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Background:  Recessive mutations in  ABCC8/KCNJ11  of β-cell K ATP  channel generally cause severe medically unresponsive hyperinsulinemic hypoglycemia (HH). Rarer dominant mutations in these genes have been described that mostly cause milder, medically responsive congenital hyperinsulinism. Rarer dominant mutations in these genes have been described that mostly cause milder, medically responsive congenital hyperinsulinism. To date the phenotype of patients with dominant mutations seems to be different from those with recessive mutations as the majority of patients are responsive to diazoxide therapy. Controversy exists on whether these dominant  ABCC8 or KCNJ11  genes mutations predispose to diabetes mellitus in adulthood or not.

journal of pediatric endocrinology and metabolism/journal of pediatric endocrinology and metabolism

Clinical characteristics of recessive and dominant congenital hyperinsulinism due to mutation(s) in the  ABCC8 / KCNJ11  genes encoding the ATP-sensitive potasium channel in the pancreatic beta cell