BSPED2025 Poster Presentations Adrenal 1 (10 abstracts)
Cortisol response to hypoglycaemia in infants with congenital hyperinsulinism: a single centre retrospective cohort 2015-2025
Francesca McFarland 1 , Zoe Yung 2 , Kelly Cassidy 2 , Joanne Blair 2 , David Cullingford 2 , Senthil Senniappan 2 , Daniel Chan 3 , Mohammed Didi 2 , Harshini Katugampola 3 & Julie Park 2
1University of Liverpool, Liverpool, United Kingdom; 2Alder Hey Children’s Hospital, Liverpool, United Kingdom; 3Great Ormond Street Hospital, London, United Kingdom
Background: In congenital hyperinsulinism (CHI), inappropriate, excessive insulin secretion leads to recurrent severe hypoglycaemia with risk of seizures and neurodevelopmental injury. Cortisol is a key counter regulatory hormone, yet published data suggests blunting of the cortisol response in hyperinsulinemic hypoglycaemia.
Aim & Methods: We retrospectively reviewed infants <6 months with CHI managed at Alder Hey Children’s Hospital (2015–2025). Inclusion required paired glucose (<3 mmol/l), and cortisol sampled at the time of hypoglycaemia; demographic and biochemical data plus short Synacthen test (SST) results were extracted. A normal response was a peak cortisol of >500 nmol/l.
Results: Eighty three infants were screened; fifty met inclusion criteria (complete glucose and cortisol dataset). (30 male; mean birthweight 2.82 kg; mean gestation 36 w; 14/50 maternal diabetes; 50 diagnosed with CHI - 7 persistent, 43 transient). Mean cortisol during hypoglycaemia was 369 nmol/l. Distribution: <100 nmol/l (n = 12), 100–150 nmol/l (n = 7), >150 nmol/l (n = 31; mean 497 nmol/l). SST data (subset): 14/18 (78%) showed normal adrenal reserve on initial Synacthen testing; failures in 4 infants (<100:3/8; >150:1/7; 100–150:0/3). These patients received hydrocortisone therapy, which was discontinued in every case, as no infant had evidence of persistent adrenal insufficiency by 21 months. Among infants with cortisol <150 nmol/l (n = 19), 6 had birthweight <2.5 kg, 6 were premature, and 7 had maternal diabetes, suggesting vulnerability of an immature HPA axis and/or low cortisol binding proteins in early life.
Conclusions: Infants with CHI commonly exhibit a suboptimal cortisol response during spontaneous hypoglycaemia, yet most have intact adrenal capacity on stimulation testing with ACTH and recover if initially insufficient. SST should be reassessed for those commenced on hydrocortisone, as it frequently normalises on repeat testing. Apparent adrenal dysfunction may be developmentally mediated and was transient in this cohort. Our findings highlight the need for further research into the maturation of the hypothalamic-pituitary-adrenal axis in neonates, including how it may be influenced in the context of hyperinsulinism.
Volume 111
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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