School of Biomedical Sciences cordially invites you to join the following seminar:

Speaker: Dr. Lydia Forestier-Zhang, MBChB, BMedSci(Hons), MRCPCH, School of Medicine and Population Health, Sheffield Children's Hospital
Talk Title: Bone and adrenal complications in paediatric patients living with spinal muscular atrophy

Date: 30 May 2025 (Friday)
Time: 3:00 pm – 4:00 pm
Venue: Seminar Room 1, G/F, Laboratory Block, 21 Sassoon Road
Host: Professor Martin Cheung

Biography

Dr. Lydia Forestier-Zhang moved to the UK from Hong Kong to study medicine at the University of Sheffield in 2008. She undertook an intercalated research degree in paediatric metabolic bone disease based at Sheffield Children’s Hospital, which is where her interest for the specialty and research began. She then completed her academic foundation training years in Oxford where she researched quality of life in rare bone diseases including osteogenesis imperfecta at the University of Oxford. Lydia completed her core paediatric training in London and Manchester before starting her paediatric endocrinology sub-specialty training in Sheffield. She is currently undertaking a PhD at the University of Sheffield, studying bone health and adrenal complications in spinal muscular atrophy.

Abstract

Recently introduced disease modifying treatments have dramatically changed the clinical course of spinal muscular atrophy and improved survival. Children are now encountering more long-term complications secondary to the disease and its new treatments. Bone fragility is a poorly understood complication and whether disease modifying drugs affect bone health outcomes is yet to be determined. Infants and children who receive onasemnogene abeparvovec gene therapy require prolonged high dose steroids which are osteotoxic and can lead to steroid induced adrenal insufficiency. My research aims to describe bone and adrenal complications in the UK paediatric SMA population treated with disease modifying drugs. I am also conducting a pre-clinical study to examine the bone phenotype in SMA mouse models to add to understanding of the pathogenesis of bone fragility.

All are welcome.