Fetal Adrenal Suppression Due to Maternal Corticosteroid Use: Case Report

Abstract

During pregnancy, steroids are usually used in maternal diseases such as adrenal failure or other autoimmune diseases, e.g. idiopathic thrombocytopenic purpura (ITP), Crohn’s disease, systemic lupus erythematosus, dermatomyositis, scleroderma, Addison’s disease and hyperemesis gravidarum, HELLP syndrome. Endogenous or exogenous maternal steroids are metabolized by the placental enzyme 11 beta-hydroxy steroid dehydrogenase type 2. Prednisolone and methylprednisolone are highly sensitive to this enzyme, while dexamethasone and betamethasone are less well metabolized. Steroids which can cross the placental barrier are administered in cases like fetal lupus, congenital adrenal hyperplasia and for enhancement of fetal lung maturation, whereas steroids used in maternal diseases are usually the ones with low affinity to the placenta; however, in case of long-term use or in high doses, placental enzyme saturation occurs and thus, resulting in fetal adrenal suppression. Antenatal steroids can lead to low birth weight, as observed in our patient. Here, we report a case with fetal adrenal suppression due to maternal methylprednisolone use presenting with early hypoglycaemia and late hyponatremia in neonatal period and requiring three-month replacement therapy. Conflict of interest:None declared.

Immunosuppression in pregnant women with systemic lupus erythematosus

“…Maternal steroids are metabolized by the placental isoenzyme, 11-b-hydroxysteroid dehydrogenase 2. Only inert products of prednisone and analogs cross the placenta [3]. Instead, dexamethasone and betamethasone are less metabolized and may cross the placenta without losing their efficacy, thus favoring low birth weight [4].…”

Neonatal hypoglycemia associated with the antenatal corticosteroids may be secondary to fetal adrenal suppression

“…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 Kurtoglu et al [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.…”

“…The corticosteroids administered during pregnancy or maternal Cushing's syndrome can cause suppression of fetal adrenal glands [3][4][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.…”

Postpartum corticosteroids in HELLP syndrome – standard to prompt recovery

“…The use of the multiple courses is controversial and may potentially harm the foetus. Increased incidence of the cerebral palsy and adrenal suppression of the neonates were described (40,41,42). Recent studies and analysis of Cochrane database reviews do not favour Dexamethason, nor Bethametasone in the management of HELLP and it is estimated, that only new studies can solve this dilemma (43).…”