hrp0084p3-744 | Diabetes | ESPE2015

Transition During Adolescence, is there Room to Improve?

Glackin Sinead , Molloy Sinead , Neylon Orla

Background: Transition is a difficult period for adolescents with type 1 diabetes. The non-linear development of the adolescent brain along with increasing insulin resistance, increasing autonomy and risk of psychopathology means that adolescents are vulnerable to poor mental and physical health and ensuing deterioration in metabolic control. It is also during this period of turmoil that adolescents often transfer from paediatric to adult services.Object...

hrp0098p1-38 | Diabetes and Insulin 2 | ESPE2024

A Retrospective Analysis of Cost of Admission Care in Children with First Presentation of T1D at University Hospital Limerick: Assessing the Feasibility of Ambulatory Care

Angela Dockery Lucy , McCaffrey Alison , Neylon Orla , O' Gorman Clodagh

Introduction: Currently in Ireland, the majority of children are admitted to hospital for education at initial diagnosis, regardless of diabetic ketoacidosis (DKA) status. ISPAD 2022 suggests that outpatient management for metabolically stable patients is a feasible management option if adequate resources are available. This study assesses the feasibility of such management in the University of Limerick (UHL) Paediatric Department by quantifying the care and e...

hrp0098fc14.5 | Fetal and Neonatal Endocrinology | ESPE2024

A novel 94bp deletion in the SLC16A1 promoter causes fasting and exercise-induced hyperinsulinaemic hypoglycaemia

Hopkins Jasmin , Mannisto Jonna , Hopkinson Jessica , Wakeling Matthew , Costigan Colm , Crowley Rachel , Gibney James , Faiz Muhamad Muhammad , Neylon Orla , O'Shea Donal , Okiro Julie , Palmer Elizabeth , Swann Niall , Houghton Jayne , Otonkoski Timo , Flanagan Sarah

Background: In 2007, non-coding variants in the promoter of SLC16A1, a beta-cell disallowed gene, were reported as a novel genetic cause of exercise-induced hyperinsulinism (HI). In this study, three different promoter variants were identified in 13 affected individuals from three families. It was proposed that these variants caused MCT1, which is encoded by SLC16A1, to be inappropriately expressed in the pancreatic beta cells resulting in insulin secretion in...