Neonatal Hyperthyroidism m Infants of Mothers Previously Thyroidectomized due to Graves’ Disease

Author(s):  
Maria Victoria Borras-Perez ◽  
David Moreno-Pérez ◽  
Amalia Zuasnabar-Cotro ◽  
Juan P. López-Siguero

AbstractNeonatal hyperthyroidism generally arises as a result of active maternal Graves’ disease via transplacental passage of thyroid stimulating immunoglobulins (TSI). On occasions, production of these antibodies may continue after thyroid ablation, either surgically or with radioiodine therapy. We present data concerning three patients (two of them twins) whose mothers had previously undergone near-total thyroidectomy prior to conception. Two of the neonates had neonatal hyperthyroidism due to persistence of TSI in the mother, and the third due to relapse of the maternal Graves’ disease during pregnancy. We recommend monitoring TSI during pregnancy in mothers with a history of Graves’ disease, even if they are in a state of post-surgical hypothyroidism.

2014 ◽  
Vol 2014 ◽  
pp. 1-3
Author(s):  
Barbara V. Parilla ◽  
Farhan Hanif ◽  
Keren Hasbani ◽  
Thomas Iannucci

Background. Fetal tachycardia may result from the transplacental passage of thyroid stimulating immunoglobulins in a patient with hypothyroidism secondary to ablation of Graves’ disease.Case. A 32-year-old woman, gravida 4, para 2, and abortus 1, with hypothyroidism and a history of Graves’ disease, presented at 23 6/7 weeks of gestation with a persistent fetal tachycardia. The treatment of the fetal tachycardia with maternally administered digoxin and Sotalol was unsuccessful. Maternal thyroid stimulating immunoglobulins were elevated, and treatment with maternally administered propylthiouracil (PTU) resulted in a normal sinus rhythm for the remainder of the pregnancy. An induction of labor was performed at 37 weeks. Four to five days after delivery, the neonate exhibited clinical signs of hyperthyroidism necessitating treatment.Conclusion. Fetal tachycardia resulting from the transplacental passage of thyroid stimulating immunoglobulins can be successfully treated with maternally administered PTU. The neonate needs to be followed up closely as clinical signs of hyperthyroidism may occur as thyroid stimulating immunoglobulins continue to circulate in the neonate, while the serum levels of PTU decline.


2004 ◽  
Vol 43 (06) ◽  
pp. 217-220 ◽  
Author(s):  
J. Dressler ◽  
F. Grünwald ◽  
B. Leisner ◽  
E. Moser ◽  
Chr. Reiners ◽  
...  

SummaryThe version 3 of the guideline for radioiodine therapy for benign thyroid diseases presents first of all a revision of the version 2. The chapter indication for radioiodine therapy, surgical treatment or antithyroid drugs bases on an interdisciplinary consensus. The manifold criteria for decision making consider the entity of thyroid disease (autonomy, Graves’ disease, goitre, goitre recurrence), the thyroid volume, suspicion of malignancy, cystic nodules, risk of surgery and co-morbidity, history of subtotal thyroidectomy, persistent or recurrent thyrotoxicosis caused by Graves’ disease including known risk factors for relapse, compression of the trachea caused by goitre, requirement of direct therapeutic effect as well as the patient’s preference. Because often some of these criteria are relevant, the guideline offers the necessary flexibility for individual decisions. Further topics are patients’ preparation, counseling, dosage concepts, procedural details, results, side effects and follow-up care. The prophylactic use of glucocorticoids during radioiodine therapy in patients without preexisting ophthalmopathy as well as dosage and duration of glucocorticoid medication in patients with preexisting ophthalmopathy need to be clarified in further studies. The pragmatic recommendations for the combined use of radioiodine and glucocorticoids remained unchanged in the 3rd version.


Thyroid ◽  
2019 ◽  
Vol 29 (1) ◽  
pp. 128-134 ◽  
Author(s):  
Ai Yoshihara ◽  
Kenji Iwaku ◽  
Jaeduk Yoshimura Noh ◽  
Natsuko Watanabe ◽  
Yo Kunii ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-3 ◽  
Author(s):  
Sarawut Summachiwakij ◽  
Issac Sachmechi

Hyperthyroidism can result in several musculoskeletal conditions such as thyrotoxic periodic paralysis, thyrotoxic myopathy, and thyroid ophthalmopathy. Rhabdomyolysis has been rarely reported to be associated with hyperthyroidism. We describe a 33-year-old man who presented with bilateral thigh pain and dark brown urine after regular squatting. He had a past medical history of hyperthyroidism but stopped taking it 2 months prior to admission. He was found to have rhabdomyolysis, myoglobinuria, and thyrotoxicosis. Presence of thyroid-stimulating immunoglobulins (TSI) and high radioiodine uptake confirmed a diagnosis of Graves' disease. He received aggressive fluid resuscitation and sodium bicarbonate intravenously along with monitoring fluid and electrolyte. Methimazole was also resumed. The patient responded to treatment and rhabdomyolysis gradually resolved. Therefore, nonstrenuous exercise can potentially induce rhabdomyolysis in patients with hyperthyroidism. Although hyperthyroidism is not widely recognized as a cause of rhabdomyolysis, it should be considered in the differential diagnosis of rhabdomyolysis.


2021 ◽  
Author(s):  
Anca Maria Panaitescu

Graves’ disease (GD) is one of the most common autoimmune conditions in women of reproductive age. The disorder is characterized by the presence of pathogenic immunoglobulins that bind the TSH receptors (TRAbs) and stimulate the production of thyroid hormones leading to hyperthyroidism (the occurrence of inhibiting or neutral antibodies being rare). Affected individuals can be treated by radioiodine therapy, surgical removal of the gland or by antithyroid drugs (ATDs). Thyroid stimulating immunoglobulins may persist for years after medical treatment, radioiodine therapy or surgical removal of the gland in those affected by GD and during pregnancy can cross the placenta and can act on the fetal thyroid gland resulting in the development of fetal and neonatal hyperthyroidism and sometimes to goiter. Antithyroid drugs used during pregnancy can also cross the placenta and may be teratogenic and act on the fetal thyroid gland, leading to fetal and neonatal hypothyroidism and goiter. This chapter will discuss specific aspects of GD during pregnancy and postpartum focusing on fetal and neonatal consequences related to this disorder.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Erica Wee ◽  
Ramya Ramachandra ◽  
Ana Maria Paez ◽  
John Brownlee ◽  
Rajan Senguttuvan

Abstract INTRODUCTION Neonatal hyperthyroidism is a transient disorder seen in neonates born to mothers with current or past history of Graves’ disease. We present a rare case of a Neonatal Graves’ disease with pulmonary hypertension (PH) which completely resolved with treatment of hyperthyroidism. CLINICAL CASE Baby B was a 3200 g term male born to a 40-year-old hypothyroid mother. He was prenatally diagnosed with Trisomy 21 and coarctation of the aorta (CoA). He developed respiratory distress soon after birth and was admitted to the NICU. His echocardiogram (echo) showed a large patent ductus arteriosus (PDA) and increased tortuosity of juxtaductal aorta with no significant gradient. Near-systemic pulmonary artery pressure was noted in the absence of any evidence of left heart failure. Cardiology determined his CoA to be hemodynamically insignificant and not the cause of his PH. Successive trials of 100% FiO2, Nitric Oxide (NO), and Sildenafil resulted in only minimal improvement of his PH. Thyroid function tests (TFT) obtained on day of life (DOL) 8 showed serum TSH of 0.01 uIU/ml [0.87 - 6.43] and FT4 of 3.5 ng/dl [0.9 - 1.5]. Further interaction with the mother revealed that she had a history of Graves’ disease treated with radioactive iodine (RAI) and resultant hypothyroidism. Baby B’s TSH receptor antibody (TRAb) and thyroid stimulating immunoglobulin levels were elevated at 7.38 IU/l [0-1.75] and 3.38 IU/l [0-0.55], respectively. He was thus diagnosed with Neonatal Graves’ disease and was started on Methimazole (MTZ) 1 mg/kg/day on DOL 8. Subsequently, potassium iodide was added. FT4 showed gradual normalization by DOL 15. Beta blockers were not added due to absence of hypertension or significant tachycardia. Serial echo showed improvement of PH, consistent with the decline in FT4 levels. Sildenafil and FiO2 were slowly weaned and discontinued by DOL 30. MTZ was then tapered and discontinued. A final echo showed complete resolution of PH, unobstructed aortic arch and persistent PDA. DISCUSSION Neonatal hyperthyroidism occurs due to transplacental transfer of TRAb from mother to fetus, stimulating the fetal thyroid to make excessive thyroid hormones. Risk correlates with TRAb titers in the mother. Our patient had pulmonary hypertension which did not resolve with FiO2, NO and Sildenafil. However, it showed complete resolution with normalization of FT4 levels by antithyroid drugs. Hyperthyroidism commonly presents with systemic HTN, but we found 3 neonatal cases in the literature presenting with PH that resolved with treatment of hyperthyroidism. The mechanism is unclear, but hypotheses include increased clearance of pulmonary vasodilators and decreased clearance of pulmonary vasoconstrictor and decreased surfactant production/function(1). REFERENCES 1) Oden J, Cheifetz IM. Neonatal thyrotoxicosis and persistent PH necessitating extracorporeal life support. Pediatrics 2005-115: e105-8.


Sign in / Sign up

Export Citation Format

Share Document