Maternally Transferred Thyroid Disease in the Infant: Recognition and Treatment

Foley, Thomas P.

doi:10.1007/978-1-4684-5973-9_12

Cited by 11 publications

(13 citation statements)

References 32 publications

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“…Uncontrolled hyperthyroidism or a high TRAb value during pregnancy is a risk for low birth weight (<2500 g), prematurity and eclampsia [28]. The transplacental transfer of TSH receptor antibodies may cause intrauterine death or fetal and neonatal hyperthyroidism [7][8][9][10][11]. Mortimer et al reported that neonatal hyperthyroidism was seen in 8% (4/48) of births in women with active Graves' disease, and that maternal TRAb values exceeded 70% at delivery in all 4 births [38].…”

Section: Discussionmentioning

confidence: 99%

“…The continuation of a high (elevated) TRAb value or an increased TRAb value after surgery may cause hyperthyroidism recurrence [3,4]. In addition, previous studies demonstrated that a high TRAb value is linked to endocrine opthalmopathy [5,6], or risk for intrauterine death, and fetal or neonatal hyperthyroidism in pregnant women with Graves' disease [7][8][9][10][11][12].…”

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confidence: 99%

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Changes in Serum TSH Receptor Antibody (TRAb) Values in Patients with Graves' Disease after Total or Subtotal Thyroidectomy

et al. 2003

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Abstract. TSH receptor antibodies (TRAb) are generally regarded as mediators of thyroid stimulation in Graves' disease. In addition, a high serum TRAb value during pregnancy is one of the risk factors for intrauterine death, prematurity, and fetal or neonatal hyperthyroidism. Recently, correlations between a high serum TRAb value and endocrine opthalmopathy were also suggested. Surgical resection of the thyroid is usually followed by a reduction of serum TRAb levels in variable degrees. The relation between the extent of the thyroidectomy and the degree of reduction is still controversial. In addition, the changes in the TRAb value after total thyroidectomy (TT) over a long period of time have never been studied. We studied the changes in serum TRAb values after TT and subtotal thyroidectomy (ST) for more than 7 years. Forty-one patients with Graves' disease underwent TT, and 99 patients underwent ST. The serum TRAb values and the ratio of the patients who achieved normal values among each group (normalization rates of TRAb) at 3 and 6 months, 1, 3, 5 and 7 years after surgery were compared between the TT group and ST group. The mean preoperative TRAb values were not significantly different between the TT and ST groups, and the mean TRAb values measured 3, 6 and 12 months after surgery were not significantly different between the groups. However, the TRAb values measured 3, 5 and 7 years after surgery were significantly (p<0.05) lower in the TT group than in the ST group (16.7 ± 3.3% vs 28.0 ± 2.6%, 12.6 ± 3.4% vs 29.3 ± 3.8%, 5.6 ± 0.9% vs 25.4 ± 4.1%, respectively). The normalization rates of TRAb were not significantly different between the groups until 1 year after surgery. However, the normalization rates 3, 5 and 7 years after surgery were significantly (p<0.05) higher in the TT group than in the ST group (65.7% vs 42.4%, 77.3% vs 46.7%, 100% vs 59.1%, respectively). The surgical complication rates of TT were similar to ST except for permanent hypoparathyroidism. TT is a treatment option for Graves' disease, especially in patients with a high TRAb value who wish to have children or who have Graves' opthalmopathy.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Changes in Serum TSH Receptor Antibody (TRAb) Values in Patients with Graves' Disease after Total or Subtotal Thyroidectomy

et al. 2003

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“…TSH-binding inhibiting antibodies, which block the binding of TSH to its receptor, can also be present in the mother. Their transplacental passage has been demon¬ strated, and the signs that result are due to the balance be¬ tween the stimulating action of the TSI and the inhibitory action of the TSH-binding inhibiting antibodies (10,11). In this form of hyperthyroidism, thyrotoxicosis disappears with the clearance of the maternal antibodies, and usually signs disappear during the first 4 months of life (10,11).…”

Section: Pathogenesis Of Neonatal Hyperthyroidismmentioning

confidence: 96%

“…This increase in cAMP is the consequence of the stimulation of the adenylate cyclase in the thyrocytes. This leads to an increase of thyroid hor¬ mone secretion, and as a consequence, to thyrotoxicosis first in utero then in the neonatal period until the disap¬ pearance of the transmitted antibodies (1,10,11). The fe¬ tal thyroid gland begins secreting thyroid hormone around 12 weeks gestation; the TSH receptor starts responding to the stimulation of TSH and therefore to the stimulation of the TSI during the second trimester of gestation (1,12).…”

Section: Pathogenesis Of Neonatal Hyperthyroidismmentioning

confidence: 98%

Hyperthyroidism in Early Infancy: Pathogenesis, Clinical Features and Diagnosis with a Focus on Neonatal Hyperthyroidism

Polak¹

1998

Thyroid

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Neonatal hyperthyroidism has mostly been described in the context of maternal Graves' disease. It has been estimated that about 0.2% of pregnant women have Graves' disease; however only 1% of the children born to these women are described as having hyperthyroidism. In most of the cases, the disease is due to maternal antibodies transferred from the mother into the fetal compartment, which stimulate the fetal thyroid by binding to the thyrotropin (TSH) receptor. In this form of neonatal hyperthyroidism, thyrotoxicosis disappears with the clearance of the maternal antibodies and usually signs disappear during the first 4 months of life. Rare forms of persistent, nonimmune neonatal hyperthyroidism are explained by molecular abnormalities of the TSH receptor. Prematurity is frequent, as well as hypotrophia. Tachycardia, goiter, hyperexcitability, poor weight gain, hepatomegaly and/or splenomegaly, stare and/or eyelid retraction are among the most frequent neonatal thyrotoxicosis clinical signs. Diagnosis is based on the determination of the blood level of thyroxine (T4), triiodothyronine (T3), and TSH. Even if these levels are normal in the cord blood, tests should be repeated 3 to 10 days later to detect possible delayed appearance of the disorder. These parameters should be interpreted according to the age of the neonate. To confirm the immune nature of this hyperthyroidism, thyroid-stimulating immunoglobulins (TSI) should be determined. The TSI determination is crucial in identifying nonimmune causes of neonatal hyperthyroidism: in this neonatal hyperthyroidism, TSI are not detected, either by radioreceptor assay and/or by functional assay, and molecular studies are needed to identify the mutation. Mutation of the TSH receptor leading to its constitutive activation and to neonatal hyperthyroidism have been described. Germline mutations are found in hereditary hyperthyroidism; de novo germline mutations can cause sporadic congenital hyperthyroidism.

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“…In three reported cases the fetus was exposed to PTU, however, these infants had a mild elevation in liver en-zymes compared to the elevation reported in unexposed cases, including our two patients who were not exposed to PTU. Enlargement of the reticuloendothelial system seen in neonatal Graves' disease may disrupt hepatic architecture and cause cholestasis [32].…”

Section: Discussionmentioning

confidence: 99%

Neonatal Graves’ Disease and Cholestatic Jaundice: Case Series and Review of the Literature

Almadhoun¹,

Rivera-Penera²,

Lipeski³

2015

OJPed

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Cholestatic jaundice and elevated liver enzymes are uncommon, but recognized, manifestations of neonatal thyrotoxicosis. Current guidelines for evaluation of cholestatic jaundice and reviews in Neonatology literature do not discuss hyperthyroidism in the differential diagnosis of cholestatic jaundice. We report two cases of neonatal thyrotoxicosis secondary to neonatal Graves' disease that presented with cholestatic jaundice and elevated liver enzymes at birth. Early recognition of thyrotoxicosis as a cause of the hepatic disease in the neonate is crucial to prevent unnecessary diagnostic procedures and to initiate timely treatment.

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Maternally Transferred Thyroid Disease in the Infant: Recognition and Treatment

Cited by 11 publications

References 32 publications

Changes in Serum TSH Receptor Antibody (TRAb) Values in Patients with Graves' Disease after Total or Subtotal Thyroidectomy

Changes in Serum TSH Receptor Antibody (TRAb) Values in Patients with Graves' Disease after Total or Subtotal Thyroidectomy

Hyperthyroidism in Early Infancy: Pathogenesis, Clinical Features and Diagnosis with a Focus on Neonatal Hyperthyroidism

Neonatal Graves’ Disease and Cholestatic Jaundice: Case Series and Review of the Literature

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