Maternal Thyroid-Blocking Immunoglobulins in Congenital Hypothyroidism*

Brown, Rosalind S.; Keating, Paula; Mitchell, Elizabeth A.

doi:10.1210/jcem-70-5-1341

Cited by 35 publications

(11 citation statements)

References 23 publications

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“…report that the finding of TBII, in the absence of thyroid stimulation, is a sensitive screening test for the presence of TSH receptor-blocking antibodies. 16 In the present study it was possible to demonstrate this pattern of high TBll activity in the absence of TSI in maternal serum at the birth of the second and third infants. After the birth of child 3, we investigated the mother's and child's sera for thyroid stimulation-blocking antibodies and found them both positive.…”

Section: Discussionsupporting

confidence: 58%

Transient congenital hypothyroidism due to maternal thyrotrophin binding inhibiting immunoglobulin

Schwingshandl

Donaghue

Luttrell

et al. 1993

J Paediatrics Child Health

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Transient congenital hypothyroidism due to maternal thyrotrophin binding inhibitor immunoglobulin (TBII), a thyroid-stimulating hormone (TSH)-receptor blocking antibody, is described in three male siblings born to a mother with autoimmune thyroiditis. These cases are believed to be the first described in Australia. The first child was found to have a serum TSH of 565 mU/L and had a negative thyroid scan when presented for neonatal screening. He was treated with thyroxine but became thyrotoxic at 3 months of age when he was on a dosage of 85 micrograms/m2 of body surface area. He was euthyroid 6 months after discontinuation of therapy. Nine years later a second hypothyroid sibling was born, with a serum TSH of 709 mU/L on day 4. Both mother and child were demonstrated to be strongly positive for TBII. Again this child was able to cease therapy by the age of 9 months. A third sibling, also TBII positive, was born 12 months after the second. His TSH was 90 mU/L and his serum thyroxine (T4) was 169 nmol/L. On this occasion, thyroid stimulation-blocking antibody was found to be present in the serum of both mother and child. Thyroxine therapy was ceased at 1 month. The family present a picture of varying degrees of transient neonatal hypothyroidism due to the transplacental passage of a maternal receptor blocking antibody. The condition is self-limiting, resolving when the immunoglobulin is cleared from the infant's circulation.

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Section: Discussionsupporting

confidence: 58%

Transient congenital hypothyroidism due to maternal thyrotrophin binding inhibiting immunoglobulin

Schwingshandl

Donaghue

Luttrell

et al. 1993

J Paediatrics Child Health

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“…However, TGBI could not be found in sporadic congenital hypothyroidism by other authors (19,26) and, consequently, the possible role of thyroid autoimmunity in the etiology of endemic cretinism remains controversial.…”

Section: Complicationsmentioning

confidence: 89%

“…8.1 ±0.1 (125) 144 ± 3 (124) 1.7 ± 1.1 (255) 0.06 ± 0.01 (27) 46.4 ±1.1 (255) 15.8 ±3.5 (12) 0.39 ± 0.04 (12) 15.5 ± 1.3 (243) 76.8 4.9 ± 0.2 (358) 166 ± 3 (299) 18.6 ± 2.1 (365) 0.17 ±0.02 (105) 65.2 ± 0.9 (167) 1.6 ±0.2 (30) 1.92 ±0.12 (24) 0.5 ± 0.01 (120) 46± 3 (109) 302 ± 20 (122) 1.09 ±0.18(19) 28.3 ± 2.6 (6) 0.01-0. \b(8) "In Brussels, Belgium and in the Idjwi Island and Ubangi endemic goiter areas, Zaire.…”

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confidence: 99%

The Disorders Induced by Iodine Deficiency

Delange¹

1994

Thyroid

558

447

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This paper reviews present knowledge on the etiology, pathophysiology, complications, prevention, and therapy of the disorders induced by iodine deficiency. The recommended dietary allowances of iodine are 100 micrograms/day for adults and adolescents, 60-100 micrograms/day for children aged 1 to 10 years, and 35-40 micrograms/day in infants aged less than 1 year. When the physiological requirements of iodine are not met in a given population, a series of functional and developmental abnormalities occur including thyroid function abnormalities and, when iodine deficiency is severe, endemic goiter and cretinism, endemic mental retardation, decreased fertility rate, increased perinatal death, and infant mortality. These complications, which constitute a hindrance to the development of the affected populations, are grouped under the general heading of iodine deficiency disorders (IDD). At least one billion people are at risk of IDD. Iodine deficiency, therefore, constitutes one of the most common preventable causes of mental deficiency in the world today. Most of the affected populations live in mountainous areas in preindustrialized countries, but 50 to 100 million people are still at risk in Europe. The most important target groups to the effects of iodine deficiency from a public health point of view are pregnant mothers, fetuses, neonates, and young infants because the main complication of IDD, i.e., brain damage resulting in irreversible mental retardation, is the consequence of thyroid failure occurring during pregnancy, fetal, and early postnatal life. The main cause of endemic goiter and cretinism is an insufficient dietary supply of iodine. The additional role of naturally occurring goitrogens has been documented in the case of certain foods (milk, cassava, millet, nuts) and bacterial and chemical water pollutants. The mechanism by which the thyroid gland adapts to an insufficient iodine supply is to increase the trapping of iodide as well as the subsequent steps of the intrathyroidal metabolism of iodine leading to preferential synthesis and secretion of triiodotyronine (T3). They are triggered and maintained by increased secretion of TSH, which is ultimately responsible for the development of goiter. The acceleration of the main steps of iodine kinetics and the degree of hyperstimulation by TSH are much more marked in the pediatric age groups, including neonates, than in adults, and the development of goiter appears as an unfavorable side effect in the process of adaptation to iodine deficiency during growth. The most serious complication of iodine deficiency is endemic cretinism, a syndrome characterized by irreversible mental retardation together with either a predominant neurological syndrome or predominant hypothyroidism, or a combination of both syndromes.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…In contrast, had we relied upon thyroid scintigraphy, the correct diagnosis might not have been made because of the ability of blocking Abs, if sufficiently potent, to inhibit TSH-induced iodine uptake [7,13]. Similarly, measurement of Abs to thyroid peroxidase or thyroglobulin, and not TSHR Abs to verify the presence of underlying maternal thyroid autoimmunity, might have led us to miss the diagnosis in one of the cases, as has been noted previously [7,14]. …”

Section: Discussionmentioning

confidence: 99%

Severe Unsuspected Maternal Hypothyroidism Discovered after the Diagnosis of Thyrotropin Receptor-Blocking Antibody-Induced Congenital Hypothyroidism in the Neonate: Failure to Recognize and Implications to the Fetus

2014

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Background: Whereas most adequately treated children with congenital hypothyroidism (CH) do well neurodevelopmentally, when both the maternal and fetal thyroid glands are compromised, significant cognitive delay can occur despite early and aggressive postnatal therapy. Maternal thyrotropin-stimulating hormone receptor (TSHR)-blocking antibodies (Abs) can be transmitted to the fetus and cause combined maternal-fetal hypothyroidism. Current guidelines recommend their measurement only if mothers have known autoimmune thyroid disease, there is a history of a previously affected sibling, or when transient CH is suspected. Results: We report 3 infants in whom the diagnosis of maternal hypothyroidism was not known and was identified only after CH was diagnosed in their babies. One of these infants had developmental delay despite rapid normalization of thyroid function postnatally. All 3 mothers had potent TSHR Abs in serum, but thyroid peroxidase Abs and thyroglobulin Abs were detectable in only 2 of them. Conclusions: TSHR-blocking Ab-induced CH should be suspected in any baby with CH irrespective of the known family history, especially if the hypothyroidism is severe and a eutopic thyroid gland is demonstrated on imaging. Measurement of TSHR Abs is necessary to establish the diagnosis; the presence of other thyroid Abs is insufficiently sensitive and may miss some cases.

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Maternal Thyroid-Blocking Immunoglobulins in Congenital Hypothyroidism*

Cited by 35 publications

References 23 publications

Transient congenital hypothyroidism due to maternal thyrotrophin binding inhibiting immunoglobulin

Transient congenital hypothyroidism due to maternal thyrotrophin binding inhibiting immunoglobulin

The Disorders Induced by Iodine Deficiency

Severe Unsuspected Maternal Hypothyroidism Discovered after the Diagnosis of Thyrotropin Receptor-Blocking Antibody-Induced Congenital Hypothyroidism in the Neonate: Failure to Recognize and Implications to the Fetus

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