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

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

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Abstrakt

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. However, in a small group of patients the hypoglycemia can be persistent and may require pancreatectomy. The mechanism of persistent hyperinsulinemic hypoglycemia in this group of patients is unclear.
OriginalsprogEngelsk
TidsskriftJournal of Clinical Endocrinology and Metabolism
Vol/bind90
Udgave nummer7
Sider (fra-til)4376-4382
ISSN0021-972X
DOI
StatusUdgivet - 2005

Fingeraftryk

Dyk ned i forskningsemnerne om 'Hyperinsulinaemic hypoglycaemia in Beckwith-Wiedemann syndrome (BWS) due to defects in the function of pancreatic ß-cell ATP-sensitive K+ channels.'. Sammen danner de et unikt fingeraftryk.

Citationsformater