Abstract:Background: Iodine is necessary for fetal thyroid development. Excess maternal intake of iodine can cause fetal hypothyroidism due to the inability to escape from the Wolff-Chaikoff effect in utero. Case Report: We report a case of fetal hypothyroid goiter secondary to inadvertent excess maternal iodine ingestion from infertility supplements. The fetus was successfully treated with intra-amniotic levothyroxine injections. Serial fetal blood sampling confirmed fetal escape from the Wolff-Chaikoff effect in the … Show more
“…Fetal goiter is a rare condition that results of either fetal hypothyroidism or hyperthyroidism. It can cause several complications 5 and has several etiologies: congenital dyshormonogenesis, deficiency or excess of iodine or transplacental passage of maternal TRAb or ATD 6 . Maternal Graves’ disease accounts for more than 60% of fetal goiter 7 .…”
We present a rare documented case with consecutive hypo‐ and hyperthyroidism during fetal life. First, hypothyroidism was due to transplacental passage of antithyroid drugs. After the mother's thyroidectomy, fetal hyperthyroidism was due to transplacental passage of persistent anti‐thyrotropin receptor antibodies. Fetal goiter disappeared after adjusting maternal treatment.
“…Fetal goiter is a rare condition that results of either fetal hypothyroidism or hyperthyroidism. It can cause several complications 5 and has several etiologies: congenital dyshormonogenesis, deficiency or excess of iodine or transplacental passage of maternal TRAb or ATD 6 . Maternal Graves ’ disease accounts for more than 60% of fetal goiter 7 .…”
We present a rare documented case with consecutive hypo‐ and hyperthyroidism during fetal life. First, hypothyroidism was due to transplacental passage of antithyroid drugs. After the mother's thyroidectomy, fetal hyperthyroidism was due to transplacental passage of persistent anti‐thyrotropin receptor antibodies. Fetal goiter disappeared after adjusting maternal treatment.
“…The Table 2 summarizes the therapeutic management, laboratory results, short‐ and long‐term outcomes of 21 cases reports of non‐immune hypothyroidism fetal goiter during the last ten years 6,31‐45 . Finally, IAIs likely prevented the hearing loss in a fetus with iodine‐induced hypothyroidism, highlighting the impact of prenatal TH substitution on complications 46,47 …”
Indications and administration of intra‐amniotic infusions of L‐thyroxine in the context of non‐immune fetal hypothyroidism with goiter lack of standardization. Systematic follow‐up of clinical features related to thyroid hormonal homeostasis may be useful to evaluate their efficiency and develop standardized management guidelines.
“…In cases of fetal thyroid dysfunction, it seems that placental deiodinases are inhibited and, moreover, the intracellular activation to triiodothyronine in the fetal brain activated, protecting the brain from permanent damage (Girling 2003 ). Nevertheless, it has also been reported that only transient hypothyroidism can impair the long-term mental development of the children or cause hearing impairments (Derksen-Lubsen et al 1996 ; Kempers et al 2006 ; Jourdain et al 2010 ; Overcash et al 2016 ), and screening at birth with postnatal treatment may not be sufficient to ascertain unimpaired neurodevelopment (Hardley et al 2018 ). Therefore, the potential risks of side effects on the fetus resulting from iodine blockade should not be underestimated.…”
In the case of a nuclear power plant accident, repetitive/prolonged radioiodine release may occur. Radioiodine accumulates in the thyroid and by irradiation enhances the risk of cancer. Large doses of non-radioactive iodine may protect the thyroid by inhibiting radioiodine uptake into the gland (iodine blockade). Protection is based on a competition at the active carrier site in the cellular membrane and the Wolff–Chaikoff effect, the latter being, however, only transient (24–48 h). Perchlorate may alternatively provide protection by a carrier competition mechanism only. Perchlorate has, however, a stronger affinity to the carrier than iodide. Based on an established biokinetic–dosimetric model developed to study iodine blockade, and after its extension to describe perchlorate pharmacokinetics and the inhibition of iodine transport through the carrier, we computed the protective efficacies that can be achieved by stable iodine or perchlorate in the case of an acute or prolonged radioiodine exposure. In the case of acute radioiodine exposure, perchlorate is less potent than stable iodine considering its ED
50.
A dose of 100 mg stable iodine has roughly the same protective efficacy as 1000 mg perchlorate. For prolonged exposures, single doses of protective agents, whether stable iodine or perchlorate, offer substantially lower protection than after acute radioiodine exposure, and thus repetitive administrations seem necessary. In case of prolonged exposure, the higher affinity of perchlorate for the carrier in combination with the fading Wolff–Chaikoff effect of iodine confers perchlorate a higher protective efficacy compared to stable iodine. Taking into account the frequency and seriousness of adverse effects, iodine and perchlorate at equieffective dosages seem to be alternatives in case of short-term acute radioiodine exposure, whereas preference should be given to perchlorate in view of its higher protective efficacy in the case of longer lasting radioiodine exposures.
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