Neonatal hypothyroidism despite maternal tri-iodothyronine toxicosis: a management problem? (original) (raw)
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Fetal Hypothyroidism Complicating Medical Treatment of Thyrotoxicosis in Pregnancy
Clinical Endocrinology, 1975
Two women with thyrotoxicosis were treated with antithyroid drugs during pregnancy. One women had inadvertently received a therapeutic dose of radioiodine at 21 weeks gestation and the other suffered from severe thyrotoxicosis with a serum LATS level of 1850%. In both patients, the serum triiodothyronine was maintained above 500 ng/dl by the concurrent oral administration of this hormone. Despite this precaution, cord serum thyrotrophin levels were markedly elevated and both infants showed clinical signs of hypothyroidism at birth. This experience indicates that triiodothyronine does not prevent fetal hypothyroidism when given to the mother in pharmacological amounts.
Careful Assessment of Maternal Thyroid Function Can Prevent Cases of Fetal Goitrous Hypothyroidism
Fetal Diagnosis and Therapy, 2013
We feel that clarification is needed with regard to the maternal MMI therapy and thyroid status. First, MMI therapy was initiated upon discovery of a low fT4 level, no detectable thyroid antibodies, but suppressed TSH levels. We wonder what the reasons were for this treatment. The low fT4 level was not consistent with a diagnosis of hyperthyroidism (more likely hypothyroidism). The suppressed TSH found only 6 months after pregnancy could be a sign of postpartum thyroiditis defined by guidelines as 'thyroid dysfunction within the first year postpartum' (although this is almost always associated with antibody positivity) . According to guidelines, such patients should not be treated with antithyroid drugs (ATD), but followed in order to detect a possible subsequent hypothyroid period. Even in cases of subclinical hyperthyroidism (low TSH, normal fT4), thyroid function tests should be repeated after 3-6 months to make sure that the TSH is persistently suppressed before considering treatment with ATD . Unless the stated fT4 value is an error, the reported beneficial effect of MMI treatment is questionable, and we believe that the woman should not have been started on MMI therapy without further investigation. However, there are no details in the article of the woman's symptoms or clinical findings be-
BMJ Case Reports, 2019
Fetal goitrous hypothyroidism is a rare entity and is caused mainly by maternal treatment of Graves’ disease (GD). We report a case of a 22-year-old woman referred at 12 weeks of gestation due to hyperthyroidism subsequent to recently diagnosed GD. She started treatment with propylthiouracil and, at 21 weeks of gestation, fetal goitre was detected. A cordocentesis confirmed the diagnosis of fetal goitrous hypothyroidism, and intra-amniotic administration of levothyroxine (LT4) was performed and repeated through the pregnancy due to maintenance of fetal goitre. The pregnancy proceeded without further complications and a healthy female infant was born at 37 weeks of gestation, with visible goitre and thyroid function within the normal range at birth. Although there is no consensus on the optimal dose, the number of injections and the interval between them, intra-amniotic LT4 administration is recommended once fetal goitrous hypothyroidism is suspected, in order to prevent long-term co...
Endokrynologia Polska, 2015
Introduction: Pregnant women require about 250 μg of iodine daily. Hypothyroid women treated with L-thyroxine do not utilise iodine, and metabolism of L-thyroxine tablets is an additional source of iodine for their foetuses. The aim of the study was to evaluate the influence of iodine supplementation in hypothyroid pregnant women treated with L-thyroxine on neonate TSH concentration and maternal thyroid parameters. Material and methods: Ninety-two pregnant women with primary hypothyroidism on adequate thyroid hormone replacement were voluntarily divided into two groups: "thyroxine" (n = 38) treated with L-thyroxine only, and "thyroxine + iodine" (n = 54) treated additionally with 150 μg/day of iodine since 10 th gestational week. Primary outcomes were the maternal thyroid function tests (TSH, fT4, fT3) and neonatal TSH concentrations at the 3-4 th day of life. Urinary iodine concentration was measured at first and third trimester to compare iodine status in both groups. Results: Iodine supplementation significantly increased median urinary ioduria in the third trimester (from 95.15 μg/L to 151.50 μg/L), but did not prevent the decrease of maternal fT4 and fT3 concentrations in the second and third trimester. Median neonate TSH concentration in both groups was within normal range, but was 33% higher in the "thyroxine + iodine" than in the "thyroxine" group (1.91 mU/L vs. 1.34 mU/L). Moreover, 8.77% of newborns in the "thyroxine + iodine" group had TSH > 5 mIU/L. Conclusions: We did not find evidence for a positive influence of iodine supplementation on thyroid function of either hypothyroid pregnant women sufficiently treated with L-thyroxine or their neonates.
The Journal of Clinical Endocrinology & Metabolism, 2009
Context: Nonimmune fetal goitrous hypothyroidism is a rare condition that can induce obstetrical and/or neonatal complications and neurodevelopmental impairments such as those still seen in some patients with congenital hypothyroidism. Prenatal treatment to prevent these adverse outcomes is appealing, but experience is limited and the risk to benefit ratio controversial. Objective: The objective of the study was to evaluate the feasibility, safety, and effectiveness of intrauterine L-thyroxine treatment in a large cohort with nonimmune fetal goitrous hypothyroidism. Design: This was a retrospective study of 12 prenatally treated fetuses diagnosed between 1991 and 2005 in France. Methods: During pregnancy, goiter size and thyroid hormone levels were compared before and after prenatal treatment. At birth, clinical, laboratory, and ultrasound data were evaluated. Results: Prenatal treatment varied widely in terms of L-thyroxine dosage (200-800 g/injection), number of injections (one to six), and frequency (every 1-4 wk). No adverse events were recorded. During pregnancy, thyroid size decreased in eight of nine cases and amniotic-fluid TSH levels decreased in the six investigated cases, returning to normal in four. However, at birth, all babies had hypothyroidism, indicating that intraamniotic TSH levels did not reliably reflect fetal thyroid function. Conclusion: Our data confirm the feasibility and safety of intraamniotic L-thyroxine treatment for nonimmune fetal goitrous hypothyroidism. Although goiter size reduction is usually obtained, thyroid hormone status remains deficient at birth. Amniocentesis seems inadequate for monitoring fetal thyroid function. Further studies are needed to determine the optimal management of this disorder.
Endocrinology, diabetes & metabolism case reports, 2017
In the absence of maternal thyroid disease or iodine deficiency, fetal goitre is rare and usually attributable to dyshormonogenesis, for which genetic ascertainment is not always undertaken in the UK. Mechanical complications include tracheal and oesophageal compression with resultant polyhydramnios, malpresentation at delivery and neonatal respiratory distress. We report an Indian kindred in which the proband (first-born son) had congenital hypothyroidism (CH) without obvious neonatal goitre. His mother's second pregnancy was complicated by fetal hypothyroid goitre and polyhydramnios, prompting amniotic fluid drainage and intraamniotic therapy (with liothyronine, T3 and levothyroxine, T4). Sadly, intrauterine death occurred at 31 weeks. Genetic studies in the proband demonstrated compound heterozygous novel (c.5178delT, p.A1727Hfs*26) and previously described (c.7123G > A, p.G2375R) thyroglobulin (TG) mutations which are the likely cause of fetal goitre in the deceased sibli...
Annales d'Endocrinologie, 2017
Disponible en ligne sur ScienceDirect www.sciencedirect.com Annales d'Endocrinologie xxx (2016) xxx-xxx Letter to the Editor Fetal hypothyroidism induced by maternal anti-TSH receptor blocking antibodies and complicated by polyhydramnios despite the absence of goiter. Treatment by intra-amniotic injections of levothyroxine Hypothyroïdie foetale induite par des anticorps bloquants antirécepteur de la TSH d'origine maternelle, compliquée de polyhydramnios malgré l'absence de goitre. Traitement par injection intra-amniotique de levothyroxine Please cite this article in press as: Menut-Ruel A, et al. Fetal hypothyroidism induced by maternal anti-TSH receptor blocking antibodies and complicated by polyhydramnios despite the absence of goiter. Treatment by intra-amniotic injections of levothyroxine. Ann Endocrinol (Paris) (2016),