Fetal/neonatal Thyrotoxicosis in a Newborn From a Hypothyroid Woman With Hashimoto’s Thyroiditis

Kiefer, Florian W.; Klebermass-Schrehof, Katrin; Steiner, Manuel; Worda, Christof; Kasprian, Gregor; Diana, Tanja; Kahaly, George J.; Gessl, Alois

doi:10.1210/jc.2016-2999

Cited by 28 publications

(29 citation statements)

References 7 publications

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“…In contrast, the highly sensitive cell-based bioassays [26][27][28][29][30][31][32][33] exclusively differentiate between the TSH-R-stimulating Ab (TSAb) and TSH-R-blocking Ab [34,35]. Also, TSAb is a highly sensitive and predictive biomarker for the extrathyroidal manifestations of GD [36][37][38][39][40][41][42] as well as a useful predictive measure of fetal or neonatal hyperthyroidism [43,44]. Finally, the incorporation and early utilization of TSAb into current diagnostic algorithms conferred a 46% shortened time to diagnosis of GD and a cost saving of 47% [45].…”

Section: Serologymentioning

confidence: 99%

“…In line with this and as a strong recommendation, all patients with a history of autoimmune thyroid disease should have their TSH-R-Ab serum levels measured at the first presentation of pregnancy using either a sensitive binding or a functional cell-based bioassay, and, DOI: 10.1159/000490384 if they are elevated, again at 18-22 weeks of gestation [5, 21-23, 43, 44, 149, 150]. Finally, fetal/neonatal hyperthyroidism requires an acute management, including MMI, beta-blockade, and cardiovascular support therapy [43].…”

Section: Pregnant Women and Gdmentioning

confidence: 99%

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2018 European Thyroid Association Guideline for the Management of Graves’ Hyperthyroidism

Kahaly¹,

Bartalena²,

Hegedüs³

et al. 2018

Eur Thyroid J

657

650

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Graves’ disease (GD) is a systemic autoimmune disorder characterized by the infiltration of thyroid antigen-specific T cells into thyroid-stimulating hormone receptor (TSH-R)-expressing tissues. Stimulatory autoantibodies (Ab) in GD activate the TSH-R leading to thyroid hyperplasia and unregulated thyroid hormone production and secretion. Diagnosis of GD is straightforward in a patient with biochemically confirmed thyrotoxicosis, positive TSH-R-Ab, a hypervascular and hypoechoic thyroid gland (ultrasound), and associated orbitopathy. In GD, measurement of TSH-R-Ab is recommended for an accurate diagnosis/differential diagnosis, prior to stopping antithyroid drug (ATD) treatment and during pregnancy. Graves’ hyperthyroidism is treated by decreasing thyroid hormone synthesis with the use of ATD, or by reducing the amount of thyroid tissue with radioactive iodine (RAI) treatment or total thyroidectomy. Patients with newly diagnosed Graves’ hyperthyroidism are usually medically treated for 12–18 months with methimazole (MMI) as the preferred drug. In children with GD, a 24- to 36-month course of MMI is recommended. Patients with persistently high TSH-R-Ab at 12–18 months can continue MMI treatment, repeating the TSH-R-Ab measurement after an additional 12 months, or opt for therapy with RAI or thyroidectomy. Women treated with MMI should be switched to propylthiouracil when planning pregnancy and during the first trimester of pregnancy. If a patient relapses after completing a course of ATD, definitive treatment is recommended; however, continued long-term low-dose MMI can be considered. Thyroidectomy should be performed by an experienced high-volume thyroid surgeon. RAI is contraindicated in Graves’ patients with active/severe orbitopathy, and steroid prophylaxis is warranted in Graves’ patients with mild/active orbitopathy receiving RAI.

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Section: Serologymentioning

confidence: 99%

Section: Pregnant Women and Gdmentioning

confidence: 99%

2018 European Thyroid Association Guideline for the Management of Graves’ Hyperthyroidism

Kahaly¹,

Bartalena²,

Hegedüs³

et al. 2018

Eur Thyroid J

657

650

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show abstract

“…Indeed, recent evidence has proven that a patient can have both TSAb and TBAb by isolating monoclonal antibodies (MAb) with stimulatory and blocking activity from the lymphocytes of the same patient [11]. The measurement of TSAb and TBAb has potential clinical implications in the differential diagnosis of AITD, in predicting the outcome of GD after antithyroid drug treatment, in evaluating the risk of extrathyroidal manifestations of GD during pregnancy, and in predicting the likelihood of fetal/neonatal hyper-or hypothyroidism [10,12]. TSHR Ab can be measured with either a bioassay or a binding assay.…”

Section: Introductionmentioning

confidence: 99%

Performance and Specificity of 6 Immunoassays for TSH Receptor Antibodies: A Multicenter Study

Diana¹,

Wüster²,

Olivo³

et al. 2017

Eur Thyroid J

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Background: The measurement of TSH receptor (TSHR) antibodies is warranted for diagnosis of Graves' disease (GD).Objective: The performance, detection sensitivity, and specificity of 6 TSHR immunoassays were compared. Methods: Two bioassays and 4 binding assays (Kronus, Immulite, Kryptor, Dynex) were compared in a dilution study performed in patients with autoimmune thyroid disease. Both bioassays were compared to 2 binding assays using stimulatory (M22) and blocking (K1-70) monoclonal antibody (MAb) mixtures. Results: Thirty samples from stimulatory (TSAb)-positive/blocking (TBAb)-negative patients with GD were diluted serially and measured in all assays. Samples were positive until dilution 1:2,187 in the TSAb bioassay, 1:81 in the Immulite (p < 0.002 vs. bioassay) and Kronus ELISA (p = 0.039) assays, and 1:27 in the Kryptor and Dynex ELISA (p < 0.001 vs. bioassay). Ten samples from TBAb-positive/TSAb-negative patients with GD or Hashimoto's thyroiditis were positive in all binding assays. None of the binding assays differentiated between TSAb and TBAb. Mixtures of 100% K1-70 (200 ng/ mL), 80% K1-70 + 20% M22, 60% K1-70 + 40% M22, 40% K1-70 + 60% M22, 20% K1-70 + 80% M22, and 100% M22 (20 ng/mL) tested positive in both Immulite (26.4, 20.2, 15.2, 10.5,6.3, 2.00 IU/L) and Kronus assays (27.1, 23.3, 19.3, 12.0, 5.7, 2.2 IU/L). These MAb mixtures were tested in the TBAb bioassay and showed 82, 61, 24 (negative), -26 (negative), -77 (negative), and -95% (negative) inhibition, respectively. Conclusions: The sample dilution study showed higher detection sensitivity for the TSAb bioassay, and the antibody mixture study demonstrated exclusive specificity of the bioassays over all automated and ELISA binding assays.

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“…Fetal hyperthyroidism is a rare and potentially life‐threatening condition which is not always easy to detect. It is most commonly observed in maternal thyroid autoimmune disorders such as poorly controlled Grave's disease.…”

mentioning

confidence: 99%

“…It is most commonly observed in maternal thyroid autoimmune disorders such as poorly controlled Grave's disease. The main cause of fetal thyroid gland stimulation is transplacental passage of maternal thyroid stimulating immunoglobulins (TSIs) and the clinical manifestations of fetal thyrotoxicosis include fetal goiter, tachycardia, intrauterine growth restriction, non‐immune hydrops, craniosynostosis, accelerated bone maturation and intrauterine death. TSIs are the major autoantigens involved in Grave's disease, whereas thyroid peroxidase (TPO) and thyroglobulin (Tg) are the major autoantigens involved in Hashimoto's disease.…”

mentioning

confidence: 99%

Recurrent fetal thyrotoxicosis in woman with history of Hashimoto's thyroiditis

Rodó

Deambrogio

Serra

et al. 2017

Ultrasound in Obstet & Gyne

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Fetal/neonatal Thyrotoxicosis in a Newborn From a Hypothyroid Woman With Hashimoto’s Thyroiditis

Abstract: Diagnosis and management of fetal hyperthyroidism can be challenging. TSH receptor antibody testing should be considered in pregnant women with any history of autoimmune thyroid disease and symptoms of fetal hyperthyroidism.

Cited by 28 publications

References 7 publications

2018 European Thyroid Association Guideline for the Management of Graves’ Hyperthyroidism

2018 European Thyroid Association Guideline for the Management of Graves’ Hyperthyroidism

Performance and Specificity of 6 Immunoassays for TSH Receptor Antibodies: A Multicenter Study

Recurrent fetal thyrotoxicosis in woman with history of Hashimoto's thyroiditis

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