Permanent Neonatal Diabetes in a Patient with a KCNJ11/Q52R Mutation Accompanied by Intermittent Hypoglycemia and Liver Failure
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Updated: Jun 18, 2026

Isolation of Neonatal Extrahepatic Cholangiocytes
Published on: June 5, 2014
Natalie D Shaw1, Joseph A Majzoub
1Division of Endocrinology, Department of Medicine, Children's Hospital Boston, 300 Longwood Avenue, Boston, MA 02115, USA.
Abstract:
The most common monogenic cause of neonatal diabetes is mutation in KCNJ11, which encodes a potassium channel in pancreatic beta cells. Some mutations in this gene, including Q52R, have been described in association with neurological deficits, but never with hepatic involvement. We report the second case of neonatal diabetes in a patient with a KCNJ11/Q52R mutation. This patient's clinical course did not include obvious neurological deficits despite the presence of prematurity, but did include transient hyperbilirubinemia, and recurrent hypoglycemia. The phenotypic spectrum of KCNJ11 mutations is variable and is likely influenced by additional genetic and environmental factors.
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