Fetal Goitrous Hypothyroidism due to Maternal Thyroid Stimulation-Blocking Antibody: A Case Report

Ohira, Satoshi; Miyake, Masako; Kobara, Hisanori; Kikuchi, Norihiko; Osada, Ryosuke; Ashida, Takashi; Hirabayashi, Kanae; Nishio, Shintaro; Kanai, Masashi; Shiozawa, Tanri

doi:10.1159/000320098

Cited by 6 publications

(4 citation statements)

References 46 publications

(12 reference statements)

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“…A positive correlation exists between a high level of maternally transmitted antibodies and the appearance of signs of hyperthyroidism in the fetus, which explains why fetal hyperthyroidism develops during the second half of pregnancy and in mothers with a high antibody level [ 14 ]. In most cases, TRAbs have a stimulating effect; however, in rare cases, their action can be inhibitory [ 15 ].…”

mentioning

confidence: 99%

Study of the Factors Leading to Fetal and Neonatal Dysthyroidism in Children of Patients With Graves Disease

Banigé

Estellat

Biran

et al. 2017

Journal of the Endocrine Society

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ContextNeonatal hyperthyroidism was first described in 1912 and in 1964 was shown to be linked to transplacental passage of maternal antibodies. Few multicenter studies have described the perinatal factors leading to fetal and neonatal dysthyroidism.ObjectiveTo show how fetal dysthyroidism (FD) and neonatal dysthyroidism (ND) can be predicted from perinatal variables, in particular, the levels of anti-thyrotropin receptor antibodies (TRAbs) circulating in the mother and child.Design and PatientsThis was a retrospective multicenter study of data from the medical records of all patients monitored for pregnancy from 2007 to 2014.SettingAmong 280,000 births, the medical records of 2288 women with thyroid dysfunction were selected and screened, and 417 women with Graves disease and positive for TRAbs during pregnancy were included.ResultsUsing the maternal TRAb levels, the cutoff value of 2.5 IU/L best predicted for FD, with a sensitivity of 100% and specificity of 64%. Using the newborn TRAb levels, the cutoff value of 6.8 IU/L best predicted for ND, with a sensitivity of 100% and a specificity of 94%. In our study, 65% of women with a history of Graves disease did not receive antithyroid drugs during pregnancy but still had infants at risk of ND.ConclusionsIn pregnant women with TRAb levels ≥2.5 IU/L, fetal ultrasound monitoring is essential until delivery. All newborns with TRAb levels ≥6.8 IU/L should be examined by a pediatrician with special attention for thyroid dysfunction and treated, if necessary.

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mentioning

confidence: 99%

Study of the Factors Leading to Fetal and Neonatal Dysthyroidism in Children of Patients With Graves Disease

Banigé

Estellat

Biran

et al. 2017

Journal of the Endocrine Society

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“…In this case, the discovery of congenital hypothyroidism in a neonate led to the diagnosis of maternal hypothyroidism. No fetal goiter was observed during pregnancy even though it has been described in a previous case report [16]. The signs and severity of hypothyroidism may vary among newborns [13].…”

Section: Discussionmentioning

confidence: 88%

Congenital Hypothyroidism due to a Low Level of Maternal Thyrotropin Receptor-Blocking Antibodies

et al. 2020

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Introduction: Maternal TSH receptor antibodies (TRAbs) can cross the placenta and affect fetal and neonatal thyroid function. Maternal TSH receptor-blocking antibodies (TBAbs) are a rare cause of congenital hypothyroidism. Case Report: Following the discovery of a highly elevated TSH on her neonatal screening test, a 10-day-old girl with no familial history of thyroid disorder was referred to the pediatric endocrinology unit. Hypothyroidism was confirmed with a highly elevated TSH (817 mIU/L, reference range 0.4–3.1) and very low levels of FT4 (1.8 pmol/L, reference range 12–22). Anti-TPO antibodies were at 81 IU/mL (reference range <34), TRAbs at 1.7 IU/L (reference range <1.75), and thyroglobulin at 9.4 µg/L (reference range 3.5–77). The thyroid appeared normal on ultrasonography, and no radioiodine uptake was seen on the scintigraphy after the perchlorate discharge test. Concomitantly, a severe maternal hypothyroidism was discovered (TSH 224 mIU/L). The maternal ultrasound appeared normal, anti-TPO antibodies were moderately elevated, and TRAbs were at 3.2 IU/L. TBAbs activity was measured in the mother and her daughter, and a very high and similar blocking activity was observed in both patients (TBAbs 89%, reference range <10%). L-thyroxine treatment was introduced in the newborn and was successfully discontinued at 6.5 months of age, as the TBAbs activity decreased. Conclusion: We report herein a case of transient congenital hypothyroidism with a normal neonatal TRAbs level. In case of maternal TBAbs, similar activity of maternal TBAbs must be expected in the neonate, independently of the neonatal level of TRAbs.

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“…As a normal thyroid gland’s signal intensity is as low as that of muscle on T2-weighted images, the presence of a signal that is higher than that associated with muscle signifies a hypofunctioning thyroid gland [16]. Table 1 summarizes our review of previous reports that describe MRI findings from fetal goiters between 2000 and 2018 [13,15,[17], [18], [19], [20], [21], [22], [23], [24], [25], [26], [27]]. Without a maternal thyroid gland abnormality, fetal hypothyroidism is characterized by a fetal thyroid gland that shows a hyperintense signal on T2-weighted images.…”

Section: Diagnosis Of Fetal Goiter and Thyroid Statusmentioning

confidence: 99%

“…ATD: antithyroid drug; GA: gestational age; WGA: weeks of gestation; TSH: thyroid-stimulating hormone; T 4 : thyroxine; LT 4 : levothyroxine; PTU: propylthiouracil; MMI: methimazol; N/A: not available; EFW: estimated fetal weight; FGR: fetal growth restriction; CS: cesarean delivery; VD: vaginal delivery; TTN: transient tachypnea of the newborn; RDS: respiratory distress syndrome. Reference ranges of fetal thyroid function according to Thorpe-Beeston et al are: TSH: 2–12 mIU/L; Free T 4 : 5.1–27 pmol/L; T 4 : 15–125 nmol/L [24]. Reference ranges of neonatal thyroid function according to Fisher are: TSH: 1–39 mIU/L; free T 4 : 28–68 pmol/L; T 4 : 142–277 nmol/L [10].…”

Section: Intrauterine Treatment Of Fetal Goitermentioning

confidence: 99%

Current knowledge about the in utero and peripartum management of fetal goiter associated with maternal Graves’ disease

Iijima

2019

European Journal of Obstetrics & Gynecology and Reproductiv

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Maternal Graves’ disease is the most common cause of fetal goiter. Fetal goiter can cause complications attributable either to the physical effects of the goiter itself or to thyroid dysfunction, which can be life-threatening and cause neurological impairment. Determining whether a goiter is caused by fetal hyperthyroidism or hypothyroidism is the main clinical problem, and in utero evaluations and management are essential. Ultrasonography combined with color Doppler and magnetic resonance imaging are helpful for the initial diagnosis and monitoring, but these imaging techniques have a limited ability to discriminate between fetal hyperthyroidism and hypothyroidism. To determine the fetal thyroid status, fetal blood sampling using cordocentesis is reliable but hazardous, and the indications must be considered carefully. Amniocentesis is an easier and safer alternative, but the correlations between the amniotic fluid and fetal serum thyroid hormone levels remain unclear. If a fetal goiter is accompanied by hypothyroidism, administering thyroid hormone intra-amniotically may be effective and relatively safe. However, the wide variety of approaches to treatment exemplifies the lack of guidelines, and no systematic studies have been conducted to date. Therefore, intrauterine treatment should be reserved for selected patients at a high risk of complications. Moreover, when intrauterine treatment fails and a fetal goiter can cause airway obstruction, intrapartum management, such as ex utero intrapartum treatment, may be required; however, reports describing the use of this procedure for fetal goiter are limited. This review summarizes the current knowledge about fetal goiter associated with maternal Graves’ disease and evaluates the most significant new findings regarding its in utero and peripartum management.

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Fetal Goitrous Hypothyroidism due to Maternal Thyroid Stimulation-Blocking Antibody: A Case Report

Cited by 6 publications

References 46 publications

Study of the Factors Leading to Fetal and Neonatal Dysthyroidism in Children of Patients With Graves Disease

Study of the Factors Leading to Fetal and Neonatal Dysthyroidism in Children of Patients With Graves Disease

Congenital Hypothyroidism due to a Low Level of Maternal Thyrotropin Receptor-Blocking Antibodies

Current knowledge about the in utero and peripartum management of fetal goiter associated with maternal Graves’ disease

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