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

doi:10.1210/jc.2005-0158

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 tidsskrift › Tidsskriftartikel › Forskning › peer review

Abstract

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.

Originalsprog	Engelsk
Tidsskrift	The Journal of Clinical Endocrinology & Metabolism
Vol/bind	90
Udgave nummer	7
Sider (fra-til)	4376-4382
ISSN	0021-972X
DOI	https://doi.org/10.1210/jc.2005-0158
Status	Udgivet - 2005

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10.1210/jc.2005-0158

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Citationsformater

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. The Journal of Clinical Endocrinology & Metabolism, 90(7), 4376-4382. https://doi.org/10.1210/jc.2005-0158

@article{fd5a6390ddda11db9628000ea68e967b,

title = "Hyperinsulinaemic hypoglycaemia in Beckwith-Wiedemann syndrome (BWS) due to defects in the function of pancreatic {\ss}-cell ATP-sensitive K+ channels.",

abstract = "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.",

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

year = "2005",

doi = "10.1210/jc.2005-0158",

language = "English",

volume = "90",

pages = "4376--4382",

journal = "The Journal of Clinical Endocrinology \& Metabolism",

issn = "0021-972X",

publisher = "Endocrine Society",

number = "7",

}

Hussain, K, Cosgrove, KE, Shepherd, RM, Luharia, A, Smith, V, Kassem, S, Gregory, JW, Sivaprasadarao, A, Christesen, HT, Jacobsen, BB, Brusgaard, K, Glaser, B, Maher, EA, Lindley, KJ, Hindmarsh, P, Dattani, M & Dunne, MJ 2005, 'Hyperinsulinaemic hypoglycaemia in Beckwith-Wiedemann syndrome (BWS) due to defects in the function of pancreatic ß-cell ATP-sensitive K+ channels.', The Journal of Clinical Endocrinology & Metabolism, bind 90, nr. 7, s. 4376-4382. https://doi.org/10.1210/jc.2005-0158

Hyperinsulinaemic hypoglycaemia in Beckwith-Wiedemann syndrome (BWS) due to defects in the function of pancreatic ß-cell ATP-sensitive K+ channels. / Hussain, K; Cosgrove, K E; Shepherd, R M et al.
I: The Journal of Clinical Endocrinology & Metabolism, Bind 90, Nr. 7, 2005, s. 4376-4382.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

TY - JOUR

T1 - Hyperinsulinaemic hypoglycaemia in Beckwith-Wiedemann syndrome (BWS) due to defects in the function of pancreatic ß-cell ATP-sensitive K+ channels.

AU - Hussain, K

AU - Cosgrove, K E

AU - Shepherd, R M

AU - Luharia, A

AU - Smith, Valdemar

AU - Kassem, S

AU - Gregory, J W

AU - Sivaprasadarao, A

AU - Christesen, H T

AU - Jacobsen, B B

AU - Brusgaard, K

AU - Glaser, B

AU - Maher, E A

AU - Lindley, K J

AU - Hindmarsh, P

AU - Dattani, M

AU - Dunne, M J

PY - 2005

Y1 - 2005

N2 - 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.

AB - 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.

U2 - 10.1210/jc.2005-0158

DO - 10.1210/jc.2005-0158

M3 - Journal article

C2 - 15811927

SN - 0021-972X

VL - 90

SP - 4376

EP - 4382

JO - The Journal of Clinical Endocrinology & Metabolism

JF - The Journal of Clinical Endocrinology & Metabolism

IS - 7

ER -

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

Abstract

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