Fetal macrosomia and neonatal hyperinsulinemic hypoglycemia associated with transplacental transfer of sulfonylurea in a mother with KCNJ11-related neonatal diabetes

Nele Myngheer, Karel Allegaert, Andrew Hattersley, Tim McDonald, Holger Kramer, Frances M. Ashcroft, Johan Verhaeghe, Chantal Mathieu, Kristina Casteels*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

20 Citations (Scopus)
15 Downloads (Pure)

Abstract

OBJECTIVE:
Sulfonylureas (SUs) are effective at controlling glycemia in permanent neonatal diabetes mellitus (PNDM) caused by KCNJ11 (Kir6.2) mutations.

RESEARCH DESIGN AND METHODS:
We report the case of a woman with PNDM who continued high doses of glibenclamide (85 mg/day) during her pregnancy. The baby was born preterm, and presented with macrosomia and severe hyperinsulinemic hypoglycemia requiring high-rate intravenous glucose infusion.

RESULTS:
Postnatal genetic testing excluded a KCNJ11 mutation in the baby. Glibenclamide was detected in both the baby's blood and the maternal milk.

CONCLUSIONS:
We hypothesize that high doses of glibenclamide in the mother led to transplacental passage of the drug and overstimulation of fetal β-cells, which resulted in severe hyperinsulinemic hypoglycemia in the neonate (who did not carry the mutation) and contributed to fetal macrosomia. We suggest that glibenclamide (and other SUs) should be avoided in mothers with PNDM if the baby does not carry the mutation or if prenatal screening has not been performed, while glibenclamide may be beneficial when the fetus is a PNDM carrier.

Original languageEnglish
Pages (from-to)3333-3335
Number of pages3
JournalDiabetes Care
Volume37
Issue number12
DOIs
Publication statusPublished - 1 Dec 2014
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2014 by the American Diabetes Association.

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