders require medical management and monitoring but typically resolve within a few weeks of birth.
•Inborn errors of thyroid hormone metabolism – A variety of inborn errors of thyroid hormone production (dyshormonogenesis) have been described. All result in varying degrees of goiter and hypothyroidism and may be detected by newborn screening for hypothyroidism. Affected individuals require lifelong thyroid hormone treatment and monitoring. (See 'Inborn errors of thyroid hormone production' above.)
•Iodine excess – Excess iodine can cause goiter and hypothyroidism in a newborn. This can be related to excess iodine exposure in utero (via excess maternal iodine, eg, from iodinated contrast media or certain drugs or nutritional supplements) or in the neonate (iodinated contrast media, drugs, or topical iodine antiseptics). (See 'Iodine excess' above.)
•Iodine deficiency – Paradoxically, iodine deficiency also can cause neonatal goiter and hypothyroidism (eg, born to mothers with iodine deficiency, who typically live in regions where iodine deficiency is endemic). (See 'Iodine deficiency' above.)
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