scholarly journals Prevalence and course of thyroid dysfunction in neonates at high risk of Graves’ disease or with non-autoimmune hyperthyroidism

2021 ◽  
Vol 184 (3) ◽  
pp. 431-440
Author(s):  
Hassina Benlarbi ◽  
Dominique Simon ◽  
Jonathan Rosenblatt ◽  
Cecile Dumaine ◽  
Nicolas de Roux ◽  
...  
Keyword(s):  
High Risk ◽  
Thyroid Function ◽  
Thyroid Dysfunction ◽  
Genetic Disorder ◽  
Care Center ◽  
Receptor Gene ◽  
High Serum ◽  
Pediatric Care ◽  
Graves Disease ◽  
Neonatal Hyperthyroidism

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.

scholarly journals Thyroid Function in Chronically Transfused Children with Beta Thalassemia Major: A Cross-Sectional Hospital Based Study

2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
Suraj Haridas Upadya ◽  
M. S. Rukmini ◽  
Sowmya Sundararajan ◽  
B. Shantharam Baliga ◽  
Nutan Kamath
Keyword(s):  
Thyroid Function ◽  
Serum Ferritin ◽  
Subclinical Hypothyroidism ◽  
Thyroid Dysfunction ◽  
Genetic Disorder ◽  
Thalassemia Major ◽  
Beta Thalassemia ◽  
P Value ◽  
Blood Transfusions ◽  
Beta Thalassemia Major

Background. Thalassemia is the most common genetic disorder worldwide. Use of iron chelators has improved survival but endocrine complications have become more frequent. The frequency of hypothyroidism in Beta Thalassemia Major (BTM) children ranges from 6 to 30 %. Thyroid dysfunction mainly occurs by gland infiltration, chronic tissue hypoxia, free radical injury, and organ siderosis. Objectives. (a) To evaluate the thyroid function status in chronically transfused children with BTM, in the first and second decade of life and (b) to study the influence of factors like duration and amount of blood transfusions, serum ferritin level, and iron chelation therapy on thyroid function. Methodology. BTM children, 3 years old and above, on regular blood transfusions with serum ferritin > 1500 mcg/l were included in the study. Thyroid function and ferritin assessment was done using ELISA kits. Autoimmune thyroiditis was ruled out by antithyroid peroxidase and antithyroglobulin antibody testing. Results. A study population of 83 children consisted of 49 boys (59%) and 34 girls (41%). 4.8% of the children had evidence of subclinical hypothyroidism. Among them two belonged to the first decade and the other two to the second decade of life. Mean TSH, FT4, and ferritin values among children with thyroid dysfunction were 6.38 ± 0.83 mIU/ml, 1.08 ± 0.45 ng/dl, and 3983.0±1698.30 ng/ml, respectively. The severity of thyroid dysfunction was statistically significantly associated with higher serum TSH values in children in the second decade of life with a p value = 0.001. No other significant correlation was found between oral chelation, amount and duration of blood transfusion, or serum ferritin levels. Conclusion. Subclinical hypothyroidism was the thyroid dysfunction observed in our study. Regular blood transfusions with adequate chelation may decrease incidence of thyroid dysfunction.

Different aetiologies in post-partum thyroiditis?

1983 ◽  
Vol 104 (2) ◽  
pp. 195-200 ◽  
Author(s):  
Per Anders Dahlberg ◽  
Rolf Jansson
Keyword(s):  
Thyroid Function ◽  
Autoimmune Thyroiditis ◽  
Thyroid Dysfunction ◽  
Post Partum ◽  
Lymphocytic Infiltration ◽  
Graves Disease ◽  
Thyroid Autoantibodies ◽  
Radioiodine Uptake ◽  
Thyroid Cytology

Abstract. During a 4 year period 19 women with post-partum onset of thyroid dysfunction have been seen in our clinic. Five women had high radioiodine uptake thyrotoxicosis (Graves' disease). Twelve women had hypothyroid symptoms starting within 3–6 months of delivery. All of these women had thyroid microsomal and/or cytoplasmic autoantibodies and thyroid lymphocytic infiltration suggesting aggravation of pre-existing subclinical autoimmune thyroiditis (Hashimoto's disease). At follow-up thyroid function gradually improved in all but signs of persistent thyroid hypofunction remained in seven. Thus women developing symptomatic postpartum hypothyroidism should be followed regularly and when thyroxine treatment is commenced in the post-partum period, it has to be continued indefinitely in many cases. Two women presented with transient low radioiodine uptake thyrotoxicosis and a small painless goitre. Thyroid cytology revealed thyroiditis but they had no thyroid autoantibodies. When followed after a succeeding delivery none of these women developed post-partum thyroid dysfunction in contrast to women in the autoimmune group. Probably the aetiology of thyroid dysfunction in these 2 women was different.

Thyroid function in patients with Prader-Willi syndrome: an Italian multicenter study of 339 patients

2019 ◽  
Vol 32 (2) ◽  
pp. 159-165 ◽  
Author(s):  
Lorenzo Iughetti ◽  
Giulia Vivi ◽  
Antonio Balsamo ◽  
Andrea Corrias ◽  
Antonino Crinò ◽  
...  
Keyword(s):  
Thyroid Function ◽  
Thyroid Dysfunction ◽  
Genetic Disorder ◽  
Hypogonadotropic Hypogonadism ◽  
Thyroid Stimulating Hormone ◽  
Hormone Deficiency ◽  
Published Data ◽  
Prader Willi Syndrome ◽  
Thyroid Function Tests ◽  
Central Hypothyroidism

AbstractBackgroundPrader-Willi syndrome (PWS) is a genetic disorder due to loss of expression of paternally transcribed genes of the imprinted region of chromosome 15q11-13. PWS is characterized by peculiar signs and symptoms and many endocrine abnormalities have been described (growth hormone deficiency, hypogonadotropic hypogonadism). The abnormalities of thyroid function are discussed in literature and published data are discordant. The aim of our study was to report the thyroid function in patients with PWS to identify the prevalence of thyroid dysfunction.MethodsThyroid function tests were carried out in 339 patients with PWS, aged from 0.2 to 50 years. A database was created to collect personal data, anthropometric data, thyroid function data and possible replacement therapy with L-thyroxine. Subjects were classified according to thyroid function as: euthyroidism (EuT), congenital hypothyroidism (C-HT), hypothyroidism (HT – high thyroid-stimulating hormone [TSH] and low free thyroxine [fT4]), central hypothyroidism (CE-H – low/normal TSH and low fT4), subclinical hypothyroidism (SH – high TSH and normal fT4), and hyperthyroidism (HyperT – low TSH and high fT4).ResultsTwo hundred and forty-three out of 339 PWS patients were younger than 18 years (71.7%). The prevalence of thyroid dysfunction was 13.6%. Specifically, C-HT was found in four children (1.18%), HT in six patients (1.77%), CE-H in 23 patients (6.78%), SH in 13 patients (3.83%), and HyperT in none. All other subjects were in EuT (86.4%).ConclusionsHypothyroidism is a frequent feature in subjects with PWS. Thyroid function should be regularly investigated in all PWS patients both at the diagnosis and annually during follow-up.

scholarly journals Management of Graves’ Disease during Pregnancy: The Key Role of Fetal Thyroid Gland Monitoring

2005 ◽  
Vol 90 (11) ◽  
pp. 6093-6098 ◽  
Author(s):  
Dominique Luton ◽  
Isabelle Le Gac ◽  
Edith Vuillard ◽  
Mireille Castanet ◽  
Jean Guibourdenche ◽  
...  
Keyword(s):  
Thyroid Gland ◽  
Thyroid Function ◽  
Thyroid Dysfunction ◽  
Tsh Receptor ◽  
Antithyroid Drugs ◽  
Graves Disease ◽  
Test Results ◽  
Bone Maturation ◽  
Normal Test ◽  
Fetal Thyroid

Abstract Background: Fetuses from mothers with Graves’ disease may experience hypothyroidism or hyperthyroidism due to transplacental transfer of antithyroid drugs (ATD) or anti-TSH receptor antibodies, respectively. Little is known about the fetal consequences. Early diagnosis is essential to successful management. We investigated a new approach to the fetal diagnosis of thyroid dysfunction and validated the usefulness of fetal thyroid ultrasonograms. Methods: Seventy-two mothers with past or present Graves’ disease and their fetuses were monitored monthly from 22 wk gestation. Fetal thyroid size and Doppler signals, and fetal bone maturation were determined on ultrasonograms, and thyroid function was evaluated at birth. Thyroid function and ATD dosage were monitored in the mothers. Results: The 31 fetuses whose mothers were anti-TSH receptor antibody negative and took no ATDs during late pregnancy had normal test results. Of the 41 other fetuses, 30 had normal test results at 32 wk, 29 were euthyroid at birth, and one had moderate hypothyroidism on cord blood tests. In the remaining 11 fetuses, goiter was visualized by ultrasonography at 32 wk, and fetal thyroid dysfunction was diagnosed and treated; there was one death, in a late referral, and 10 good outcomes with normal or slightly altered thyroid function at birth. The sensitivity and specificity of fetal thyroid ultrasound at 32 wk for the diagnosis of clinically relevant fetal thyroid dysfunction were 92 and 100%, respectively. Conclusion: In pregnant women with past or current Graves’ disease, ultrasonography of the fetal thyroid gland by an experienced ultrasonographer is an excellent diagnostic tool. This tool in conjunction with close teamwork among internists, endocrinologists, obstetricians, echographists, and pediatricians can ensure normal fetal thyroid function.

scholarly journals Management of neonates born to women with Graves' disease: a cohort study

2014 ◽  
Vol 170 (6) ◽  
pp. 855-862 ◽  
Author(s):  
Alix Besançon ◽  
Jacques Beltrand ◽  
Isabelle Le Gac ◽  
Dominique Luton ◽  
Michel Polak
Keyword(s):  
Cord Blood ◽  
Thyroid Function ◽  
Prospective Observational Study ◽  
Graves Disease ◽  
Thyroid Function Tests ◽  
Third Trimester ◽  
Free Triiodothyronine ◽  
Bone Maturation ◽  
Thyrotropin Receptor Antibody ◽  
Neonatal Hyperthyroidism

ObjectiveHyperthyroidism in neonates born to mothers with Graves' disease (GD) can be associated with significant morbidity and mortality, but is still overlooked by clinicians. Management of neonatal hyperthyroidism would be improved by a better understanding of the predictive factors involved. The aim of this study was to evaluate the course of thyroid function and clinical outcomes during the first postnatal month in babies born to mothers with GD.DesignProspective observational study.MethodsSixty-eight neonates born to mothers with GD were managed from birth and divided into three groups based on thyrotropin receptor antibody (TRAb) and anti-thyroid drug (ATD) status in the mother: TRAb−ve/ATD−ve,n=27; TRAb−ve/ATD+ve,n=8; and TRAb+ve/ATD+ve,n=33. The main outcome measures were clinical examination, thyroid function tests (TSH, free thyroxine (FT4), free triiodothyronine, and TRAb), echocardiography, thyroid ultrasonography, and bone maturation assessment.ResultsNone of the infants born to TRAb−vemothers with GD developed neonatal hyperthyroidism. Of the 33 TRAb+ve/ATD+veneonates, 24 (72.7%) had positive TRAb on cord blood assays, and seven of these developed neonatal hyperthyroidism. FT4elevation between days 3 and 7 but not at birth was predictive of the development of hyperthyroidism.ConclusionsTRAb status should be checked in the third trimester in mothers with GD and on cord blood in their neonates; if positive, it indicates a high risk of neonatal hyperthyroidism. FT4measurement at birth should be repeated between days 3 and 5 (and by day 7 at the latest); rapid FT4elevation during the first postnatal week is predictive of hyperthyroidism and warrants ATD therapy.

scholarly journals Erratic movement disorders disclosing Graves’ disease and paralleling thyroid function but not autoantibody levels

2019 ◽  
Vol 47 (3) ◽  
pp. 1378-1386 ◽  
Author(s):  
Sébastien Delhasse ◽  
Ines Debove ◽  
Gabriella Arnold-Kunz ◽  
Joseph-André Ghika ◽  
Joelle Nsimire Chabwine
Keyword(s):  
Thyroid Function ◽  
Movement Disorders ◽  
Thyroid Dysfunction ◽  
Neurological Symptoms ◽  
Graves Disease ◽  
Thyroid Antibodies ◽  
Autoimmune Pathology ◽  
The Impact ◽  
Complex Movement

Graves’ disease (GD) is an autoimmune pathology characterized by hyperthyroidism and the presence of specific anti-thyroid antibodies. Neurological symptoms such as seizures, cognitive impairment, and tremor can be observed during the course of GD, but more complex movement disorders such as chorea and myoclonus are less frequent. The mechanisms underlying movement disorders in GD are not fully understood. While some authors relate movement disorders to thyroid dysfunction, others claim an autoimmune origin. We herein report a case involving a 60-year-old woman who presented with erratic, intricate movement disorders for which a medical workup revealed GD. During the 2-year follow-up period, her neurological symptoms evolved in parallel with her thyroid function, but not with her autoimmune anti-thyroid antibody level. Her neurological symptoms completely disappeared when she became euthyroid. We herein discuss the complicated clinicobiological relationship between thyroid function and movement disorders. This relationship involves several factors, including the impact of radioactive treatment. The present case emphasizes the importance of including thyroid function screening in the workup of unexplained movement disorders.

scholarly journals SAT-463 Thyrotoxicosis from Nivolumab in a Patient with Preexisting Graves’ Disease

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Preethi Polavarapu ◽  
Padmaja Akkireddy
Keyword(s):  
Adverse Events ◽  
Thyroid Function ◽  
Autoimmune Thyroiditis ◽  
Immune Checkpoint ◽  
Immune Checkpoint Inhibitors ◽  
Thyroid Dysfunction ◽  
Checkpoint Inhibitors ◽  
Graves Disease ◽  
Thyroid Function Tests ◽  
Free T4

Abstract Introduction Thyroid dysfunction is one of the common immune-related adverse events associated with immune checkpoint inhibitors like Nivolumab. Thyroiditis or primary hypothyroidism is the most commonly reported presentation. Graves’ disease is less frequently reported. We report a case of preexisting Graves’ disease patient, on antithyroid meds who developed thyrotoxicosis followed by hypothyroidism after receiving Nivolumab therapy. Case 66 y/o female patient with newly diagnosed metastatic melanoma presented to us for evaluation of abnormal thyroid test after her second cycle of Nivolumab. She has a long-standing history of Graves’ disease and has been on methimazole since her diagnosis. Her baseline thyroid labs before the start of Nivolumab were within normal limits (on methimazole 2.5 mg daily). She presented with weight loss, palpitations, and tremors four weeks after the start of Nivolumab. On exam, she was tachycardic with tremors noted to outstretched hands and had diffusely enlarged thyroid. Repeat lab work done before her second cycle revealed suppressed TSH 0.02 (0.4-4.5 uIU/ml) with elevated free T4 and T3. Her TSI titers were elevated. Methimazole dose was increased to 10 mg daily, and follow up labs done in a month revealed TSH of 89 uIU/ml, Free T4 0.16 (0.76-1.8 ng/dl). Methimazole was completely stopped at this time. She continued to have elevated TSH despite being off of methimazole for more than a month, concerning for the development of hypothyroidism. She was started on levothyroxine, after which labs returned to normal. The patient continued on immunotherapy during this period. Discussion Immune checkpoint inhibitors have been increasingly used for cancer therapy. Endocrinopathies are the most common immune-related adverse events associated with the use of these agents, with thyroid dysfunction being more common. Our patient had well-controlled Graves’ disease and was on a stable dose of methimazole for years. She developed autoimmune thyroiditis four weeks after receiving immunotherapy and subsequently developed hypothyroidism. The literature search did not reveal cases of autoimmune thyroiditis in a patient with preexisting Graves’ disease. One study reported that the timeline for developing the thyrotoxic phase is five weeks, which is followed by the rapid development of either euthyroid or hypothyroid phase. Management during the thyrotoxic phase is usually beta-blockers. Current guidelines recommend checking thyroid function test before initiation of therapy and every two weeks after the diagnosis of thyrotoxicosis until they become euthyroid or hypothyroid. Our case illustrates that patients with preexisting Graves’ disease can develop thyroiditis after receiving immune checkpoint inhibitors, and hence, frequent monitoring with thyroid function tests is needed.

Abstract #1202: A Case of Graves’ Disease With Fluctuating Thyroid Function

2016 ◽  
Vol 22 ◽  
pp. 305-306
Author(s):  
Sheela Metgud ◽  
Anup Kumar ◽  
Erin Drever ◽  
Tahira Yasmeen
Keyword(s):  
Thyroid Function ◽  
Graves Disease
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