BSPED2011 Oral Communications Oral Communications 3 (4 abstracts)
The impact of GH deficiency (GHD) and GH treatment (GHTx) on cardiovascular risk in survivors of bone marrow transplantation with total body irradiation (BMT/TBI) in childhood
Nikki Davis 2 , Michael Stevens 1 , Jacqueline Cornish 1 , Claire Stewart 3 , Andrew Moss 3 , Wolf Woltersdorf 1 , Ruth Elson 1 & Elizabeth Crowne 1
1Bristol University Hospitals NHS Foundation Trust, Bristol, UK; 2Southampton University Hospitals NHS Trust, Southampton, UK; 3Manchester Metropolitan University, Manchester, UK.
Introduction: Survivors of childhood BMT/TBI have increased cardiovascular morbidity and GH deficiency (GHD). We aimed to investigate the relationship between cardiovascular risk and GHD and GHTx in BMT/TBI survivors.
Methods: BMT/TBI survivors (n=36) and non-BMT control subjects (n=19) were sub-divided according to GH status assessed by insulin tolerance test: i) survivors with untreated GHD (N=18,11M), ii) survivors on GHTx (N=18,10M), iii) controls with untreated GHD (N=7,5M), iv) controls with normal GH status (N=12,8M). All had body composition assessment (DEXA), and fasted lipids, insulin, glucose, leptin, adiponectin, and IL6.
Results: Results were expressed as mean (S.D.) or geometric mean (range). The ages of the groups were 1.17.1 (6.1–23.5), 2.14.7 (10.9–24.5), 3.12.2 (7.9–15.6) and 4.16.3 (7.8–20.1) years. Survivors with untreated GHD demonstrated increased central adiposity compared with normal controls using LSD but not the more stringent Scheffe test due to group size and heterogeneity (% trunk fat 33.4 (13.4) vs (22.2 (11.1), P=0.04). Survivors on GHTx had higher fasted insulin (15.0 (2.6–68.3) vs 5.2 (0.1–48.1) μIU/l, P=0.05) and HOMAR (3.29 (0.53–18.31) vs 1.11 (0.02–10.48), P=0.05) than survivors with untreated GHD. They also had higher total cholesterol (4.9 (0.8) vs 3.6 (0.7) mmol/l, P=0.001) and triglycerides (1.6 (0.5–4.8) vs 0.8 (0.5–1.6) mmol/l, P=0.03) compared to normal controls and higher triglycerides than controls with isolated GHD (1.6 (0.5–4.8) vs 0.7 (0.5–1.4) mmol/l, P=0.05). Leptin and adiponectin were not different. IL6 was reduced in all groups with GHD i) <0.05 (<0.05–4.73), P=0.01, ii) <0.05 (<0.05–14.04), P=0.01, and iii) <0.05 (<0.05–19.18, P=0.05) compared to normal controls (5.92 (<0.05–39.8) pg/ml).
Conclusion: Adverse cardiovascular profiles persisted in survivors on GHTx, indicating additional factors are involved and alternative strategies targeting cardiovascular risk are needed to improve long-term outcome.
Volume 27
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Endocrine Abstracts
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