Neonatal Hyperthyroidism Causes Premature Development of Baroreceptor-Mediated Cardiac Sympathetic Reflexes

1982 ◽  
Vol 5 (2-3) ◽  
pp. 208-215 ◽  
Author(s):  
Jorge Bartolome ◽  
Christopher Lau ◽  
Theodore A. Slotkin
1991 ◽  
Vol 85 (3) ◽  
Author(s):  
C. Pavlides ◽  
A.I. Westlind-Danielsson ◽  
H. Nyborg ◽  
B.S. McEwen

Author(s):  
J. Chester ◽  
D. Rotenstein ◽  
U. Ringkananont ◽  
G. Steuer ◽  
Β. Carlin ◽  
...  

1976 ◽  
Vol 82 (5) ◽  
pp. 1677-1680
Author(s):  
G. V. Kovalev ◽  
I. S. Morozov ◽  
V. I. Petrov
Keyword(s):  

Author(s):  
Juliane Léger ◽  
Clemence Delcour ◽  
Jean-Claude Carel

Abstract Fetal and neonatal dysfunctions include rare serious disorders involving abnormal thyroid function during the second half of gestation, which may persist throughout life, as for most congenital thyroid disorders, or be transient, resolving in the first few weeks of life, as in autoimmune hyperthyroidism or hypothyroidism and some cases of congenital hypothyroidism (CH) with the thyroid gland in situ. Primary CH is diagnosed by neonatal screening, which has been implemented for 40 years in developed countries and should be introduced worldwide, as early treatment prevents irreversible neurodevelopmental delay.Central CH is a rarer entity occurring mostly in association with multiple pituitary hormone deficiencies. Other rare disorders impair the action of thyroid hormones. Neonatal Grave’s disease (GD) results from the passage of thyrotropin receptor antibodies (TRAb) across the placenta, from mother to fetus. It may affect the fetuses and neonates of mothers with a history of current or past GD, but hyperthyroidism develops only in those with high levels of stimulatory TRAb activity. The presence of antibodies predominantly blocking TSH receptors may result in transient hypothyroidism, possibly followed by neonatal hyperthyroidism, depending on the balance between the antibodies present. Antithyroid drugs taken by the mother cross the placenta, treating potential fetal hyperthyroidism,but they may also cause transient fetal and neonatal hypothyroidism. Early diagnosis and treatment are key to optimizing the child’s prognosis. This review focuses on the diagnosis and management of these patients during the fetal and neonatal periods. It includes the description of a case of fetal and neonatal autoimmune hyperthyroidism.


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

1994 ◽  
Vol 179 (1-2) ◽  
pp. 71-74 ◽  
Author(s):  
Johannes Zanzinger ◽  
Jens Doutheil ◽  
Jürgen Czachurski ◽  
Horst Seller

2019 ◽  
Vol 25 (19) ◽  
pp. 2315-2326 ◽  
Author(s):  
Meng-Jiang Lu ◽  
Zhi Yu ◽  
Yan He ◽  
Yin Yin ◽  
Bin Xu

2021 ◽  
Vol 184 (3) ◽  
pp. 431-440
Author(s):  
Hassina Benlarbi ◽  
Dominique Simon ◽  
Jonathan Rosenblatt ◽  
Cecile Dumaine ◽  
Nicolas de Roux ◽  
...  

Objective Neonatal hyperthyroidism may be caused by a permanent non-autoimmune genetic disorder or, more frequently, by maternally transmitted high serum TRAb levels. Variable thyroid dysfunction may be observed in this second context. We aimed to evaluate the prevalence of neonatal non-autoimmune hyperthyroidism and of the different types of thyroid function in neonates with a high risk of hyperthyroidism due to maternal Graves’ disease (GD). Design and methods This observational cohort study included all neonates identified in the database of a single academic pediatric care center, over a period of 13 years, as having non-autoimmune hyperthyroidism or an autoimmune disorder with high TRAb levels (above 6 IU/L) transmitted by their mothers. Patients were classified as having neonatal hyperthyroidism, hypothyroidism, or euthyroidism with a permanent or transient disorder. Results Two of the 34 consecutive neonates selected (6%) had permanent non-autoimmune hyperthyroidism due to germline (n = 1) or somatic (n = 1) mutations of the TSH receptor gene. The patients with high serum TRAb levels at birth had transient hyperthyroidism (n = 23), hypothyroidism (primary n = 2, central n = 3) or persistent euthyroidism (n = 4). Conclusion These original findings highlight the need for careful and appropriate monitoring of thyroid function in the long term, not only for the rare patients with non-autoimmune neonatal hyperthyroidism, but also for repeat monitoring during the first month of life in neonates with maternally transmitted high TRAb levels, to ensure the early identification of thyrotoxicosis in more than two thirds of cases and to detect primary or central hypothyroidism, thereby potentially decreasing associated morbidity.


2005 ◽  
Vol 1 (1) ◽  
pp. 97-104
Author(s):  
John H Lazarus

Pregnancy has marked effects on thyroid physiology and autoimmune thyroid disease tends to ameliorate through gestation due to the general immunosuppression seen in pregnancy. There is a need for trimester-specific thyroid hormone reference ranges. Hyperthyroidism in pregnancy – usually due to Graves' disease – is not common but, if the patient is compliant, a good outcome can be expected for both mother and child if treatment with anti-thyroid drugs (propylthiouracil is preferred) is instituted. Thyroid-stimulating hormone receptor antibody should be measured at 36 weeks in such patients in order to predict the possibility of neonatal hyperthyroidism. Transient gestational hyperthyroidism is often associated with hyperemesis gravidarum and thyroid function should be checked in patients severely affected by this condition. Radioiodine therapy is contraindicated in pregnancy but thyroid surgery may be performed safely in the second trimester. Autoimmune thyroiditis and Graves’ hyperthyroidism occur quite commonly in postpartum women.


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