Diagnosis and Management of Fetal and Neonatal Thyrotoxicosis

Abstract

Background and Objectives: Clinical fetal thyrotoxicosis is a rare disorder occurring in 1-5% of pregnancies with Graves’ disease. Although transplacental passage of maternal TSH receptor stimulating autoantibodies (TRAb) to the fetus occurs early in gestation, their concentration in the fetus is reduced until the late second trimester, and reaches maternal levels in the last period of pregnancy. The mortality of fetal thyrotoxicosis is 12–20%, mainly due to heart failure. Case report: We present a case of fetal and neonatal thyrotoxicosis with favorable evolution under proper treatment in a 37-year-old woman. From her surgical history, we noted a thyroidectomy performed 12 years ago for Graves’ disease with orbitopathy and ophthalmopathy; the patient was hormonally balanced under substitution treatment for post-surgical hypothyroidism and hypoparathyroidism. From her obstetrical history, we remarked a untreated pregnancy complicated with fetal anasarca, premature birth, and neonatal death. The current pregnancy began with maternal euthyroid status and persistently increased TRAb, the value of which reached 101 IU/L at 20 weeks gestational age and decreased rapidly within 1 month to 7.5 IU/L, probably due to the placental passage, and occurred simultaneously with the development of fetal tachycardia, without any other fetal thyrotoxicosis signs. In order to treat fetal thyrotoxicosis, the patient was administered methimazole, in addition to her routine substitution of 137.5 ug L-Thyroxine daily, with good control of thyroid function in both mother and fetus. Conclusions: Monitoring for fetal thyrotoxicosis signs and maternal TRAb concentration may successfully guide the course of a pregnancy associated with Graves’ disease. An experienced team should be involved in the management.

Diagnosis and Management of Fetal Arrhythmias in the Current Era

“…Over the past 15 to 20 years, fetal cardiologists and obstetricians have become increasingly aware of the shortcomings of these definitions, with much research demonstrating that “subtle” arrhythmias may be missed with these broad heart rate limits [ 3 , 8 , 9 ]. Persistent FHR elevations just above the upper limit of “normal” may go unrecognized as markers of fetal thyrotoxicosis, for example [ 10 , 11 ]. Even more problematic are FHRs within the “normal” range that mask potentially lethal channelopathies, like long QT syndrome (LQTS) [ 8 , 9 ].…”

Atualizações sobre a doença de Graves neonatal: Principais avaliações diagnósticas e tratamentos

“…Esses hormônios são substanciais para o desenvolvimento adequado do sistema nervoso central, crescimento ósseo, metabolismo e função cardiovascular. No caso do hipertireoidismo neonatal, a tireoide do bebê produz quantidades excessivas de hormônios tireoidianos, resultando em um estado de hiperatividade (Bohîlțea et al, 2022).…”

“…O Hipertireoidismo neonatal permanente, por sua vez, ocorre quando o hipertireoidismo persiste ao longo do tempo, não sendo transitório como na condição anterior. Pode estar associado a distúrbios genéticos hereditários, como a doença de Graves neonatal ou defeitos na produção ou ação dos hormônios tireoidianos (Bohîlțea et al, 2022).…”