J Pediatr Endocr Met 2015; 28(3-4): 463–466
Patient report Aslıhan Abbasoğlu*, Ayşe Ecevit, Ali Ulaş Tuğcu, İlkay Erdoğan, Sibel Tulgar Kınık and Aylin Tarcan
Neonatal thyrotoxicosis with severe supraventricular tachycardia: case report and review of the literature Abstract: Neonatal thyrotoxicosis is a rare condition caused by the transplacental passage of thyroid stimulating immunoglobulins from mothers with Graves’ disease. We report a case of neonatal thyrotoxicosis with concurrent supraventricular tachycardia (SVT). The female infant, who was born by section due to breech delivery and meconium in the amniotic fluid at 36 weeks of gestation, presented with tachycardia on day 7. Her heart rate was between 260 and 300 beats/min, and an electrocardiogram revealed ongoing SVT. Sotalol was effective after two cardioversions in maintaining sinus rhythm. Thyroid function studies revealed hyperthyroidism in the infant, and her mother was found to have Graves’ disease. Since symptoms and signs can vary, especially in preterm infants with neonatal hyperthyroidism, we want to emphasize the importance of prenatal care and follow-ups of Graves’ disease associated pregnancies and management of newborns after birth.
Introduction
Keywords: newborn; thyrotoxicosis.
The female infant was born by cesarean section due to breech delivery and meconium in the amniotic fluid with 2470 g birth weight at 36 weeks of gestation. She needed resuscitation with APGAR scores of 4, 6, and 7 at 1, 5, and 10 min, respectively. She was intubated and transferred to the neonatal intensive care unit (NICU). She was in need of mechanical ventilation for 12 h. Then, clinical features of early-onset sepsis and respiratory distress were determined. After taking a blood culture, intravenous ampicillin (100 mg/kg/day) and gentamicin (4 mg/kg/day) treatment was started. On day 7 of her admission, tachycardia was started. Her heart rate was between 260 and 300 beats/min. Electrocardiogram revealed ongoing supraventricular tachycardia (SVT) at a rate of 243 bpm (Figure 1). Treatment was started with vagal stimulation. A plastic bag filled with iced-water was applied on the face and unilateral carotid sinus massage was made. An intravenous adenosine 0.1 mg/kg dose was also administered. Two trials of electric cardioversion of
supraventricular
tachycardia;
DOI 10.1515/jpem-2014-0166 Received April 15, 2014; accepted July 22, 2014; previously published online August 19, 2014
*Corresponding author: Aslıhan Abbasoğlu, MD, Division of Neonatology, Department of Pediatrics, Baskent University Faculty of Medicine, Çankaya/Ankara, Turkey, Phone: +90-312-212-6868, Fax: +90-312-223-7333, E-mail: [email protected] Ayşe Ecevit, Ali Ulaş Tuğcu and Aylin Tarcan: Division of Neonatology, Department of Pediatrics, Başkent University Faculty of Medicine, Ankara, Turkey İlkay Erdoğan: Division of Pediatric Cardiology, Department of Pediatrics, Başkent University Faculty of Medicine, Ankara, Turkey Sibel Tulgar Kınık: Division of Pediatric Endocrinology, Department of Pediatrics, Başkent University Faculty of Medicine, Ankara, Turkey
Neonatal thyrotoxicosis is a rare but potentially fatal thyroid disease, with an incidence of roughly 1 out of 50,000 infants (1). It may have a varied clinical presentation and can range from a totally asymptomatic healthy newborn to the one with severe thyroid storm (2–5). In this case, we report a late preterm infant with neonatal thyrotoxicosis presenting with supraventricular tachycardia (SVT). SVT is the most common significant arrhythmia in neonatal and infancy age group which is characterized by abrupt onset and termination with narrow QRS complexes and a regular RR interval (6). This case report also emphasizes the importance of prenatal care and follow-ups.
Case report
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464 Abbasoğlu et al.: Neonatal thyrotoxicosis with severe supraventricular tachycardia
Figure 1 Electrocardiogram of the case.
1 J/kg were unsuccessful in maintaining a stable sinus rhythm. A dose of 1 mg/kg sotalol was administered orally. Persistent sinus rhythm was obtained 15 min following the start of this therapy. Echocardiography showed a structurally normal heart with a normal ejection fraction. On same day, high thyroxine (T4) of 22.7 ng/dL (0.7–1.48) and low thyroid-stimulating hormone (TSH) levels of 0.005 μIU/mL (1.7–9.1) were determined in the infant’s serum samples. Thyrotropin receptor antibodies (TRAb) were 250 U/L. Laboratory evaluation revealed a white blood count of 11,300/μL with hemoglobin 24.5 g/dL, hematocrit 62%, platelet count 208,000/μL, with normal electrolytes and biochemical parameters. Our patient was diagnosed to have thyroid storm due to thyrotoxicosis. Intensive medical therapy was started with 10 mg/kg/day of propylthiouracil, 1 drop of Lugol’s iodine solution three times per day, 2 mg/kg/day propranolol, and 2 mg/kg/day of oral prednisolone. The short-acting propylthiouracil was the preferred antithyroid drug compared to methimazole, because it has the extra benefit of decreasing the conversion of T4 into T3. On days 2 and 3 of treatment, her heart rate was decreased
to 172 and 130, respectively. After the control of thyroid crisis, propylthiouracil was replaced with methimazole at a dose of 1 mg/kg/day. Lugol’s iodine was discontinued after day 5 of therapy, as serum T4 level decreased to 3.12 ng/dL. In the first week, the dose of steroid was reduced to half. During this time, her tachypnea continued with a respiratory rate between 72 and 80 breaths/min, and tachypnea resolved after 10 days. On day 12 of treatment, she was discharged from hospital on methimazole, propranolol, and prednisolone, with a plan to follow-up in the pediatric-endocrinology outpatient clinic, with a weight of 2650 g and 0.84 ng/dL of serum T4 and 0.004 μIU/mL of TSH. After the diagnosis of neonatal thyrotoxicosis, the mother in our case was found to have hyperthyroidism with TSH: 0.035 μIU/mL (normal: 0.35–4.94). She was immediately started methimazole treatment. On the follow-up visit to the endocrinology outpatient clinic 7 days after the discharge, she was found to be doing well with a normal heart rate and appropriate weight gain. Propranolol and prednisolone treatment were discontinued. Methimazole was gradually
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Abbasoğlu et al.: Neonatal thyrotoxicosis with severe supraventricular tachycardia 465
decreased and eventually discontinued at 2 months of age. Repeated thyroid function tests at 2 and 3 months of age were all normal.
Discussion Neonatal thyrotoxicosis is rare condition caused by the transplacental passage of thyroid stimulating immunoglobulins from mothers with Graves’ disease. Graves’ disease is an autoimmune disorder, characterized by the presence of specific immunoglobulins directed against the TSH receptors in the thyroid gland. It complicates 0.1% to 0.2% of pregnancies. Maternal Graves’ disease is associated with an increased risk of spontaneous abortion, preterm labor, and perinatal mortality (7). The incidence of hyperthyroidism in babies of mothers who require treatment with antithyroid drugs to term may be as high as 22%. The mortality has been reported to be 12%–20%, usually due to heart failure (8). Thyrotoxicosis is the syndrome caused by an excess of free thyroid hormones. Thyroid storm, also referred to as thyrotoxic crisis, is an acute, life-threatening, hypermetabolic state, induced by excessive release of thyroid hormones in individuals with thyrotoxicosis (9, 10). Thyroid storm may be the initial presentation of thyrotoxicosis in undiagnosed children, particularly in neonates (11–13). Symptoms and signs of neonatal thyrotoxicosis can be apparent at birth or may be delayed due to the effect of transplacental passage of maternal antithyroid drugs or effect of coexisting blocking antibodies, but they are apparent by 10 days of life, rarely can be delayed up to 45 days (1). In premature infants like the one in our case, other issues related to prematurity (oxygen requirements, polycythemia, and nutrition) should be considered. These issues both complicate the clinical picture and delay diagnosis and treatment. Smith et al. (13) examined 7 low birth-weight infants with thyrotoxicosis, and in 6 out of the 7 cases, diagnosis was delayed (after day 7). Our case was a late preterm infant with oxygen requirement for 10 days and poor weight gain. The diagnosis of neonatal thyrotoxicosis was made on the day 7. Neonatal thyrotoxicosis often present with hyperkinesis, hyperexcitability, diarrhea, poor weight gain, exophthalmos, hepatosplenomegaly, thrombocytopenia, craniosynostosis, and several cardiac complications including supraventricular tachycardia, cardiomyopathy and congestive cardiac failure (2). In our case, SVT was the initial manifestation of neonatal thyrotoxicosis. The presentation of SVT in the neonate is frequently subtle and may include pallor, cyanosis, restlessness, irritability, feeding difficulty,
tachypnea, and grunting. Besides these symptoms, during the examination of an infant with SVT thyrotoxicosis should be kept in mind (14). Cardiovascular signs of thyrotoxicosis may progress to cardiac failure (15–19). Neonatal SVT can be difficult to control with traditional antiarrhythmic agents (20). Amiodarone is an effective and safe therapy for tachycardia control in infancy, but the iodine released from amiodarone can affect thyroid function. Because of our patient’s status about hyperthyroidism, intravenous amiodaroneinfusion was not preferred. Sotalol is also efficacious in the conversion of acute supraventricular arrhythmia, and in our case, sotalol proved to be effective after two cardioversions in maintaining sinus rhythm afterward (21). Appropriate management of any premature infant exhibiting possible signs of hyperthyroidism should include thorough investigation into past or active thyroid disease in the mother, quantitative assessment of maternal thyrotropin binding inhibitory immunoglobulin (TBII), cord TSH and venous free T4, and TSH (1). Since our patient was in the NICU for prematurity, we were able to observe the manifestations of the hyperthyroidism, and as a result, timely management was instituted. However, in the scenario of a full-term infant with an unknown maternal thyroid history, the patient may be sent home from the nursery and then later present with these signs and symptoms in an emergency department. Physicians in these settings need to keep thyroid disease of the newborn on their list of differential diagnoses. The purpose of presenting this patient is to emphasize the importance of prenatal care and follow-ups. Obstetricians, endocrinologists, and pediatricians need to work together in their management of Graves’ disease associated pregnancies (22, 23).
References 1. Ogilvy-Stuart AL. Neonatal thyroid disorders. Arch Dis Child Fetal Neonatal Ed 2002;87165–71. 2. Batra CM. Fetal and neonatal thyrotoxicosis. Indian J Endocrinol Metab 2013;17:50–4. 3. Zimmerman D. Fetal and neonatal hyperthyroidism. Thyroid 1999;9:727–33. 4. Polak M. Hyperthyroidism in early infancy: pathogenesis, clinical features and diagnosis with a focus on neonatal hyperthyroidism. Thyroid 1998;8:1171–7. 5. Radetti G, Zavallone A, Gentili L, Beck-Peccoz P, Bona G. Foetal and Neonatal thyroid disorders. Minerva Pediatr 2002;54:383–400. 6. Moak JP. Supraventricular tachycardia in the neonate and infant. Prog Pediatr Cardiol 2000;11:25–38. 7. Mestman JH. Hyperthyroidism in pregnancy. Clin Obstet Gynecol 1997;40:45–64.
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466 Abbasoğlu et al.: Neonatal thyrotoxicosis with severe supraventricular tachycardia 8. Mortimer RH, Tyack SA, Galligan JP, Perry-Keene DA, Tan YM. Graves’ disease in pregnancy: TSH receptor binding inhibiting immunoglobulins and maternal and neonatal thyroid function. Clin Endocrinol 1990;32:141–52. 9. Johnstone HC, Dharmaraj P, Cheetham TD. The evaluation and management of thyrotoxicosis. Curr Paediatrics 2004;14:430–37. 10. Mittra ES, Niederkohr RD, Rodriguez C, El-Maghraby T, McDougall IR. Uncommon causes of thyrotoxicosis. J Nucl Med 2008;49:265–78. 11. Nayak B, Burman K. Thyrotoxicosis and thyroid storm. Endocrinol Metab Clin North Am 2006;35:663–86. 12. Bahn Chair RS, Burch HB, Cooper DS, Garber JR, Greenlee MC, et al., American Thyroid Association; American Association of Clinical Endocrinologists. Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists. Thyroid 2011;21:593–646. 13. Smith C, Thomsett M, Choong C, Rodda C, McIntyre HD, et al. Congenital thyrotoxicosis in premature infants. Clin Endocrinol 2001;54:371–76. 14. Hecht T, Brand J, Vlaho S. Encephalopathy and sinus tachycardia in childhood – a possible differential diagnosis. J Pediatr Endocrinol Metab 2012;25:149–51.
15. Lozano HF, Sharma CN. Reversible pulmonary hypertension, tricuspid regurgitation and right-sided heart failure associated with hyperthyroidism: case report and review of the literature. Cardiol Rev 2004;12:299–305. 16. Oden J, Cheifetz IM. Neonatal thyrotoxicosis and persistent pulmonary hypertension necessitating extracorporeal life support. Pediatrics 2005;115:105–8. 17. Woeber KA. Thyrotoxicosis and the heart. N Engl J Med 1992;327:94–8. 18. Skelton CL. The heart and hyperthyroidism: editorial. N Engl J Med 1982;307:1206–8. 19. Fadel BM, Ellahham S, Ringel MD, Lindsay J Jr, Wartofsky L, et al. Hyperthyroid heart disease. Clin Cardiol 2000;23:402–8. 20. Wren C. Cardiac arrhythmias in the fetus and newborn. Semin Fetal Neonatal Med 2006;11:182–90. 21. Wong KK, Potts JE, Etheridge SP, Sanatani S. Medications used to manage supraventricular tachycardia in the infant a North American survey. Pediatr Cardiol 2006;27:199–203. 22. Smith CM, Gavranich J, Cotterill A, Rodda CP. Congenital neonatal thyrotoxicosis and previous maternal radioiodine therapy. Br Med J 2000;320:1260–1. 23. Aslam M, Inayat M. Fetal and neonatal Graves disease: a case report and review of the literature. South Med J 2008;101:840–1.
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Patient report Aslıhan Abbasoğlu*, Ayşe Ecevit, Ali Ulaş Tuğcu, İlkay Erdoğan, Sibel Tulgar Kınık and Aylin Tarcan
Neonatal thyrotoxicosis with severe supraventricular tachycardia: case report and review of the literature Abstract: Neonatal thyrotoxicosis is a rare condition caused by the transplacental passage of thyroid stimulating immunoglobulins from mothers with Graves’ disease. We report a case of neonatal thyrotoxicosis with concurrent supraventricular tachycardia (SVT). The female infant, who was born by section due to breech delivery and meconium in the amniotic fluid at 36 weeks of gestation, presented with tachycardia on day 7. Her heart rate was between 260 and 300 beats/min, and an electrocardiogram revealed ongoing SVT. Sotalol was effective after two cardioversions in maintaining sinus rhythm. Thyroid function studies revealed hyperthyroidism in the infant, and her mother was found to have Graves’ disease. Since symptoms and signs can vary, especially in preterm infants with neonatal hyperthyroidism, we want to emphasize the importance of prenatal care and follow-ups of Graves’ disease associated pregnancies and management of newborns after birth.
Introduction
Keywords: newborn; thyrotoxicosis.
The female infant was born by cesarean section due to breech delivery and meconium in the amniotic fluid with 2470 g birth weight at 36 weeks of gestation. She needed resuscitation with APGAR scores of 4, 6, and 7 at 1, 5, and 10 min, respectively. She was intubated and transferred to the neonatal intensive care unit (NICU). She was in need of mechanical ventilation for 12 h. Then, clinical features of early-onset sepsis and respiratory distress were determined. After taking a blood culture, intravenous ampicillin (100 mg/kg/day) and gentamicin (4 mg/kg/day) treatment was started. On day 7 of her admission, tachycardia was started. Her heart rate was between 260 and 300 beats/min. Electrocardiogram revealed ongoing supraventricular tachycardia (SVT) at a rate of 243 bpm (Figure 1). Treatment was started with vagal stimulation. A plastic bag filled with iced-water was applied on the face and unilateral carotid sinus massage was made. An intravenous adenosine 0.1 mg/kg dose was also administered. Two trials of electric cardioversion of
supraventricular
tachycardia;
DOI 10.1515/jpem-2014-0166 Received April 15, 2014; accepted July 22, 2014; previously published online August 19, 2014
*Corresponding author: Aslıhan Abbasoğlu, MD, Division of Neonatology, Department of Pediatrics, Baskent University Faculty of Medicine, Çankaya/Ankara, Turkey, Phone: +90-312-212-6868, Fax: +90-312-223-7333, E-mail: [email protected] Ayşe Ecevit, Ali Ulaş Tuğcu and Aylin Tarcan: Division of Neonatology, Department of Pediatrics, Başkent University Faculty of Medicine, Ankara, Turkey İlkay Erdoğan: Division of Pediatric Cardiology, Department of Pediatrics, Başkent University Faculty of Medicine, Ankara, Turkey Sibel Tulgar Kınık: Division of Pediatric Endocrinology, Department of Pediatrics, Başkent University Faculty of Medicine, Ankara, Turkey
Neonatal thyrotoxicosis is a rare but potentially fatal thyroid disease, with an incidence of roughly 1 out of 50,000 infants (1). It may have a varied clinical presentation and can range from a totally asymptomatic healthy newborn to the one with severe thyroid storm (2–5). In this case, we report a late preterm infant with neonatal thyrotoxicosis presenting with supraventricular tachycardia (SVT). SVT is the most common significant arrhythmia in neonatal and infancy age group which is characterized by abrupt onset and termination with narrow QRS complexes and a regular RR interval (6). This case report also emphasizes the importance of prenatal care and follow-ups.
Case report
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464 Abbasoğlu et al.: Neonatal thyrotoxicosis with severe supraventricular tachycardia
Figure 1 Electrocardiogram of the case.
1 J/kg were unsuccessful in maintaining a stable sinus rhythm. A dose of 1 mg/kg sotalol was administered orally. Persistent sinus rhythm was obtained 15 min following the start of this therapy. Echocardiography showed a structurally normal heart with a normal ejection fraction. On same day, high thyroxine (T4) of 22.7 ng/dL (0.7–1.48) and low thyroid-stimulating hormone (TSH) levels of 0.005 μIU/mL (1.7–9.1) were determined in the infant’s serum samples. Thyrotropin receptor antibodies (TRAb) were 250 U/L. Laboratory evaluation revealed a white blood count of 11,300/μL with hemoglobin 24.5 g/dL, hematocrit 62%, platelet count 208,000/μL, with normal electrolytes and biochemical parameters. Our patient was diagnosed to have thyroid storm due to thyrotoxicosis. Intensive medical therapy was started with 10 mg/kg/day of propylthiouracil, 1 drop of Lugol’s iodine solution three times per day, 2 mg/kg/day propranolol, and 2 mg/kg/day of oral prednisolone. The short-acting propylthiouracil was the preferred antithyroid drug compared to methimazole, because it has the extra benefit of decreasing the conversion of T4 into T3. On days 2 and 3 of treatment, her heart rate was decreased
to 172 and 130, respectively. After the control of thyroid crisis, propylthiouracil was replaced with methimazole at a dose of 1 mg/kg/day. Lugol’s iodine was discontinued after day 5 of therapy, as serum T4 level decreased to 3.12 ng/dL. In the first week, the dose of steroid was reduced to half. During this time, her tachypnea continued with a respiratory rate between 72 and 80 breaths/min, and tachypnea resolved after 10 days. On day 12 of treatment, she was discharged from hospital on methimazole, propranolol, and prednisolone, with a plan to follow-up in the pediatric-endocrinology outpatient clinic, with a weight of 2650 g and 0.84 ng/dL of serum T4 and 0.004 μIU/mL of TSH. After the diagnosis of neonatal thyrotoxicosis, the mother in our case was found to have hyperthyroidism with TSH: 0.035 μIU/mL (normal: 0.35–4.94). She was immediately started methimazole treatment. On the follow-up visit to the endocrinology outpatient clinic 7 days after the discharge, she was found to be doing well with a normal heart rate and appropriate weight gain. Propranolol and prednisolone treatment were discontinued. Methimazole was gradually
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Abbasoğlu et al.: Neonatal thyrotoxicosis with severe supraventricular tachycardia 465
decreased and eventually discontinued at 2 months of age. Repeated thyroid function tests at 2 and 3 months of age were all normal.
Discussion Neonatal thyrotoxicosis is rare condition caused by the transplacental passage of thyroid stimulating immunoglobulins from mothers with Graves’ disease. Graves’ disease is an autoimmune disorder, characterized by the presence of specific immunoglobulins directed against the TSH receptors in the thyroid gland. It complicates 0.1% to 0.2% of pregnancies. Maternal Graves’ disease is associated with an increased risk of spontaneous abortion, preterm labor, and perinatal mortality (7). The incidence of hyperthyroidism in babies of mothers who require treatment with antithyroid drugs to term may be as high as 22%. The mortality has been reported to be 12%–20%, usually due to heart failure (8). Thyrotoxicosis is the syndrome caused by an excess of free thyroid hormones. Thyroid storm, also referred to as thyrotoxic crisis, is an acute, life-threatening, hypermetabolic state, induced by excessive release of thyroid hormones in individuals with thyrotoxicosis (9, 10). Thyroid storm may be the initial presentation of thyrotoxicosis in undiagnosed children, particularly in neonates (11–13). Symptoms and signs of neonatal thyrotoxicosis can be apparent at birth or may be delayed due to the effect of transplacental passage of maternal antithyroid drugs or effect of coexisting blocking antibodies, but they are apparent by 10 days of life, rarely can be delayed up to 45 days (1). In premature infants like the one in our case, other issues related to prematurity (oxygen requirements, polycythemia, and nutrition) should be considered. These issues both complicate the clinical picture and delay diagnosis and treatment. Smith et al. (13) examined 7 low birth-weight infants with thyrotoxicosis, and in 6 out of the 7 cases, diagnosis was delayed (after day 7). Our case was a late preterm infant with oxygen requirement for 10 days and poor weight gain. The diagnosis of neonatal thyrotoxicosis was made on the day 7. Neonatal thyrotoxicosis often present with hyperkinesis, hyperexcitability, diarrhea, poor weight gain, exophthalmos, hepatosplenomegaly, thrombocytopenia, craniosynostosis, and several cardiac complications including supraventricular tachycardia, cardiomyopathy and congestive cardiac failure (2). In our case, SVT was the initial manifestation of neonatal thyrotoxicosis. The presentation of SVT in the neonate is frequently subtle and may include pallor, cyanosis, restlessness, irritability, feeding difficulty,
tachypnea, and grunting. Besides these symptoms, during the examination of an infant with SVT thyrotoxicosis should be kept in mind (14). Cardiovascular signs of thyrotoxicosis may progress to cardiac failure (15–19). Neonatal SVT can be difficult to control with traditional antiarrhythmic agents (20). Amiodarone is an effective and safe therapy for tachycardia control in infancy, but the iodine released from amiodarone can affect thyroid function. Because of our patient’s status about hyperthyroidism, intravenous amiodaroneinfusion was not preferred. Sotalol is also efficacious in the conversion of acute supraventricular arrhythmia, and in our case, sotalol proved to be effective after two cardioversions in maintaining sinus rhythm afterward (21). Appropriate management of any premature infant exhibiting possible signs of hyperthyroidism should include thorough investigation into past or active thyroid disease in the mother, quantitative assessment of maternal thyrotropin binding inhibitory immunoglobulin (TBII), cord TSH and venous free T4, and TSH (1). Since our patient was in the NICU for prematurity, we were able to observe the manifestations of the hyperthyroidism, and as a result, timely management was instituted. However, in the scenario of a full-term infant with an unknown maternal thyroid history, the patient may be sent home from the nursery and then later present with these signs and symptoms in an emergency department. Physicians in these settings need to keep thyroid disease of the newborn on their list of differential diagnoses. The purpose of presenting this patient is to emphasize the importance of prenatal care and follow-ups. Obstetricians, endocrinologists, and pediatricians need to work together in their management of Graves’ disease associated pregnancies (22, 23).
References 1. Ogilvy-Stuart AL. Neonatal thyroid disorders. Arch Dis Child Fetal Neonatal Ed 2002;87165–71. 2. Batra CM. Fetal and neonatal thyrotoxicosis. Indian J Endocrinol Metab 2013;17:50–4. 3. Zimmerman D. Fetal and neonatal hyperthyroidism. Thyroid 1999;9:727–33. 4. Polak M. Hyperthyroidism in early infancy: pathogenesis, clinical features and diagnosis with a focus on neonatal hyperthyroidism. Thyroid 1998;8:1171–7. 5. Radetti G, Zavallone A, Gentili L, Beck-Peccoz P, Bona G. Foetal and Neonatal thyroid disorders. Minerva Pediatr 2002;54:383–400. 6. Moak JP. Supraventricular tachycardia in the neonate and infant. Prog Pediatr Cardiol 2000;11:25–38. 7. Mestman JH. Hyperthyroidism in pregnancy. Clin Obstet Gynecol 1997;40:45–64.
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466 Abbasoğlu et al.: Neonatal thyrotoxicosis with severe supraventricular tachycardia 8. Mortimer RH, Tyack SA, Galligan JP, Perry-Keene DA, Tan YM. Graves’ disease in pregnancy: TSH receptor binding inhibiting immunoglobulins and maternal and neonatal thyroid function. Clin Endocrinol 1990;32:141–52. 9. Johnstone HC, Dharmaraj P, Cheetham TD. The evaluation and management of thyrotoxicosis. Curr Paediatrics 2004;14:430–37. 10. Mittra ES, Niederkohr RD, Rodriguez C, El-Maghraby T, McDougall IR. Uncommon causes of thyrotoxicosis. J Nucl Med 2008;49:265–78. 11. Nayak B, Burman K. Thyrotoxicosis and thyroid storm. Endocrinol Metab Clin North Am 2006;35:663–86. 12. Bahn Chair RS, Burch HB, Cooper DS, Garber JR, Greenlee MC, et al., American Thyroid Association; American Association of Clinical Endocrinologists. Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists. Thyroid 2011;21:593–646. 13. Smith C, Thomsett M, Choong C, Rodda C, McIntyre HD, et al. Congenital thyrotoxicosis in premature infants. Clin Endocrinol 2001;54:371–76. 14. Hecht T, Brand J, Vlaho S. Encephalopathy and sinus tachycardia in childhood – a possible differential diagnosis. J Pediatr Endocrinol Metab 2012;25:149–51.
15. Lozano HF, Sharma CN. Reversible pulmonary hypertension, tricuspid regurgitation and right-sided heart failure associated with hyperthyroidism: case report and review of the literature. Cardiol Rev 2004;12:299–305. 16. Oden J, Cheifetz IM. Neonatal thyrotoxicosis and persistent pulmonary hypertension necessitating extracorporeal life support. Pediatrics 2005;115:105–8. 17. Woeber KA. Thyrotoxicosis and the heart. N Engl J Med 1992;327:94–8. 18. Skelton CL. The heart and hyperthyroidism: editorial. N Engl J Med 1982;307:1206–8. 19. Fadel BM, Ellahham S, Ringel MD, Lindsay J Jr, Wartofsky L, et al. Hyperthyroid heart disease. Clin Cardiol 2000;23:402–8. 20. Wren C. Cardiac arrhythmias in the fetus and newborn. Semin Fetal Neonatal Med 2006;11:182–90. 21. Wong KK, Potts JE, Etheridge SP, Sanatani S. Medications used to manage supraventricular tachycardia in the infant a North American survey. Pediatr Cardiol 2006;27:199–203. 22. Smith CM, Gavranich J, Cotterill A, Rodda CP. Congenital neonatal thyrotoxicosis and previous maternal radioiodine therapy. Br Med J 2000;320:1260–1. 23. Aslam M, Inayat M. Fetal and neonatal Graves disease: a case report and review of the literature. South Med J 2008;101:840–1.
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