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​Cihat Şen, ​Nicola Volpe

Cecilia Villalain, Daniel Rolnik, M. Mar Gil

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Murat Yayla

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Resul Arısoy

OP-002 Excessive prenatal supplementation of ıodine and fetal goiter; report of managment conservatively of fetal goiter: a case report

Birsen Konukcu

Article info

OP-002 Excessive prenatal supplementation of ıodine and fetal goiter; report of managment conservatively of fetal goiter: a case report. Perinatal Journal 2024;32(2024):1-3 DOI: 10.59215/prn.24.032supp002

Author(s) Information

Birsen Konukcu

  1. Antalya City Hospital, Department of Perinatology Antalya, Turkiye

Birsen Konukcu, Antalya City Hospital, Department of Perinatology Antalya, Turkiye, [email protected]

Publication History

Manuscript Received: April 25, 2024

Manuscript Accepted: May 01, 2024

Publication date: May 18, 2024

Conflicts of Interest

No conflicts declared.

Iodine is an essential mineral for the synthesis of thyroid hormones, so its deficiency can lead to serious problems. Therefore, routine iodine supplementation is recommended for pregnant women by World Health Organization .
Fetal thyroid disorder is uncommon, and typically arises in the context of a managed maternal thyroid condition. Antithyroid therapy in mothers contributes to 10–15% of cases of congenital hypothyroidism in fetuses.

The excessive iodine ingestion above daily intake limits during the pregnancy is a well-known mechanism  among the known causes of fetal goiter. The occurrence of fetal goiter in babies of euthyroid mothers is quite rare.

Fetal goiter, due to the maternal and fetal complications it causes, affects long-term morbidity and mortality. Among these complications are polyhydramnios, intrauterine growth restriction (IUGR), preterm birth, labor dystocia, hypoxia and brain damage resulting from airway obstruction caused by this mass.
At 24 weeks pregnant, a 27-year-old primigravida was referred for a routine second trimester ultrasound evaluation despite not having a relevant family history or any personal thyroid or autoimmune illness. which showed cervical hyperextension and a high vascularized, bilobed, and symmetric mass in the anterior region of the fetal neck measuring 2.6 cm cranio-caudal × 1.5 cm transverse >%95 SD, suggesting fetal goiter.  No signs of polyhydramnios, and no other fetal anomalies were found. Overall, these findings stated fetal goiter.
The patient seemed to be clinically euthyroid and denied having ever had thyroid problems. Thyroid function tests performed on the mother's serum were also normal. Thyroid peroxidase and anti-thyroglobulin antibodies were both within the reference range. No known medication exposures occurred. The only prescription she was known to be taking was a prenatal vitamin.
On the 24th week of gestation, the mother's urine iodine content was 972 µg/L /24 h (normal range: 150–249 µg /24 h).
When a detailed anamnesis was taken, it was learned that the patient had misunderstood the recommended dose of medication. It was learned that instead of two drops (250 µg), she used two droppers full of medicine (estimated 5000 µg) starting from the 4th week of pregnancy. Supplements were immediately discontinued and followed up at two week intervals.The patient was informed about the possibility of fetal goiter and hypothyroidism due to excessive iodine intake, along with all associated risks. Amniocentesis and cordocentesis were discussed, and it was explained that fetal TSH measurement would determine the treatment plan as needed, but she did not accept this  and intra-amniotic therapy because of the potential risks of the procedures. She declined the invasive procedures  and preferred to proceed with expectant management. Subsequent ultrasounds demonstrated resolution of the fetal goiter. During follow -up late onset IUGR was observed.
 At 37 weeks gestation, she had ceserian delivery, and the result was a 2340 g girl baby. The thyroid was not palpable at delivery. By the day of birth, postnatal thyroid scans showed a steady state of euthyroidism. The newborn's hearing screen confirmed both sides of the response to be normal. The baby was euthyroid, healthy, and reaching all developmental milestones at eight months of age.
This case report sheds light on the consequences of maternal excessive iodine intake, which can result in conditions such as fetal goiter, as seen in our case. Additionally, this case presentation demonstrates the immaturity of the Wolff-Chaikoff effect in fetuses, indicating that they have not yet developed the ability to escape from it. The fetus is thought to be particularly susceptible to the suppressive effects of excessive iodine because it cannot avoid the Wolff-Chaikoff effect, a defensive mechanism that stops the creation of excess thyroid hormone in the event that plasma iodine levels abruptly rise.Excessive iodine consumption in healthy individuals momentarily and abruptly impairs thyroid hormone secretion and thyroid biosynthesis. Following an extended period of exposure to high levels of iodine, organification and thyroid hormone biosynthesis proceed normally. The developing fetal and neonatal thyroid gland is unable to reduce intracellular iodine transport, in contrast to adults and children. Thus, the fetus continues to be hypothyroid. Because fetuses have not yet developed the ability to escape from the Wolff-Chaikoff effect before 36 weeks, excess iodine can result in persistent fetal hypothyroidism . This effect resolves when the excessive iodine supplementation is removed. During pregnancy and childbirth, complications associated with fetal goiter may occur. Tracheal compression can result in postnatal asphyxia, intrathyroidal arteriovenous shunting can lead to high-output cardiac failure in the fetus and subsequent hydrops, and esophageal compression may diminish the fetus's capacity to ingest amniotic fluid, contributing to polyhydramnios, thereby increasing the likelihood of preterm delivery. In addition, neck hyperextension from the goiter could result in malpresentation during delivery and delivery dystocia may occur. In our case, three weeks after discontinuation of iodine, fetal goiter had resolved, and fetal neck hyperextension had improved on examination. Therefore, these complications were not observed in our case.
One of the obstetric complications seen in cases of fetal goiter is intrauterine growth retardation (IUGR).IUGR developed.
Our case highlights the importance of timely diagnosis and management of fetal goiter to prevent potential obstetric complications . While antenatal detection and treatment options were limited in our case due to patient preferences, postnatal assessments showed positive outcomes, including the resolution of fetal goiter and normal bilateral hearing tests.
Another point we want to emphasize with this study is that clinicians and healthcare providers should carefully review the medications and supplements used by patients and ensure they are being used at the correct dosage. Improper use of any medication can lead to teratogenic effects.

Hypothyroidism, intrauterine treatment, euthyroid, fetal goiter, iodine supplementation

Figure 1
Coronal view of the one lobule of visible thyroid goiter on the anterior face
Figure 2
Sagittal view of the 24-week fetus with a visible thyroid goiter on the anterior face and hyperextension neck
Figure 3
Ultrasound demonstrating two hypoechogenic symetric masses measuring 30 mm transvers lenght
Figure 4
Color Doppler of the fetal goiter, hypervascularization of the fetal thyroid gland