http://informahealthcare.com/jmf ISSN: 1476-7058 (print), 1476-4954 (electronic) J Matern Fetal Neonatal Med, Early Online: 1 ! 2014 Informa UK Ltd. DOI: 10.3109/14767058.2014.936002
LETTER TO THE EDITOR
Neonatal hypoglycemia associated with the antenatal corticosteroids may be secondary to fetal adrenal suppression Mustafa Aydin1, Ugur Deveci1, and Nilay Hakan2 J Matern Fetal Neonatal Med Downloaded from informahealthcare.com by Nyu Medical Center on 05/13/15 For personal use only.
1
Department of Pediatrics-division of Neonatology, Elazig Training and Research Hospital, Elazig, Turkey and 2Department of Pediatrics-division of Neonatology, Erzurum Training and Research Hospital, Erzurum, Turkey
Keywords
We read with great interest the article by Pettit et al. [1] that reported the association of antenatal betamethasone with neonatal hypoglycemia and hyperbilirubinemia. They proposed that antenatal corticosteroid administration may cause maternal hyperglycemia, and then maternal hyperglycemia leads to fetal pancreatic beta cell hyperplasia/hyperinsulinemia and subsequent neonatal hypoglycemia [1]. The advocated possible mechanism of corticosteroid-induced hyperglycemia in mothers is directly promotion of hepatic gluconeogenesis, thus hyperglycemia [2]. However, secondary fetal adrenal suppression may be another, possibly the main, mechanism for neonatal hypoglycemia due to antenatal corticosteroids which never mentioned by the authors in their article. The corticosteroids administered during pregnancy or maternal Cushing’s syndrome can cause suppression of fetal adrenal glands [3–5]. During pregnancy taken high doses and/or long period prednisolone and methylprednisolone itself can saturate the placental enzymes and, as a result, large amount of corticosteroids can cross the placental barrier causing significant suppression of the fetal adrenal glands. So, the neonate develops hyponatremia, hypoglycemia and hypotension due to adrenal gland insufficiency which becomes prominent on postnatal day three [5]. Saulnier et al. [4] reported a case of neonatal acute adrenal insufficiency following the administration of low-doses corticosteroid during pregnancy. Similarly, a case of fetal adrenal suppression due to maternal methylprednisolone use presenting with early hypoglycemia and late hyponatremia in neonatal period and requiring three-month replacement therapy reported by Kurtog˘lu et al. [5].
Address for correspondence: Dr. Mustafa Aydin, Neonatology, Department of Pediatrics, Elazig Training _ ¨ nu¨ Cad. No: 74, Elazig, Hospital, Rızaiye Mah. Ino +90(424)238 10 00. Fax: +90(424)212 14 [email protected]
Division of and Research Turkey. Tel: 61. E-mail:
Antenatal corticosteroid, adrenal suppression, betamethasone, fetus, maternal hyperglycemia, neonatal hypoglycemia History Received 25 May 2014 Accepted 15 June 2014 Published online 3 July 2014
In conclusion, corticosteroid use in pregnancy may cause to fetal adrenal suppression and thus would be the main reason of presenting neonatal hypoglycemia. Therefore, primary or secondary hypoadrenalism should be taken in mind in the etiology of neonatal hypoglycemia.
References 1. Pettit KE, Tran SH, Lee E, Caughey AB. The association of antenatal corticosteroids with neonatal hypoglycemia and hyperbilirubinemia. J Matern Fetal Neonatal Med 2014;27:683–6. 2. Mazziotti G, Gazzaruso C, Giustina A. Diabetes in Cushing syndrome: basic and clinical aspects. Trends Endocrinol Metab 2011;22:499–506. 3. Homar V, Grosek S, Battelino T. High-dose methylprednisolone in a pregnant woman with Crohn’s disease and adrenal suppression in her newborn. Neonatology 2008;94:306–9. 4. Saulnier PJ, Piguel X, Perault-Pochat MC, et al. Hypoglycemic seizure and neonatal acute adrenal insufficiency after maternal exposure to prednisone during pregnancy: a case report. Eur J Pediatr 2010;169:763–5. 5. Kurtog˘lu S, Sarıcı D, Akın MA, et al. Fetal adrenal suppression due to maternal corticosteroid use: case report. J Clin Res Pediatr Endocrinol 2011;3:160–2.
LETTER TO THE EDITOR
Neonatal hypoglycemia associated with the antenatal corticosteroids may be secondary to fetal adrenal suppression Mustafa Aydin1, Ugur Deveci1, and Nilay Hakan2 J Matern Fetal Neonatal Med Downloaded from informahealthcare.com by Nyu Medical Center on 05/13/15 For personal use only.
1
Department of Pediatrics-division of Neonatology, Elazig Training and Research Hospital, Elazig, Turkey and 2Department of Pediatrics-division of Neonatology, Erzurum Training and Research Hospital, Erzurum, Turkey
Keywords
We read with great interest the article by Pettit et al. [1] that reported the association of antenatal betamethasone with neonatal hypoglycemia and hyperbilirubinemia. They proposed that antenatal corticosteroid administration may cause maternal hyperglycemia, and then maternal hyperglycemia leads to fetal pancreatic beta cell hyperplasia/hyperinsulinemia and subsequent neonatal hypoglycemia [1]. The advocated possible mechanism of corticosteroid-induced hyperglycemia in mothers is directly promotion of hepatic gluconeogenesis, thus hyperglycemia [2]. However, secondary fetal adrenal suppression may be another, possibly the main, mechanism for neonatal hypoglycemia due to antenatal corticosteroids which never mentioned by the authors in their article. The corticosteroids administered during pregnancy or maternal Cushing’s syndrome can cause suppression of fetal adrenal glands [3–5]. During pregnancy taken high doses and/or long period prednisolone and methylprednisolone itself can saturate the placental enzymes and, as a result, large amount of corticosteroids can cross the placental barrier causing significant suppression of the fetal adrenal glands. So, the neonate develops hyponatremia, hypoglycemia and hypotension due to adrenal gland insufficiency which becomes prominent on postnatal day three [5]. Saulnier et al. [4] reported a case of neonatal acute adrenal insufficiency following the administration of low-doses corticosteroid during pregnancy. Similarly, a case of fetal adrenal suppression due to maternal methylprednisolone use presenting with early hypoglycemia and late hyponatremia in neonatal period and requiring three-month replacement therapy reported by Kurtog˘lu et al. [5].
Address for correspondence: Dr. Mustafa Aydin, Neonatology, Department of Pediatrics, Elazig Training _ ¨ nu¨ Cad. No: 74, Elazig, Hospital, Rızaiye Mah. Ino +90(424)238 10 00. Fax: +90(424)212 14 [email protected]
Division of and Research Turkey. Tel: 61. E-mail:
Antenatal corticosteroid, adrenal suppression, betamethasone, fetus, maternal hyperglycemia, neonatal hypoglycemia History Received 25 May 2014 Accepted 15 June 2014 Published online 3 July 2014
In conclusion, corticosteroid use in pregnancy may cause to fetal adrenal suppression and thus would be the main reason of presenting neonatal hypoglycemia. Therefore, primary or secondary hypoadrenalism should be taken in mind in the etiology of neonatal hypoglycemia.
References 1. Pettit KE, Tran SH, Lee E, Caughey AB. The association of antenatal corticosteroids with neonatal hypoglycemia and hyperbilirubinemia. J Matern Fetal Neonatal Med 2014;27:683–6. 2. Mazziotti G, Gazzaruso C, Giustina A. Diabetes in Cushing syndrome: basic and clinical aspects. Trends Endocrinol Metab 2011;22:499–506. 3. Homar V, Grosek S, Battelino T. High-dose methylprednisolone in a pregnant woman with Crohn’s disease and adrenal suppression in her newborn. Neonatology 2008;94:306–9. 4. Saulnier PJ, Piguel X, Perault-Pochat MC, et al. Hypoglycemic seizure and neonatal acute adrenal insufficiency after maternal exposure to prednisone during pregnancy: a case report. Eur J Pediatr 2010;169:763–5. 5. Kurtog˘lu S, Sarıcı D, Akın MA, et al. Fetal adrenal suppression due to maternal corticosteroid use: case report. J Clin Res Pediatr Endocrinol 2011;3:160–2.
