Hyperinsulinaemic hypoglycaemia in Beckwith-Wiedemann syndrome (BWS) due to defects in the function of pancreatic ß-cell ATP-sensitive K+ channels

Autor: Hussain, K, Cosgrove, K E, Shepherd, R M, Luharia, A, Smith, Valdemar, Kassem, S, Gregory, J W, Sivaprasadarao, A, Christesen, H T, Jacobsen, B B, Brusgaard, K, Glaser, B, Maher, E A, Lindley, K J, Hindmarsh, P, Dattani, M, Dunne, M J

Publikováno v: Hussain, K, Cosgrove, K E, Shepherd, R M, Luharia, A, Smith, V, Kassem, S, Gregory, J W, Sivaprasadarao, A, Christesen, H T, Jacobsen, B B, Brusgaard, K, Glaser, B, Maher, E A, Lindley, K J, Hindmarsh, P, Dattani, M & Dunne, M J 2005, ' Hyperinsulinaemic hypoglycaemia in Beckwith-Wiedemann syndrome (BWS) due to defects in the function of pancreatic ß-cell ATP-sensitive K+ channels. ', Journal of Clinical Endocrinology and Metabolism, vol. 90, no. 7, pp. 4376-4382 . https://doi.org/10.1210/jc.2005-0158

Beckwith-Wiedemann syndrome (BWS) is a congenital overgrowth syndrome that is clinically and genetically heterogeneous. Hyperinsulinemic hypoglycemia occurs in about 50% of children with BWS and, in the majority of infants, it resolves spontaneously.

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