Search Results
Leeds Institute for Cardiovascular and Metabolic Medicine (LICAMM), University of Leeds, Leeds, UK
Search for other papers by Nikolaos Kyriakakis in
Google Scholar
PubMed
Search for other papers by Marilena Giannoudi in
Google Scholar
PubMed
Search for other papers by Satish S Kumar in
Google Scholar
PubMed
Leeds Institute for Cardiovascular and Metabolic Medicine (LICAMM), University of Leeds, Leeds, UK
Search for other papers by Khyatisha Seejore in
Google Scholar
PubMed
Search for other papers by Georgios K Dimitriadis in
Google Scholar
PubMed
Search for other papers by Harpal Randeva in
Google Scholar
PubMed
Leeds Institute of Medical Research, University of Leeds, UK
Search for other papers by Adam Glaser in
Google Scholar
PubMed
Search for other papers by Michelle Kwok-Williams in
Google Scholar
PubMed
Search for other papers by Georgina Gerrard in
Google Scholar
PubMed
Search for other papers by Carmel Loughrey in
Google Scholar
PubMed
Search for other papers by Ahmed Al-Qaissi in
Google Scholar
PubMed
Search for other papers by Ramzi Ajjan in
Google Scholar
PubMed
Search for other papers by Julie Lynch in
Google Scholar
PubMed
Leeds Institute for Cardiovascular and Metabolic Medicine (LICAMM), University of Leeds, Leeds, UK
Search for other papers by Robert D Murray in
Google Scholar
PubMed
Background
Survivors of childhood brain tumours (SCBT) and teenage and young adult cancer survivors have an adverse cardiovascular risk profile, which translates into an increased vascular mortality. Data on cardiovascular risk profiles in SCBT are limited, and furthermore, there are no data in adult-onset (AO) brain tumours.
Patients and
methods: Fasting lipids, glucose, insulin, 24-h blood pressure (BP), and body composition were measured in 36 brain tumour survivors (20 AO; 16 childhood-onset (CO)) and 36 age- and gender-matched controls.
Results
Compared with controls, patients had elevated total cholesterol (5.3 ± 1.1 vs 4.6 ± 1.0 mmol/L, P = 0.007), LDL-C (3.1 ± 0.8 vs 2.7 ± 0.9 mmol/L, P = 0.011), insulin (13.4 ± 13.1 vs 7.6 ± 3.3 miu/L, P = 0.014), and increased insulin resistance (homeostatic model assessment for insulin resistance (HOMA-IR) 2.90 ± 2.84 vs 1.66 ± 0.73, P = 0.016). Patients showed adverse body composition, with increased total body fat mass (FM) (24.0 ± 12.2 vs 15.7 ± 6.6 kg, P < 0.001) and truncal FM (13.0 ± 6.7 vs 8.2 ± 3.7 kg, P < 0.001).
After stratification by timing of onset, CO survivors showed significantly increased LDL-C, insulin, and HOMA-IR compared with controls. Body composition was characterized by the increased total body and truncal FM. Truncal fat mass was increased by 84.1% compared with controls. AO survivors showed similar adverse cardiovascular risk profiles, with increased total cholesterol and HOMA-IR. Truncal FM was increased by 41.0% compared with matched controls (P = 0.029). No difference in mean 24-h BP was noted between patients and controls irrespective of the timing of cancer diagnosis.
Conclusion
The phenotype of both CO and AO brain tumour survivors is characterized by an adverse metabolic profile and body composition, putatively placing long-term survivors at increased risk of vascular morbidity and mortality.