Hyperthyroid Fetal Goiter: A Case Report

Vedi Loue

doi:10.11648/j.jgo.20190703.14

Abstract

The persistent presence of maternal thyroid-stimulating hormone receptor antibody in patients with Graves’disease could cause fetal hyperthyroid goiter during pregnancy. The recognition and treatment of hyperthyroid fetal goiter are believed to be very important to optimize growth and intellectual development in affected fetuses. We report here, a case of a hyperthyroid fetal goiter identified by ultrasound exam at 27 weeks 5 days of gestation in a women having Graves’ disease and on antithyroid drugs therapy. This observation shows the fetal risk associated with the persistence of anti-TSH receptor antibodies in mothers with Graves' disease and the possibility of fetal approach.

Highlights

Fetal goiter, which signals a thyroid dysfunction, is a rare condition
The second, which is very rare, is of genetic origin and is linked either to the mutation of the thyroid stimulating hormone (TSH) receptor or to an activating mutation of Guanine Nucleotide binding protein Alpha Stimulating (GNAS) gene: this gene encodes the alpha subunit of the G protein coupled to adenylate cyclase, whose role is to induce the synthesis of thyroid hormones [5]
Graves’ disease is the most common cause of hyperthyroidism. It is an autoimmune thyroiditis in which maternal autoantibodies stimulate the overproduction of thyroid hormones by the thyroid follicular cells, inducing a state of hyperthyroidism. These immunoglobulins, IgG type, have two types of possible action: some stimulate the synthesis of Cyclic Adenosine Monophosphate by these cells, these are the thyroid stimulating immunoglobulins (TSI) while other antibodies will block the binding of TSH with its receptor, these are the thyroid binding inhibiting Immunoglobulins (TBII)

Summary

Introduction

Fetal goiter, which signals a thyroid dysfunction, is a rare condition. It can be caused by several different pathologies: including dysgenesis, dyshormonogenesis, maternal ingestion of antithyroid drugs, transplacental passage of maternal antibodies, thyroid stimulating hormone receptor mutation, or tumors [1]. The persistent presence of maternal thyroid-stimulating hormone receptor antibody (Trab) in patients with Graves’ disease could cause fetal hyperthyroid goiter during pregnancy by stimulating the thyroid gland, leading to excessive thyroid hormone secretion. Graves’ disease and on antithyroid drugs therapy. Through this case, we recall the physiopathological, diagnostic and therapeutic aspects of this pathology

Case Presentation

Physiopathology

Diagnosis

Treatment

Findings

Conclusion