Growth During Pubertal Induction in Girls With Turner Syndrome: A Retrospective Cohort Analysis

Author:

Nicholls Joshua12ORCID,Harris Mark23,Hughes Ian4,Huynh Tony356,McMahon Sarah K23

Affiliation:

1. Department of Paediatrics, Queensland Children's Hospital , South Brisbane 4101, Queensland , Australia

2. Children's Health Queensland Clinical Unit, Faculty of Medicine, The University of Queensland , South Brisbane 4101, Queensland , Australia

3. Department of Endocrinology and Diabetes, Queensland Children's Hospital , South Brisbane 4101, Queensland , Australia

4. Office for Research Governance and Development, Gold Coast University Hospital , Southport 4215, Queensland , Australia

5. Children's Health Research Centre, Faculty of Medicine, The University of Queensland , South Brisbane 4101, Queensland , Australia

6. Department of Chemical Pathology, Mater Pathology , South Brisbane 4101, Queensland , Australia

Abstract

Abstract Context Patients with Turner syndrome (TS) often present with short stature and ovarian insufficiency. The optimal method of pubertal induction to maximize adult height (AH) is unknown. Objective To identify variables related to pubertal induction that are associated with growth and AH. Methods This retrospective cohort analysis of patients attending a specialized TS clinic at a quaternary children's hospital included patients with TS (n = 107) who attended the clinic between 2015 and 2021. Among them, 51 received estradiol for pubertal induction. Main outcome measures were changes in height SD score (ΔHeightSDS) during pubertal induction and AH. Age at pubertal induction, bone age delay, mid-parental height (MPH), growth hormone treatment, and karyotype were assessed as predictors of AH and ΔHeightSDS. Associations between karyotype and comorbidities were also assessed. Results AH was predicted by MPH (0.8 cm/cm, P = .0001) and bone age delay (−1.84 cm/year, P = .006). ΔHeightSDS was predicted by growth hormone dose (0.09 SDS/mg/m2/week; P = .017), bone age delay (−1.37 SDS/year; P = .003), and age at pubertal induction (0.44 SDS/year; P = .001). There was an interaction between bone age delay and pubertal induction age (P = .013), with the combination of younger age at pubertal induction and a less-delayed bone age associated with a lower ΔHeightSDS. Karyotype did not influence AH or ΔHeightSDS but did affect rates of other comorbidities. Conclusion Decisions around timing of pubertal induction in patients with TS should be tailored to the individual. The current approach to estrogen supplementation needs to be refined in order to facilitate pubertal induction in a physiological manner without compromising height.

Publisher

The Endocrine Society

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