Abstract
Permanent neonatal diabetes (PND) is a rare disease characterized by hyperglycemia diagnosed within the first 6 months of life (1). Activating mutation of the KCNJ11 gene encoding Kir6.2 subunit of the ATP-potassium (KATP) channel has been described as the most frequent cause of PND. Under physiologic circumstances, KATP channel closure plays a central role in glucose-stimulated insulin secretion from pancreatic β-cells. Sulfonylureas (SUs) stimulate insulin secretion by closing KATP channels via an ATP-independent mechanism. Since 2004, SUs are best choice of treatment in PND with such mutations and allow better glycemic control in children and adults than insulin (2). Some authors report that adult patients are unable to switch successfully from insulin to SU and that the doses required to get the insulin independence are higher (3,4). We present our …
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