Endocrine Abstracts (2015) 38 P156 | DOI: 10.1530/endoabs.38.P156

Adverse metabolic profile in long-term survivors of adult and childhood-onset brain tumours: the role of growth hormone deficiency

Julie Lynch1, Nikolaos Kyriakakis1,2, Satish S Kumar1, Ramzi Ajjan2, Georgina Gerrard3, Carmel Loughrey3, Adam Glaser4 & Robert D Murray1,2


1Leeds Centre for Diabetes and Endocrinology, St James’s University Hospital, Leeds, UK; 2Division of Cardiovascular and Diabetes Research, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, UK; 3Clinical Oncology, Leeds Cancer Centre, St James’s University Hospital, Leeds, UK; 4Paediatric Haematology and Oncology, Leeds Teaching Hospitals NHS Trust, Leeds, UK.


Introduction: Childhood-onset brain tumour (CO-BT) survivors demonstrate elevated standardized mortality rates for cardiac disease. Adverse lipid profile and body composition contribute to the increased cardiovascular risk. Little is known about the metabolic changes in long-term survivors of adult-onset brain tumours (AO-BT).

Methods: We performed a cross-sectional study to compare cardiovascular risk parameters in CO-BT with AO-BT survivors and healthy controls. Measurements of lipid profile, fasting glucose and body composition were performed. Basal anterior pituitary hormone profile and dynamic tests (ITT or GST) were also undertaken.

Results: patients with AO-BT (mean age 39.5±13.2 years), 17 patients with CO-BT (mean age 20.4±4.9 years) and 36 healthy controls were assessed. All patients received cranial radiotherapy. 89.5% (17/19) of adult-onset and 94.1% (16/17) of childhood-onset patients developed growth hormone deficiency (GHD), partial or severe. No difference in the lipid profile and body composition was noted between the AO-BT and CO-BT groups. Fasting glucose was higher in the adult-onset compared with the childhood-onset group (5.07±0.99 mmol/l vs 4.56±0.33 mmol/l, P=0.04), however no difference was observed in the HbA1c. Patients with GHD, not on GH replacement, demonstrated significantly elevated total (5.64±1.06 mmol/l vs 4.66±0.9 mmol/l, P=0.004) and LDL cholesterol (3.28±0.66 mmol/l vs 2.76±0.82 mmol/l, P=0.016), BMI (28.3±6.6 vs 24.8±3.5, P=0.046), waist/hip ratio (0.89±0.07 vs 0.82±0.07, P=0.001) total (26.6±12.5 kg vs 15.4±7.5 kg, P=0.001) and truncal (14.76±6.35 kg vs 8.1±4.1 kg, P<0.001) fat mass and skinfold thickness (78.9±33.1 mm vs 41.32±17.2 mm P<0.001), compared with controls. On the contrary, patients on GH replacement did not differ for the above parameters from controls, with the exception of summative skinfold thickness, which was higher in the patient group (73.95±31.03 mm vs 45.38±14.18 mm, P=0.038).

Conclusions: Our results demonstrate an adverse cardiovascular risk profile in long-term brain tumour survivors of both adult and childhood onset. GHD has a pivotal role in patients’ metabolic status, while GH therapy improves most of the metabolic parameters.

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