Congenital Hypothyroidism due to Unexpected Iodine Sources

Stagi, Stefano; Manoni, Cristina; Chiarelli, Francesco; Martino, Maurizio de

doi:10.1159/000295697

Cited by 4 publications

(3 citation statements)

References 5 publications

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“…1 de Vasconcellos and Collett-Solberg 6 reported 8 cases of neonatal goiter thought to have developed as a result of maternal ingestion of a prenatal vitamin that was contaminated with excess iodine. Stagi et al 10 presented 2 neonates born with goiter and positive screening tests for CH whose mothers were later found to have taken an herbal supplement throughout their pregnancies high in iodine-containing alga kelp. The urinary iodine concentrations were elevated in both mothers and neonates.…”

Section: Discussionmentioning

confidence: 99%

Congenital Hypothyroidism Caused by Excess Prenatal Maternal Iodine Ingestion

Connelly

Boston

Pearce

et al. 2012

The Journal of Pediatrics

120

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We report the cases of 3 infants with congenital hypothyroidism detected with the use of our newborn screening program, with evidence supporting excess maternal iodine ingestion (12.5 mg/d) as the etiology. Levels of whole blood iodine extracted from their newborn screening specimens were 10 times above mean control levels. Excess iodine ingestion from nutritional supplements is often unrecognized.

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Section: Discussionmentioning

confidence: 99%

Congenital Hypothyroidism Caused by Excess Prenatal Maternal Iodine Ingestion

Connelly

Boston

Pearce

et al. 2012

The Journal of Pediatrics

120

View full text Add to dashboard Cite

show abstract

“…However, the immature neonatal thyroid gland is unable to escape from the acute Wolff-Chaikoff effect, making infants and children more susceptible to iodine-induced hypothyroidism [63, 64]. Further work has led to the important discovery that excess iodine exposure in utero and in the postnatal period, in the form of iodine-containing antiseptics, contrast agents, medications, and supplements, can lead to transient or permanent neonatal hypothyroidism [63, 65, 66].…”

Section: Eradication Of Cretinism By Salt Iodinationmentioning

confidence: 99%

History of the Thyroid

2022

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The history of the thyroid dates from 2697 BCE when the “Yellow Emperor” Hung Ti described the use of seaweed to treat goiter. The English name “thyroid” was coined by Thomas Wharton in 1656 from the Greek word for a shield. Bernard Courtois discovered iodine in 1811 when he noted a residual purplish ash while burning seaweed. Robert Graves is known for his classic 1835 report of “palpitations, goiter, and exophthalmos” in three women, but Caleb Parry observed the same clinical features in 1786. The clinical syndrome we now recognize as hypothyroidism was characterized as “myxoedema” in 1878 by William Ord at St. Thomas Hospital. In 1891, George Murray reported that injection of thyroid extract from sheep led to improvement in symptoms in a woman with myxedema. Thomas Kocher, who reported that patients with goiter who underwent complete thyroidectomy developed <i>cachexia strumipriva</i>, was awarded the Nobel Prize in Physiology and Medicine in 1909. Edward Kendall discovered “thyroxin” on Christmas day in 1914. Studies by David Marine that iodine treatment prevented endemic goiter led to salt iodination, which has largely eradicated endemic cretinism. In 1973, Jean Dussault reported detection of congenital hypothyroidism by screening newborn populations.

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“…Maternal intentional or inadvertent consumption of iodine supplements (e.g. in herbal remedies) may also result in TCH and maternal consumption of inorganic iodine (4–100 mg/day) for thyrotoxicosis, while breastfeeding has been associated with mild TCH in 10% infants ( 74 , 75 , 76 ).…”

Section: Excess Iodine Consumptionmentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: The pathophysiology of transient congenital hypothyroidism

Peters

Schoenmakers

2022

European Journal of Endocrinology

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Transient congenital hypothyroidism (TCH) refers to congenital hypothyroidism which spontaneously resolves in the first few months or years of life. Currently, there is a paucity of reliable markers predicting TCH at diagnosis, and the diagnosis is established following withdrawal of levothyroxine therapy around 3 years of age. The incidence of TCH is increasing, and it is a major contributor to the overall increase in incidence of CH in recent studies. Both genetic factors, in particular mutations affecting DUOX2 and DUOXA2, and environmental factors, e.g iodine deficiency and excess, anti- TSHR antibodies and exposure to anti-thyroid or iodine-rich medications may cause TCH. Resolution of TCH in childhood may reflect both normal thyroid physiology (decreased thyroid hormone biosynthesis requirements after the neonatal period) and clearance or cessation of environmental precipitants. The relative contributions and interactions of genetic and environmental factors to TCH, and the extent to which TCH may be prevented, require evaluation in future population-based studies.

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Congenital Hypothyroidism due to Unexpected Iodine Sources

Cited by 4 publications

References 5 publications

Congenital Hypothyroidism Caused by Excess Prenatal Maternal Iodine Ingestion

Congenital Hypothyroidism Caused by Excess Prenatal Maternal Iodine Ingestion

History of the Thyroid

MECHANISMS IN ENDOCRINOLOGY: The pathophysiology of transient congenital hypothyroidism

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