BSPED2013 Poster Presentations (1) (89 abstracts)
Increasing weight in children with congenital hyperinsulinism is linked to KATP channel gene mutations
Zainaba Mohamed 1 , Rajesh Chidanandaswamy 1 , Abigail Swancott 1 , Caroline Steele 1 , Philip Murray 1 , Lindsey Rigby 1 , Raja Padidela 1 , Sarah Ehtisham 1 , Mars Skae 1 , Leena Patel 1 , Sian Ellard 4 , Mohammed Didi 5 , Karen E Cosgrove 3 , Mark Dunne 3 , Indi Banerjee 1 & Peter Clayton 2
1Department of Paediatric Endocrinology, Royal Manchester Children’s Hospital, Manchester, UK; 2Faculty of Medical and Human Sciences, University of Manchester, Manchester, UK; 3Faculty of Life Sciences, University of Mancheser, Manchester, UK; 4Molecular Genetics, Royal Devon and Exeter NHS Foundation Trust, Exeter, UK; 5Department of Paediatric Endocrinology, Alder Hey Children’s NHS Foundation Trust, Liverpool, UK.
Introduction: Congenital hyperinsulinism (CHI) is a cause of severe hypoglycaemia due to insulin over-secretion. The medical management of CHI involves supplementary glucose, which combined with insulin excess, may be obesogenic. However, increased weight in CHI patients has not been reported. We have investigated if children with CHI increase in weight and if genetic or treatment factors influence the weight trajectory.
Methods: Weights were measured and expressed as SDS in children with CHI at birth (n=70) and at ages 1 (n=51), 2 (n=44), 3 (n=30) and 4 (n=23) years. Weight SDS at follow-up was tested for correlation with ATP-sensitive K+ channel (KATP) gene mutation status (n=65) and with treatment variables, which included medical/surgical treatment, resolution of CHI, supplemental glucose and response to diazoxide, in a backward regression model.
Results: Weight SDS increased from birth (median (range) −0.2 (−4.4; 5.7)) to ages 2 (+0.1 (−3.7; +5.0)), 3 (+0.5 (−2.2; +2.9) and 4 (+0.5 (−3.3; +3.1)) years. The weight increment was most significant at age 2 years (P=0.02). KATP channel mutations, either heterozygous or homozygous, were present in 25 (39%) children. Children with mutations were heavier at birth (P<0.001) and remained so at 2 years (P=0.02). Mutation status, but not treatment variables were correlated with weight SDS at 2 years (R2=0.5, p=0.004) implying that genetic factors alone may associate with an increased weight trajectory in CHI.
Conclusions: Weight SDS may increase in the first 2 years of life, which is correlated with KATP channel mutation status but not to the treatment of CHI. Further follow-up is required to assess if weight trajectory in later childhood leads to obesity.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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