Diabetes Care
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Diabetes Care 30:e104 2007
DOI: 10.2337/dc07-1318
© 2007 by the American Diabetes Association
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Online Letters: Observations

Early Glibenclamide Treatment in a Clinical Newborn With KCNJ11 Gene Mutation

Gerhard Däublin, MD1, Bettina Lorenz-Depiereux, PHD2,3, Tim M. Strom, MD2,3, Oliver Blankenstein, MD4 and Klemens Raile, MD4

1 Children's Hospital Aurich, Aurich, Germany
2 GSF National Research Center for Environment and Health, Munich-Neuherberg, Germany
3 Institute of Human Genetics, Technical University, Munich, Germany
4 Department of Pediatric Endocrinology and Diabetes, Charité Campus Virchow, Berlin, Germany

Address correspondence to Klemens Raile, MD, Department of Pediatric Endocrinology and Diabetes, Charité Children's Hospital, Augustenburger Platz 1, 13353 Berlin, Germany. E-mail: klemens.raile@charite.de

The first 20% of the full text of this article appears below.

Activating mutations in the KCNJ11 gene, which code for the ATP-sensitive K+ channel subunit Kir6.2, are the most common cause of permanent neonatal diabetes. Recently, a switch from insulin treatment to oral sulfonylurea has been proposed if genetic testing reveals sulfonylurea-sensitive KCNJ11 mutations (1). Until now, hurdles for early treatment were 1) the time until the mutation analysis is finished and 2) the lack of knowledge about adverse effects . . . [Full Text of this Article]


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Copyright © 2007 by the American Diabetes Association.